Artykuły w czasopismach: „Intracellular redox homeostasis”

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Colgan, Stephen M., i Richard C. Austin. "Homocysteinylation of Metallothionein Impairs Intracellular Redox Homeostasis". Arteriosclerosis, Thrombosis, and Vascular Biology 27, nr 1 (styczeń 2007): 8–11. http://dx.doi.org/10.1161/01.atv.0000254151.00086.26.

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Süzen, Sibel, Mehmet C. Atayik, Hanif Sirinzade, Bita Entezari, Hande Gurer-Orhan i Ufuk Cakatay. "Melatonin and redox homeostasis". Melatonin Research 5, nr 3 (30.09.2022): 304–24. http://dx.doi.org/10.32794/mr112500134.

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Redox homeostasis and redox signaling are constituents of preservation of a normal physiological state. Whereas the equilibrium between oxidants and nucleophiles is conserved in redox homeostasis, oxidative stress promotes the formation of a radically altered redox state. It is known that modification of circadian clock may lead to severe alteration in redox balance. Melatonin [N-acetyl-5-methoxytryptamine, (MLT)] regulates numerous physiological functions including circadian rhythm, sleep-wake cycle, gonadal activity, redox homeostasis, neuroprotection, immune-modulation, and anticancer activity in organisms. Insufficient MLT production is closely related to development of aging process, tumorigenesis, visceral adiposity, neurodegenerative disorders, etc. Reactive oxygen species (ROS) are not intrinsically harmful or beneficial in cellular redox metabolism. Redox homeostasis is an integrative status for both of the hormetic response to ROS overproduction and subsequent redox signaling. MLT and its derivatives are traditionally classified as hormone-like substances. Their redox sensitive regulatory activity and direct interaction with intracellular ROS serve as second messenger in cell signaling. This review involves the role of redox homeostasis in the pathogenesis of age-related disorders and its relationship with MLT, therefore, targeting the circadian rhythm may propose new therapeutic approach for these disorders.

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Merker, Marilyn P., Bruce R. Pitt, Augustine M. Choi, Paul M. Hassoun, Christopher A. Dawson i Aron B. Fisher. "Lung redox homeostasis: emerging concepts". American Journal of Physiology-Lung Cellular and Molecular Physiology 279, nr 3 (1.09.2000): L413—L417. http://dx.doi.org/10.1152/ajplung.2000.279.3.l413.

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This symposium was organized to present some aspects of current research pertaining to lung redox function. Focuses of the symposium were on roles of pulmonary endothelial NADPH oxidase, xanthine oxidase (XO)/xanthine dehydrogenase (XDH), heme oxygenase (HO), transplasma membrane electron transport (TPMET), and the zinc binding protein metallothionein (MT) in the propagation and/or protection of the lung or other organs from oxidative injury. The presentations were chosen to reflect the roles of both intracellular (metallothionein, XO/XDH, and HO) and plasma membrane (NADPH oxidase, XO/XDH, and unidentified TPMET) redox proteins in these processes. Although the lung endothelium was the predominant cell type under consideration, at least some of the proposed mechanisms operate in or affect other cell types and organs as well.

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Monti, Daria Maria, Nicola Montesano Gesualdi, Josef Matoušek, Franca Esposito i Giuseppe D’Alessio. "The cytosolic ribonuclease inhibitor contributes to intracellular redox homeostasis". FEBS Letters 581, nr 5 (6.02.2007): 930–34. http://dx.doi.org/10.1016/j.febslet.2007.01.072.

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Bagur Quetglas, Rafaela, Péter Várnai, Gyorgy Csordás i Gyorgy Hajnóczky. "Effect of Arsenic on Intracellular Calcium & Redox Homeostasis". Biophysical Journal 112, nr 3 (luty 2017): 132a. http://dx.doi.org/10.1016/j.bpj.2016.11.730.

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Xie, Zhi-Zhong, Yang Liu i Jin-Song Bian. "Hydrogen Sulfide and Cellular Redox Homeostasis". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/6043038.

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Intracellular redox imbalance is mainly caused by overproduction of reactive oxygen species (ROS) or weakness of the natural antioxidant defense system. It is involved in the pathophysiology of a wide array of human diseases. Hydrogen sulfide (H2S) is now recognized as the third “gasotransmitters” and proved to exert a wide range of physiological and cytoprotective functions in the biological systems. Among these functions, the role of H2S in oxidative stress has been one of the main focuses over years. However, the underlying mechanisms for the antioxidant effect of H2S are still poorly comprehended. This review presents an overview of the current understanding of H2S specially focusing on the new understanding and mechanisms of the antioxidant effects of H2S based on recent reports. Both inhibition of ROS generation and stimulation of antioxidants are discussed. H2S-induced S-sulfhydration of key proteins (e.g., p66Shc and Keap1) is also one of the focuses of this review.

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Sang, Dongmiao, Xiaofeng Li, Zhikun Xu, Huiming Lin, Changhong Guo i Fengyu Qu. "Disrupted intracellular redox balance with enhanced ROS generation and sensitive drug release for cancer therapy". Biomaterials Science 8, nr 21 (2020): 6045–55. http://dx.doi.org/10.1039/d0bm00765j.

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Walker, Cheryl L., Laura C. D. Pomatto, Durga Nand Tripathi i Kelvin J. A. Davies. "Redox Regulation of Homeostasis and Proteostasis in Peroxisomes". Physiological Reviews 98, nr 1 (1.01.2018): 89–115. http://dx.doi.org/10.1152/physrev.00033.2016.

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Peroxisomes are highly dynamic intracellular organelles involved in a variety of metabolic functions essential for the metabolism of long-chain fatty acids, d-amino acids, and many polyamines. A byproduct of peroxisomal metabolism is the generation, and subsequent detoxification, of reactive oxygen and nitrogen species, particularly hydrogen peroxide (H2O2). Because of its relatively low reactivity (as a mild oxidant), H2O2 has a comparatively long intracellular half-life and a high diffusion rate, all of which makes H2O2 an efficient signaling molecule. Peroxisomes also have intricate connections to mitochondria, and both organelles appear to play important roles in regulating redox signaling pathways. Peroxisomal proteins are also subject to oxidative modification and inactivation by the reactive oxygen and nitrogen species they generate, but the peroxisomal LonP2 protease can selectively remove such oxidatively damaged proteins, thus prolonging the useful lifespan of the organelle. Peroxisomal homeostasis must adapt to the metabolic state of the cell, by a combination of peroxisome proliferation, the removal of excess or badly damaged organelles by autophagy (pexophagy), as well as by processes of peroxisome inheritance and motility. More recently the tumor suppressors ataxia telangiectasia mutate (ATM) and tuberous sclerosis complex (TSC), which regulate mTORC1 signaling, have been found to regulate pexophagy in response to variable levels of certain reactive oxygen and nitrogen species. It is now clear that any significant loss of peroxisome homeostasis can have devastating physiological consequences. Peroxisome dysregulation has been implicated in several metabolic diseases, and increasing evidence highlights the important role of diminished peroxisomal functions in aging processes.

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Fatma, Homa, Mohd Jameel i Hifzur R. Siddique. "An Update on Phytochemicals in Redox Homeostasis: “Virtuous or Evil” in Cancer Chemoprevention?" Chemistry 5, nr 1 (4.02.2023): 201–22. http://dx.doi.org/10.3390/chemistry5010017.

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Redox homeostasis, a dynamic process ensuring a balance between cellular oxidizing and reducing reactions, is crucial for maintaining healthy cellular physiology and regulating many biological processes, requiring continuous monitoring and fine-tuning. Reactive species play a critical role in intra/intercellular signaling, and each cell has a specific system guarding cellular redox homeostasis. ROS signaling and oxidative stress are involved in cancer initiation and progression. However, the generation of reactive species beyond the threshold level inside the tumor microenvironment is considered one of the therapeutic approaches. Various studies have shown that some phytochemicals can target the redox homeostasis of the tumor microenvironment. Recent advances have focused on developing and introducing phytochemical interventions as favorable therapeutic options against cancer. However, studies have also suggested the “virtuous” and “evil” impacts of phytochemicals. Some phytochemicals enhance therapeutic efficacy by promoting intracellular oxidant accumulation. However, under certain conditions, some phytochemicals may harm the cellular microenvironment to promote cancer and tend to target different pathways for cancer initiation and development instead of targeting redox homeostasis. In this context, this review is focused on providing an overall understanding of redox homeostasis and intends to highlight the potential positive and negative impacts of phytochemicals in redox homeostasis and disease development. We also discuss the recent nanotechnology-based advancements in combating cancer development.

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Shi, Jiayan, Hailong Tian, Liyuan Peng, Canhua Huang, Edouard C. Nice, Bingwen Zou i Haiyuan Zhang. "A nanoplatform reshaping intracellular osmolarity and redox homeostasis against colorectal cancer". Journal of Controlled Release 352 (grudzień 2022): 766–75. http://dx.doi.org/10.1016/j.jconrel.2022.11.003.

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Kang, Jia, i Shazib Pervaiz. "Mitochondria: Redox Metabolism and Dysfunction". Biochemistry Research International 2012 (2012): 1–14. http://dx.doi.org/10.1155/2012/896751.

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Mitochondria are the main intracellular location for fuel generation; however, they are not just power plants but involved in a range of other intracellular functions including regulation of redox homeostasis and cell fate. Dysfunction of mitochondria will result in oxidative stress which is one of the underlying causal factors for a variety of diseases including neurodegenerative diseases, diabetes, cardiovascular diseases, and cancer. In this paper, generation of reactive oxygen/nitrogen species (ROS/RNS) in the mitochondria, redox regulatory roles of certain mitochondrial proteins, and the impact on cell fate will be discussed. The current state of our understanding in mitochondrial dysfunction in pathological states and how we could target them for therapeutic purpose will also be briefly reviewed.

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Li, Ying, Eun Ha Choi i Ihn Han. "Regulation of Redox Homeostasis by Nonthermal Biocompatible Plasma Discharge in Stem Cell Differentiation". Oxidative Medicine and Cellular Longevity 2019 (31.03.2019): 1–15. http://dx.doi.org/10.1155/2019/2318680.

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Recently, a growing body of evidence has shown the role of reactive species as secondary messengers in cell proliferation and differentiation, as opposed to the harmful metabolism byproducts that they were previously solely recognized as. Thus, the balance of intracellular reduction-oxidation (redox) homeostasis plays a vital role in the regulation of stem cell self-renewal and differentiation. Nonthermal biocompatible plasma (NBP) has emerged as a novel tool in biomedical applications. Recently, NBP has also emerged as a powerful tool in the tissue engineering field for the surface modification of biomaterial and the promotion of stem cell differentiation by the regulation of intracellular redox biology. NBP can generate various kinds of reactive oxygen species (ROS) and reactive nitrogen species (RNS), which may play the role of the second passenger in the cell signaling network and active antioxidant system in cells. Herein, we review the current knowledge on mechanisms by which NBP regulates cell proliferation and differentiation through redox modification. Considering the importance of redox homeostasis in the regulation of stem cell differentiation, understanding the underlying molecular mechanisms involved will provide important new insights into NBP-induced stem cell differentiation for tissue engineering.

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Yang, Ni, Rong-Rong Zheng, Zi-Ying Chen, Rui-Xin Wang, Lin-Ping Zhao, Xia-Yun Chen, Lei Chen, Lin Xu, Shi-Ying Li i A.-Li Chen. "A carrier free photodynamic oxidizer for enhanced tumor therapy by redox homeostasis disruption". Biomaterials Science 10, nr 6 (2022): 1575–81. http://dx.doi.org/10.1039/d1bm01876k.

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In this work, we developed a carrier free photodynamic oxidizer to decrease intracellular glutathione (GSH) levels and disrupt the redox homeostasis for enhanced photodynamic therapy (PDT) efficacy on tumor inhibition.

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Galinina, Nina, Zane Lasa, Inese Strazdina, Reinis Rutkis i Uldis Kalnenieks. "Effect of ADH II Deficiency on the Intracellular Redox Homeostasis inZymomonas mobilis". Scientific World Journal 2012 (2012): 1–6. http://dx.doi.org/10.1100/2012/742610.

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Mutant strain of the facultatively anaerobic, ethanol-producing bacteriumZymomonas mobilis, deficient in the Fe-containing alcohol dehydrogenase isoenzyme (ADH II), showed impaired homeostasis of the intracellular NAD(P)H during transition from anaerobic to aerobic conditions, and also in steady-state continuous cultures at various oxygen supplies. At the same time, ADH II deficiency in aerobically grown cells was accompanied by a threefold increase of catalase activity and by about 50% increase of hydrogen peroxide excretion. It is concluded that ADH II under aerobic conditions functions to maintain intracellular redox homeostasis and to protect the cells from endogenous hydrogen peroxide.

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Fraternale, Alessandra, Carolina Zara, Marta De Angelis, Lucia Nencioni, Anna Teresa Palamara, Michele Retini, Tomas Di Mambro, Mauro Magnani i Rita Crinelli. "Intracellular Redox-Modulated Pathways as Targets for Effective Approaches in the Treatment of Viral Infection". International Journal of Molecular Sciences 22, nr 7 (30.03.2021): 3603. http://dx.doi.org/10.3390/ijms22073603.

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Host-directed therapy using drugs that target cellular pathways required for virus lifecycle or its clearance might represent an effective approach for treating infectious diseases. Changes in redox homeostasis, including intracellular glutathione (GSH) depletion, are one of the key events that favor virus replication and contribute to the pathogenesis of virus-induced disease. Redox homeostasis has an important role in maintaining an appropriate Th1/Th2 balance, which is necessary to mount an effective immune response against viral infection and to avoid excessive inflammatory responses. It is known that excessive production of reactive oxygen species (ROS) induced by viral infection activates nuclear factor (NF)-kB, which orchestrates the expression of viral and host genes involved in the viral replication and inflammatory response. Moreover, redox-regulated protein disulfide isomerase (PDI) chaperones have an essential role in catalyzing formation of disulfide bonds in viral proteins. This review aims at describing the role of GSH in modulating redox sensitive pathways, in particular that mediated by NF-kB, and PDI activity. The second part of the review discusses the effectiveness of GSH-boosting molecules as broad-spectrum antivirals acting in a multifaceted way that includes the modulation of immune and inflammatory responses.

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Szentmihályi, Klára. "Fémelem-homeosztázis és oxidatív stressz patológiás folyamatokban". Orvosi Hetilap 160, nr 36 (wrzesień 2019): 1407–16. http://dx.doi.org/10.1556/650.2019.31499.

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Abstract: The author briefly summarizes the relationship between oxidative stress and changes in metal ion metabolism in pathological processes. Essential metal ions such as Ca, Mg, Fe, Cu, Zn, Se are essential in the living organisms, their metabolism and intracellular concentration are strictly regulated. Externally or intrinsically, altered metal ion metabolism can lead to metal ion accumulation or metal ion deficiency. Excess amounts of redox-active essential metals such as Fe, Cu, Co, Cr, Ni can induce free radicals under certain circumstances that cause inflammation, cell damage, and cancerous changes, although the molecular mechanism is still unclear in every detail. Changes in the metabolism of non-essential and non-variable valence metal ions also affect redox homeostasis. Despite the fact that each metal can react in a unique way and with different mechanisms, similar processes occur, where both metal deficiency and excessive metal induce oxidative stress. Antioxidant defense system is damaged, free radicals produced alter the redox balance, and redox homeostasis changed induces the production of cytokines and other transcription factors that affect the intracellular signaling pathways and affect the development of various diseases, including metabolic, cardiovascular, neurological diseases and cancer. Orv Hetil. 2019; 160(36): 1407–1416.

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Sugiura, Kazunori, Shoko Mihara, Nae Fu i Toru Hisabori. "Real-time monitoring of the in vivo redox state transition using the ratiometric redox state sensor protein FROG/B". Proceedings of the National Academy of Sciences 117, nr 27 (23.06.2020): 16019–26. http://dx.doi.org/10.1073/pnas.1918919117.

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The intracellular redox state is one of the key factors regulating various physiological phenomena in the cell. Monitoring this state is therefore important for understanding physiological homeostasis in cells. Various fluorescent sensor proteins have already been developed to monitor intracellular redox state. We also developed fluorescent redox sensor proteins named Oba-Q and Re-Q, the emissions of which are quenched under oxidized and reduced conditions, respectively. Although these sensors were useful to visualize the redox changes in the cell over time, they have the weakness that their emission signals are directly influenced by their in situ expression levels. To overcome this problem, we developed a redox sensor protein with a single excitation peak and dual variable emission peaks. This sensor protein shows green emission under oxidized conditions and blue emission under reduced conditions. We therefore named this sensor FROG/B, fluorescent protein with redox-dependent change in green/blue. By using this sensor, we successfully measured the changes in intracellular redox potentials in cyanobacterial cells quantitatively caused by light/dark transition just by calculating the ratio of emission between green and blue signals.

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Liu, Xinping, Zhengqing Yan, Yuhuan Sun, Jinsong Ren i Xiaogang Qu. "A label-free ratiometric electrochemical DNA sensor for monitoring intracellular redox homeostasis". Chemical Communications 53, nr 46 (2017): 6215–18. http://dx.doi.org/10.1039/c7cc03239k.

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Rose, Shannon, Stepan Melnyk, Timothy A. Trusty, Oleksandra Pavliv, Lisa Seidel, Jingyun Li, Todd Nick i S. Jill James. "Intracellular and Extracellular Redox Status and Free Radical Generation in Primary Immune Cells from Children with Autism". Autism Research and Treatment 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/986519.

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The modulation of the redox microenvironment is an important regulator of immune cell activation and proliferation. To investigate immune cell redox status in autism we quantified the intracellular glutathione redox couple (GSH/GSSG) in resting peripheral blood mononuclear cells (PBMCs), activated monocytes and CD4 T cells and the extracellular cysteine/cystine redox couple in the plasma from 43 children with autism and 41 age-matched control children. Resting PBMCs and activated monocytes from children with autism exhibited significantly higher oxidized glutathione (GSSG) and percent oxidized glutathione equivalents and decreased glutathione redox status (GSH/GSSG). In activated CD4 T cells from children with autism, the percent oxidized glutathione equivalents were similarly increased, and GSH and GSH/GSSG were decreased. In the plasma, both glutathione and cysteine redox ratios were decreased in autistic compared to control children. Consistent with decreased intracellular and extracellular redox status, generation of free radicals was significantly elevated in lymphocytes from the autistic children. These data indicate primary immune cells from autistic children have a more oxidized intracellular and extracellular microenvironment and a deficit in glutathione-mediated redox/antioxidant capacity compared to control children. These results suggest that the loss of glutathione redox homeostasis and chronic oxidative stress may contribute to immune dysregulation in autism.

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Noctor, Graham, Sonja Veljovic-Jovanovic i Christine H. Foyer. "Peroxide processing in photosynthesis: antioxidant coupling and redox signalling". Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 355, nr 1402 (29.10.2000): 1465–75. http://dx.doi.org/10.1098/rstb.2000.0707.

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Photosynthesis has a high capacity for production of hydrogen peroxide (H 2 O 2 ), but the intracellular levels of this relatively weak oxidant are controlled by the antioxidant system, comprising a network of enzymatic and non-enzymatic components that notably includes reactions linked to the intracellular ascorbate and glutathione pools. Mutants and transformed plants with specific decreases in key components offer the opportunity to dissect the complex system that maintains redox homeostasis. Since H 2 O 2 is a signal-transducing molecule relaying information on intracellular redox state, the pool size must be rigorously controlled within each compartment of the cell. This review focuses on compartment-specific differences in the stringency of redox coupling between ascorbate and glutathione, and the significance this may have for the flexibility of the control of gene expression that is linked to photosynthetic H 2 O 2 production.

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Sumandea, Marius P., i Susan F. Steinberg. "Redox Signaling and Cardiac Sarcomeres". Journal of Biological Chemistry 286, nr 12 (21.01.2011): 9921–27. http://dx.doi.org/10.1074/jbc.r110.175489.

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Oxidative stress is common in many clinically important cardiac disorders, including ischemia/reperfusion, diabetes, and hypertensive heart disease. Oxidative stress leads to derangements in pump function due to changes in the expression or function of proteins that regulate intracellular Ca2+ homeostasis. There is growing evidence that the cardiodepressant actions of reactive oxygen species (ROS) also are attributable to ROS-dependent signaling events in the sarcomere. This minireview focuses on myofilament protein post-translational modifications induced by ROS or ROS-activated signaling enzymes that regulate cardiac contractility.

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Price-Whelan, Alexa, Lars E. P. Dietrich i Dianne K. Newman. "Pyocyanin Alters Redox Homeostasis and Carbon Flux through Central Metabolic Pathways in Pseudomonas aeruginosa PA14". Journal of Bacteriology 189, nr 17 (25.05.2007): 6372–81. http://dx.doi.org/10.1128/jb.00505-07.

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ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa produces colorful, redox-active antibiotics called phenazines. Excretion of pyocyanin, the best-studied natural phenazine, is responsible for the bluish tint of sputum and pus associated with P. aeruginosa infections in humans. Although the toxicity of pyocyanin for other bacteria, as well as its role in eukaryotic infection, has been studied extensively, the physiological relevance of pyocyanin metabolism for the producing organism is not well understood. Pyocyanin reduction by P. aeruginosa PA14 is readily observed in standing liquid cultures that have consumed all of the oxygen in the medium. We investigated the physiological consequences of pyocyanin reduction by assaying intracellular concentrations of NADH and NAD+ in the wild-type strain and a mutant defective in phenazine production. We found that the mutant accumulated more NADH in stationary phase than the wild type. This increased accumulation correlated with a decrease in oxygen availability and was relieved by the addition of nitrate. Pyocyanin addition to a phenazine-null mutant also decreased intracellular NADH levels, suggesting that pyocyanin reduction facilitates redox balancing in the absence of other electron acceptors. Analysis of extracellular organic acids revealed that pyocyanin stimulated stationary-phase pyruvate excretion in P. aeruginosa PA14, indicating that pyocyanin may also influence the intracellular redox state by decreasing carbon flux through central metabolic pathways.

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Perelmuter, Karen, Inés Tiscornia, Marcelo A. Comini i Mariela Bollati-Fogolín. "Generation and Characterization of Stable Redox-Reporter Mammalian Cell Lines of Biotechnological Relevance". Sensors 22, nr 4 (9.02.2022): 1324. http://dx.doi.org/10.3390/s22041324.

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Cellular functions such as DNA replication and protein translation are influenced by changes in the intracellular redox milieu. Exogenous (i.e., nutrients, deterioration of media components, xenobiotics) and endogenous factors (i.e., metabolism, growth) may alter the redox homeostasis of cells. Thus, monitoring redox changes in real time and in situ is deemed essential for optimizing the production of recombinant proteins. Recently, different redox-sensitive variants of green fluorescent proteins (e.g., rxYFP, roGFP2, and rxmRuby2) have been engineered and proved suitable to detect, in a non-invasive manner, perturbations in the pool of reduced and oxidized glutathione, the major low molecular mass thiol in mammals. In this study, we validate the use of cytosolic rxYFP on two cell lines widely used in biomanufacturing processes, namely, CHO-K1 cells expressing the human granulocyte macrophage colony-stimulating factor (hGM-CSF) and HEK-293. Flow cytometry was selected as the read-out technique for rxYFP signal given its high-throughput and statistical robustness. Growth kinetics and cellular metabolism (glucose consumption, lactate and ammonia production) of the redox reporter cells were comparable to those of the parental cell lines. The hGM-CSF production was not affected by the expression of the biosensor. The redox reporter cell lines showed a sensitive and reversible response to different redox stimuli (reducing and oxidant reagents). Under batch culture conditions, a significant and progressive oxidation of the biosensor occurred when CHO-K1-hGM-CSF cells entered the late-log phase. Medium replenishment restored, albeit partially, the intracellular redox homeostasis. Our study highlights the utility of genetically encoded redox biosensors to guide metabolic engineering or intervention strategies aimed at optimizing cell viability, growth, and productivity.

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Jin, Jun-Xue, Jing-Tao Sun, Chao-Qian Jiang, Hong-Di Cui, Ya Bian, Sanghoon Lee, Lianjin Zhang, Byeong Chun Lee i Zhong-Hua Liu. "Melatonin Regulates Lipid Metabolism in Porcine Cumulus–Oocyte Complexes via the Melatonin Receptor 2". Antioxidants 11, nr 4 (31.03.2022): 687. http://dx.doi.org/10.3390/antiox11040687.

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Previous studies suggest that the inclusion of melatonin (MTn) in in vitro maturation protocols improves the developmental competence of oocytes by scavenging reactive oxygen species (ROS). However, the molecular mechanisms integrating melatonin receptor (MT)-mediated lipid metabolism and redox signaling during in vitro cumulus–oocyte complex (COC) development still remain unclear. Here, we aimed to elucidate the potential role of MTn receptors in lipid metabolic adjustments during in vitro porcine COC development. We observed that MTn-mediated Gsα–cAMP/PKA signaling facilitated lipolysis primarily through the MT2 receptor and subsequently increased fatty acid (FA) release by hydrolyzing intracellular triglycerides (TGs) in cumulus cells. Furthermore, CD36 was a critical FA transporter that transported available FAs from cumulus cells to oocytes and promoted de novo TG synthesis in the latter. In addition, MTn regulated lipogenesis and intracellular lipolysis to maintain lipid homeostasis and limit ROS production, thereby supporting oocyte cytoplasmic maturation and the subsequent embryo development. Taken together, these findings provide insight into the possible mechanism integrating MT2-mediated lipid homeostasis and redox signaling, which limits ROS production during in vitro COC development. Therefore, understanding the dynamics of the interactions between lipid homeostasis and redox signaling driven by MT2 is necessary in order to predict drug targets and the effects of therapeutics used to improve female reproductive health.

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Mourenza, Álvaro, Natalia Bravo-Santano, Inés Pradal, Jose A. Gil, Luis M. Mateos i Michal Letek. "Mycoredoxins Are Required for Redox Homeostasis and Intracellular Survival in the Actinobacterial Pathogen Rhodococcus equi". Antioxidants 8, nr 11 (15.11.2019): 558. http://dx.doi.org/10.3390/antiox8110558.

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Rhodococcus equi is a facultative intracellular pathogen that can survive within macrophages of a wide variety of hosts, including immunosuppressed humans. Current antibiotherapy is often ineffective, and novel therapeutic strategies are urgently needed to tackle infections caused by this pathogen. In this study, we identified three mycoredoxin-encoding genes (mrx) in the genome of R. equi, and we investigated their role in virulence. Importantly, the intracellular survival of a triple mrx-null mutant (Δmrx1Δmrx2Δmrx3) in murine macrophages was fully impaired. However, each mycoredoxin alone could restore the intracellular proliferation rate of R. equi Δmrx1Δmrx2Δmrx3 to wild type levels, suggesting that these proteins could have overlapping functions during host cell infection. Experiments with the reduction-oxidation sensitive green fluorescent protein 2 (roGFP2) biosensor confirmed that R. equi was exposed to redox stress during phagocytosis, and mycoredoxins were involved in preserving the redox homeostasis of the pathogen. Thus, we studied the importance of each mycoredoxin for the resistance of R. equi to different oxidative stressors. Interestingly, all mrx genes did have overlapping roles in the resistance to sodium hypochlorite. In contrast, only mrx1 was essential for the survival against high concentrations of nitric oxide, while mrx3 was not required for the resistance to hydrogen peroxide. Our results suggest that all mycoredoxins have important roles in redox homeostasis, contributing to the pathogenesis of R. equi and, therefore, these proteins may be considered interesting targets for the development of new anti-infectives.

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Aki, Toshihiko, Kana Unuma i Koichi Uemura. "The Role of Peroxiredoxins in the Regulation of Sepsis". Antioxidants 11, nr 1 (6.01.2022): 126. http://dx.doi.org/10.3390/antiox11010126.

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Oxidative stress, a result of a disturbance in redox homeostasis, is considered to be one of the main aggravating events in the pathogenesis of immune disorders. Peroxiredoxins (Prdxs) are an enzyme family that catalyzes the reduction of peroxides, including hydrogen peroxide, lipid peroxides, and nitrogen peroxides. Although the maintenance of cellular redox homeostasis through Prdxs is essential for surviving in adverse environments, Prdxs also participate in the regulation of cellular signal transduction by modulating the activities of a panel of molecules involved in the signal transduction process. Although Prdxs were discovered as intracellular anti-oxidative enzymes, recent research has revealed that Prdxs also play important roles in the extracellular milieu. Indeed, Prdxs have been shown to have the capacity to activate immune cells through ligation with innate immune receptors such as toll-like receptors (TLRs). In this review, we will summarize the intracellular as well as extracellular roles of Prdxs for and against the pathogenesis of inflammatory disorders including sepsis, hemorrhagic shock, and drug-induced liver injury.

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Song, Yong-Seok, Ismail S. Zaitoun, Shoujian Wang, Soesiawati R. Darjatmoko, Christine M. Sorenson i Nader Sheibani. "Cytochrome P450 1B1 Expression Regulates Intracellular Iron Levels and Oxidative Stress in the Retinal Endothelium". International Journal of Molecular Sciences 24, nr 3 (26.01.2023): 2420. http://dx.doi.org/10.3390/ijms24032420.

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Cytochrome P450 (CYP) 1B1 is a heme-containing monooxygenase found mainly in extrahepatic tissues, including the retina. CYP1B1 substrates include exogenous aromatic hydrocarbons, such as dioxins, and endogenous bioactive compounds, including 17β-estradiol (E2) and arachidonic acid. The endogenous compounds and their metabolites are mediators of various cellular and physiological processes, suggesting that CYP1B1 activity is likely important in maintaining proper cellular and tissue functions. We previously demonstrated that lack of CYP1B1 expression and activity are associated with increased levels of reactive oxygen species and oxidative stress in the retinal vasculature and vascular cells, including retinal endothelial cells (ECs). However, the detailed mechanism(s) of how CYP1B1 activity modulates redox homeostasis remained unknown. We hypothesized that CYP1B1 metabolism of E2 affects bone morphogenic protein 6 (BMP6)-hepcidin-mediated iron homeostasis and lipid peroxidation impacting cellular redox state. Here, we demonstrate retinal EC prepared from Cyp1b1-deficient (Cyp1b1−/−) mice exhibits increased estrogen receptor-α (ERα) activity and expresses higher levels of BMP6. BMP6 is an inducer of the iron-regulatory hormone hepcidin in the endothelium. Increased hepcidin expression in Cyp1b1−/− retinal EC resulted in decreased levels of the iron exporter protein ferroportin and, as a result, increased intracellular iron accumulation. Removal of excess iron or antagonism of ERα in Cyp1b1−/− retinal EC was sufficient to mitigate increased lipid peroxidation and reduce oxidative stress. Suppression of lipid peroxidation and antagonism of ERα also restored ischemia-mediated retinal neovascularization in Cyp1b1−/− mice. Thus, CYP1B1 expression in retinal EC is important in the regulation of intracellular iron levels, with a significant impact on ocular redox homeostasis and oxidative stress through modulation of the ERα/BMP6/hepcidin axis.

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Granatiero, Veronica, Csaba Konrad, Kirsten Bredvik, Giovanni Manfredi i Hibiki Kawamata. "Nrf2 signaling links ER oxidative protein folding and calcium homeostasis in health and disease". Life Science Alliance 2, nr 5 (październik 2019): e201900563. http://dx.doi.org/10.26508/lsa.201900563.

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We report a signaling pathway linking two fundamental functions of the ER, oxidative protein folding, and intracellular calcium regulation. Cells sense ER oxidative protein folding through H2O2, which induces Nrf2 nuclear translocation. Nrf2 regulates the expression of GPx8, an ER glutathione peroxidase that modulates ER calcium levels. Because ER protein folding is dependent on calcium, this pathway functions as rheostat of ER calcium levels. Protein misfolding and calcium dysregulation contribute to the pathophysiology of many diseases, including amyotrophic lateral sclerosis, in which astrocytic calcium dysregulation participates in causing motor neuron death. In human-derived astrocytes harboring mutant SOD1 causative of familial amyotrophic lateral sclerosis, we show that impaired ER redox signaling decreases Nrf2 nuclear translocation, resulting in ER calcium overload and increased calcium-dependent cell secretion, leading to motor neuron death. Nrf2 activation in SOD1 mutant astrocytes with dimethyl fumarate restores calcium homeostasis and ameliorates motor neuron death. These results highlight a regulatory mechanism of intracellular calcium homeostasis by ER redox signaling and suggest that this mechanism could be a therapeutic target in SOD1 mutant astrocytes.

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Zhu, Xiao-Hong, Ming Lu, Byeong-Yeul Lee, Kamil Ugurbil i Wei Chen. "In vivo NAD assay reveals the intracellular NAD contents and redox state in healthy human brain and their age dependences". Proceedings of the National Academy of Sciences 112, nr 9 (17.02.2015): 2876–81. http://dx.doi.org/10.1073/pnas.1417921112.

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NAD is an essential metabolite that exists in NAD+or NADH form in all living cells. Despite its critical roles in regulating mitochondrial energy production through the NAD+/NADH redox state and modulating cellular signaling processes through the activity of the NAD+-dependent enzymes, the method for quantifying intracellular NAD contents and redox state is limited to a few in vitro or ex vivo assays, which are not suitable for studying a living brain or organ. Here, we present a magnetic resonance (MR) -based in vivo NAD assay that uses the high-field MR scanner and is capable of noninvasively assessing NAD+and NADH contents and the NAD+/NADH redox state in intact human brain. The results of this study provide the first insight, to our knowledge, into the cellular NAD concentrations and redox state in the brains of healthy volunteers. Furthermore, an age-dependent increase of intracellular NADH and age-dependent reductions in NAD+, total NAD contents, and NAD+/NADH redox potential of the healthy human brain were revealed in this study. The overall findings not only provide direct evidence of declined mitochondrial functions and altered NAD homeostasis that accompany the normal aging process but also, elucidate the merits and potentials of this new NAD assay for noninvasively studying the intracellular NAD metabolism and redox state in normal and diseased human brain or other organs in situ.

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Lv, Huanhuan, Chenxiao Zhen, Junyu Liu, Pengfei Yang, Lijiang Hu i Peng Shang. "Unraveling the Potential Role of Glutathione in Multiple Forms of Cell Death in Cancer Therapy". Oxidative Medicine and Cellular Longevity 2019 (10.06.2019): 1–16. http://dx.doi.org/10.1155/2019/3150145.

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Glutathione is the principal intracellular antioxidant buffer against oxidative stress and mainly exists in the forms of reduced glutathione (GSH) and oxidized glutathione (GSSG). The processes of glutathione synthesis, transport, utilization, and metabolism are tightly controlled to maintain intracellular glutathione homeostasis and redox balance. As for cancer cells, they exhibit a greater ROS level than normal cells in order to meet the enhanced metabolism and vicious proliferation; meanwhile, they also have to develop an increased antioxidant defense system to cope with the higher oxidant state. Growing numbers of studies have implicated that altering the glutathione antioxidant system is associated with multiple forms of programmed cell death in cancer cells. In this review, we firstly focus on glutathione homeostasis from the perspectives of glutathione synthesis, distribution, transportation, and metabolism. Then, we discuss the function of glutathione in the antioxidant process. Afterwards, we also summarize the recent advance in the understanding of the mechanism by which glutathione plays a key role in multiple forms of programmed cell death, including apoptosis, necroptosis, ferroptosis, and autophagy. Finally, we highlight the glutathione-targeting therapeutic approaches toward cancers. A comprehensive review on the glutathione homeostasis and the role of glutathione depletion in programmed cell death provide insight into the redox-based research concerning cancer therapeutics.

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31

Skoko, John, Shireen Attaran i Carola Neumann. "Signals Getting Crossed in the Entanglement of Redox and Phosphorylation Pathways: Phosphorylation of Peroxiredoxin Proteins Sparks Cell Signaling". Antioxidants 8, nr 2 (23.01.2019): 29. http://dx.doi.org/10.3390/antiox8020029.

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Reactive oxygen and nitrogen species have cell signaling properties and are involved in a multitude of processes beyond redox homeostasis. The peroxiredoxin (Prdx) proteins are highly sensitive intracellular peroxidases that can coordinate cell signaling via direct reactive species scavenging or by acting as a redox sensor that enables control of binding partner activity. Oxidation of the peroxidatic cysteine residue of Prdx proteins are the classical post-translational modification that has been recognized to modulate downstream signaling cascades, but increasing evidence supports that dynamic changes to phosphorylation of Prdx proteins is also an important determinant in redox signaling. Phosphorylation of Prdx proteins affects three-dimensional structure and function to coordinate cell proliferation, wound healing, cell fate and lipid signaling. The advent of large proteomic datasets has shown that there are many opportunities to understand further how phosphorylation of Prdx proteins fit into intracellular signaling cascades in normal or malignant cells and that more research is necessary. This review summarizes the Prdx family of proteins and details how post-translational modification by kinases and phosphatases controls intracellular signaling.

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32

Arrigo, André-Patrick, Sophie Virot, Sylvain Chaufour, Wance Firdaus, Carole Kretz-Remy i Chantal Diaz-Latoud. "Hsp27 Consolidates Intracellular Redox Homeostasis by Upholding Glutathione in Its Reduced Form and by Decreasing Iron Intracellular Levels". Antioxidants & Redox Signaling 7, nr 3-4 (marzec 2005): 414–22. http://dx.doi.org/10.1089/ars.2005.7.414.

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Wang, Chuan, Yi Mao, Jia Yu, Lin Zhu, Ming Li, Decheng Wang, Dandan Dong, Jun Liu i Qian Gao. "PhoY2 of Mycobacteria Is Required for Metabolic Homeostasis and Stress Response". Journal of Bacteriology 195, nr 2 (2.11.2012): 243–52. http://dx.doi.org/10.1128/jb.01556-12.

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ABSTRACTThe ability of pathogenic mycobacteria to adapt to diverse environments is essential for their success as pathogens. Here we describe a transposon-inactivatedphoY2mutant ofMycobacterium marinum. PhoY2 of mycobacteria is a functional homologue of PhoU inEscherichia coliand an important component of the Pho regulon. We found that PhoY2 is required for maintaining intracellular inorganic phosphate (Pi) homeostasis and balanced energy and redox states. Disruption ofphoY2resulted in elevated levels of intracellular poly-Piand ATP and an elevated NAD+/NADH ratio, and the mutant strain exhibited increased sensitivity to environmental stress conditions, including nutrient deprivation as well as SDS and antibiotic treatments. Taken together, our results suggest that PhoY2 is required for maintaining metabolic homeostasis and adaptation to stress conditions, which may provide an explanation for the suggested role of PhoY2 in drug tolerance.

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34

Quan, Yumeng, Yu Du, Yuxin Tong, Sumin Gu i Jean X. Jiang. "Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis". Antioxidants 10, nr 9 (28.08.2021): 1374. http://dx.doi.org/10.3390/antiox10091374.

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The lens is continuously exposed to oxidative stress insults, such as ultraviolet radiation and other oxidative factors, during the aging process. The lens possesses powerful oxidative stress defense systems to maintain its redox homeostasis, one of which employs connexin channels. Connexins are a family of proteins that form: (1) Hemichannels that mediate the communication between the intracellular and extracellular environments, and (2) gap junction channels that mediate cell-cell communication between adjacent cells. The avascular lens transports nutrition and metabolites through an extensive network of connexin channels, which allows the passage of small molecules, including antioxidants and oxidized wastes. Oxidative stress-induced post-translational modifications of connexins, in turn, regulates gap junction and hemichannel permeability. Recent evidence suggests that dysfunction of connexins gap junction channels and hemichannels may induce cataract formation through impaired redox homeostasis. Here, we review the recent advances in the knowledge of connexin channels in lens redox homeostasis and their response to cataract-related oxidative stress by discussing two major aspects: (1) The role of lens connexins and channels in oxidative stress and cataractogenesis, and (2) the impact and underlying mechanism of oxidative stress in regulating connexin channels.

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Dhaoui, Manel, Françoise Auchère, Pierre-Louis Blaiseau, Emmanuel Lesuisse, Ahmed Landoulsi, Jean-Michel Camadro, Rosine Haguenauer-Tsapis i Naïma Belgareh-Touzé. "Gex1 is a yeast glutathione exchanger that interferes with pH and redox homeostasis". Molecular Biology of the Cell 22, nr 12 (15.06.2011): 2054–67. http://dx.doi.org/10.1091/mbc.e10-11-0906.

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In the yeast Saccharomyces cerevisiae, glutathione plays a major role in heavy metal detoxification and protection of cells against oxidative stress. We show that Gex1 is a new glutathione exchanger. Gex1 and its paralogue Gex2 belong to the major facilitator superfamily of transporters and display similarities to the Aft1-regulon family of siderophore transporters. Gex1 was found mostly at the vacuolar membrane and, to a lesser extent, at the plasma membrane. Gex1 expression was induced under conditions of iron depletion and was principally dependent on the iron-responsive transcription factor Aft2. However, a gex1Δ gex2Δ strain displayed no defect in known siderophore uptake. The deletion mutant accumulated intracellular glutathione, and cells overproducing Gex1 had low intracellular glutathione contents, with glutathione excreted into the extracellular medium. Furthermore, the strain overproducing Gex1 induced acidification of the cytosol, confirming the involvement of Gex1 in proton transport as a probable glutathione/proton antiporter. Finally, the imbalance of pH and glutathione homeostasis in the gex1Δ gex2Δ and Gex1-overproducing strains led to modulations of the cAMP/protein kinase A and protein kinase C1 mitogen-activated protein kinase signaling pathways.

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36

Stepovaya, E. A., E. V. Shakhristova, N. V. Ryazantseva, O. L. Nosareva, V. D. Yakushina, A. I. Nosova, V. S. Gulaya, E. A. Stepanova, R. I. Chil'chigashev i V. V. Novitsky. "The role of oxidative protein modification and the gluthatione system in modulation of the redox status of breast epithelial cells". Biomeditsinskaya Khimiya 62, nr 1 (styczeń 2016): 64–68. http://dx.doi.org/10.18097/pbmc20166201064.

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The effects of the SH-group blocker N-ethylmaleimide (NEM) and thiol group protector 1,4-dithioerythritol (DTE) on the redox status of cells HBL-100 cells, oxidative modification of their proteins and the state of glutathione and thioredoxin systems have been investigated. Breast epithelial cells cultivated in the presence of NEM were characterized by decreased redox status, increased glutathione reductase activity, and increased concentrations of products of irreversible oxidative modification of protein and amino acids. Cultivation of HBL-100 cells in the presence of DTE resulted in a shift of the redox status towards reduction processes and increased reversible protein modification by glutathionylation. The proposed model of intracellular redox modulation may be used in the development of new therapeutic approaches to treat diseases accompanied by impaired redox homeostasis (e.g. oncologic, inflammatory, cardiovascular and neurodegenerative disease).

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Jimenez-Moreno, Natalia, i Jon D. Lane. "Autophagy and Redox Homeostasis in Parkinson’s: A Crucial Balancing Act". Oxidative Medicine and Cellular Longevity 2020 (10.11.2020): 1–38. http://dx.doi.org/10.1155/2020/8865611.

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Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are generated primarily from endogenous biochemical reactions in mitochondria, endoplasmic reticulum (ER), and peroxisomes. Typically, ROS/RNS correlate with oxidative damage and cell death; however, free radicals are also crucial for normal cellular functions, including supporting neuronal homeostasis. ROS/RNS levels influence and are influenced by antioxidant systems, including the catabolic autophagy pathways. Autophagy is an intracellular lysosomal degradation process by which invasive, damaged, or redundant cytoplasmic components, including microorganisms and defunct organelles, are removed to maintain cellular homeostasis. This process is particularly important in neurons that are required to cope with prolonged and sustained operational stress. Consequently, autophagy is a primary line of protection against neurodegenerative diseases. Parkinson’s is caused by the loss of midbrain dopaminergic neurons (mDANs), resulting in progressive disruption of the nigrostriatal pathway, leading to motor, behavioural, and cognitive impairments. Mitochondrial dysfunction, with associated increases in oxidative stress, and declining proteostasis control, are key contributors during mDAN demise in Parkinson’s. In this review, we analyse the crosstalk between autophagy and redoxtasis, including the molecular mechanisms involved and the detrimental effect of an imbalance in the pathogenesis of Parkinson’s.

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38

Hatori, Yuta, i Svetlana Lutsenko. "The Role of Copper Chaperone Atox1 in Coupling Redox Homeostasis to Intracellular Copper Distribution". Antioxidants 5, nr 3 (27.07.2016): 25. http://dx.doi.org/10.3390/antiox5030025.

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Quan, Yingyao, Shengni Hua, Wei Li, Meixiao Zhan, Yong Li i Ligong Lu. "Resveratrol bidirectionally regulates insulin effects in skeletal muscle through alternation of intracellular redox homeostasis". Life Sciences 242 (luty 2020): 117188. http://dx.doi.org/10.1016/j.lfs.2019.117188.

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Ju, Youngjun, Weihua Zhang, Yanxi Pei i Guangdong Yang. "H2S signaling in redox regulation of cellular functions". Canadian Journal of Physiology and Pharmacology 91, nr 1 (styczeń 2013): 8–14. http://dx.doi.org/10.1139/cjpp-2012-0293.

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Hydrogen sulfide (H2S) is traditionally recognized as a toxic gas with a rotten-egg smell. In just the last few decades, H2S has been found to be one of a family of gasotransmitters, together with nitric oxide and carbon monoxide, and various physiologic effects of H2S have been reported. Among the most acknowledged molecular mechanisms for the cellular effects of H2S is the regulation of intracellular redox homeostasis and post-translational modification of proteins through S-sulfhydration. On the one side, H2S can promote an antioxidant effect and is cytoprotective; on the other side, H2S stimulates oxidative stress and is cytotoxic. This review summarizes our current knowledge of the antioxidant versus pro-oxidant effects of H2S in mammalian cells and describes the Janus-faced properties of this novel gasotransmitter. The redox regulation for the cellular effects of H2S through S-sulfhydration and the role of H2S in glutathione generation is also recapitulated. A better understanding of H2S-regualted redox homeostasis will pave the way for future design of novel pharmacological and therapeutic interventions for various diseases.

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41

Campagna, Roberto, i Arianna Vignini. "NAD+ Homeostasis and NAD+-Consuming Enzymes: Implications for Vascular Health". Antioxidants 12, nr 2 (4.02.2023): 376. http://dx.doi.org/10.3390/antiox12020376.

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Nicotinamide adenine dinucleotide (NAD+) is a ubiquitous metabolite that takes part in many key redox reactions. NAD+ biosynthesis and NAD+-consuming enzymes have been attracting markedly increasing interest since they have been demonstrated to be involved in several crucial biological pathways, impacting genes transcription, cellular signaling, and cell cycle regulation. As a consequence, many pathological conditions are associated with an impairment of intracellular NAD+ levels, directly or indirectly, which include cardiovascular diseases, obesity, neurodegenerative diseases, cancer, and aging. In this review, we describe the general pathways involved in the NAD+ biosynthesis starting from the different precursors, analyzing the actual state-of-art of the administration of NAD+ precursors or blocking NAD+-dependent enzymes as strategies to increase the intracellular NAD+ levels or to counteract the decline in NAD+ levels associated with ageing. Subsequently, we focus on the disease-related and age-related alterations of NAD+ homeostasis and NAD+-dependent enzymes in endothelium and the consequent vascular dysfunction, which significantly contributes to a wide group of pathological disorders.

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Boysen, Jana Marie, Nauman Saeed, Thomas Wolf, Gianni Panagiotou i Falk Hillmann. "The Peroxiredoxin Asp f3 Acts as Redox Sensor in Aspergillus fumigatus". Genes 12, nr 5 (29.04.2021): 668. http://dx.doi.org/10.3390/genes12050668.

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The human pathogenic fungus Aspergillus fumigatus is readily eradicated by the innate immunity of immunocompetent human hosts, but can cause severe infections, such as invasive aspergillosis (IA), in immunocompromised individuals. During infection, the fungal redox homeostasis can be challenged by reactive oxygen species (ROS), either derived from the oxidative burst of innate immune cells or the action of antifungal drugs. The peroxiredoxin Asp f3 was found to be essential to cause IA in mice, but how Asp f3 integrates with fungal redox homeostasis remains unknown. Here, we show that in vivo, Asp f3 acts as a sensor for ROS. While global transcription in fungal hyphae under minimal growth conditions was fully independent of Asp f3, a robust induction of the oxidative stress response required the presence of the peroxiredoxin. Hyphae devoid of Asp f3 failed to activate several redox active genes, like members of the gliotoxin biosynthesis gene cluster and integral members of the Afyap1 regulon, the central activator of the ROS defense machinery in fungi. Upon deletion of the asp f3 gene Afyap1 displayed significantly reduced nuclear localization during ROS exposure, indicating that Asp f3 can act as an intracellular redox sensor for several target proteins.

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Farris, Patricia K., i Giuseppe Valacchi. "Ultraviolet Light Protection: Is It Really Enough?" Antioxidants 11, nr 8 (29.07.2022): 1484. http://dx.doi.org/10.3390/antiox11081484.

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Our current understanding of the pathogenesis of skin aging includes the role of ultraviolet light, visible light, infrared, pollution, cigarette smoke and other environmental exposures. The mechanism of action common to these exposures is the disruption of the cellular redox balance by the directly or indirectly increased formation of reactive oxygen species that overwhelm the intrinsic antioxidant defense system, resulting in an oxidative stress condition. Altered redox homeostasis triggers downstream pathways that contribute to tissue oxinflammation (cross-talk between inflammation and altered redox status) and accelerate skin aging. In addition, both ultraviolet light and pollution increase intracellular free iron that catalyzes reactive oxygen species generation via the Fenton reaction. This disruption of iron homeostasis within the cell further promotes oxidative stress and contributes to extrinsic skin aging. More recent studies have demonstrated that iron chelators can be used topically and can enhance the benefits of topically applied antioxidants. Thus, an updated, more comprehensive approach to environmental or atmospheric aging protection should include sun protective measures, broad spectrum sunscreens, antioxidants, chelating agents, and DNA repair enzymes.

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Sági-Kazár, Máté, Katalin Solymosi i Ádám Solti. "Iron in leaves: chemical forms, signalling, and in-cell distribution". Journal of Experimental Botany 73, nr 6 (1.02.2022): 1717–34. http://dx.doi.org/10.1093/jxb/erac030.

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Abstract Iron (Fe) is an essential transition metal. Based on its redox-active nature under biological conditions, various Fe compounds serve as cofactors in redox enzymes. In plants, the photosynthetic machinery has the highest demand for Fe. In consequence, the delivery and incorporation of Fe into cofactors of the photosynthetic apparatus is the focus of Fe metabolism in leaves. Disturbance of foliar Fe homeostasis leads to impaired biosynthesis of chlorophylls and composition of the photosynthetic machinery. Nevertheless, mitochondrial function also has a significant demand for Fe. The proper incorporation of Fe into proteins and cofactors as well as a balanced intracellular Fe status in leaf cells require the ability to sense Fe, but may also rely on indirect signals that report on the physiological processes connected to Fe homeostasis. Although multiple pieces of information have been gained on Fe signalling in roots, the regulation of Fe status in leaves has not yet been clarified in detail. In this review, we give an overview on current knowledge of foliar Fe homeostasis, from the chemical forms to the allocation and sensing of Fe in leaves.

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45

Puigpinós, Judit, Celia Casas i Enrique Herrero. "Altered intracellular calcium homeostasis and endoplasmic reticulum redox state in Saccharomyces cerevisiae cells lacking Grx6 glutaredoxin". Molecular Biology of the Cell 26, nr 1 (styczeń 2015): 104–16. http://dx.doi.org/10.1091/mbc.e14-06-1137.

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Glutaredoxin 6 (Grx6) of Saccharomyces cerevisiae is an integral thiol oxidoreductase protein of the endoplasmic reticulum/Golgi vesicles. Its absence alters the redox equilibrium of the reticulum lumen toward a more oxidized state, thus compensating the defects in protein folding/secretion and cell growth caused by low levels of the oxidase Ero1. In addition, null mutants in GRX6 display a more intense unfolded protein response than wild-type cells upon treatment with inducers of this pathway. These observations support a role of Grx6 in regulating the glutathionylation of thiols of endoplasmic reticulum/Golgi target proteins and consequently the equilibrium between reduced and oxidized glutathione in the lumen of these compartments. A specific function influenced by Grx6 activity is the homeostasis of intracellular calcium. Grx6-deficient mutants have reduced levels of calcium in the ER lumen, whereas accumulation occurs at the cytosol from extracellular sources. This results in permanent activation of the calcineurin-dependent pathway in these cells. Some but not all the phenotypes of the mutant are coincident with those of mutants deficient in intracellular calcium transporters, such as the Golgi Pmr1 protein. The results presented in this study provide evidence for redox regulation of calcium homeostasis in yeast cells.

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46

Bielefeldt, K., C. A. Whiteis, R. V. Sharma, F. M. Abboud i J. L. Conklin. "Reactive oxygen species and calcium homeostasis in cultured human intestinal smooth muscle cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 272, nr 6 (1.06.1997): G1439—G1450. http://dx.doi.org/10.1152/ajpgi.1997.272.6.g1439.

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Reactive oxygen species (ROS) significantly alter cell function. We examined the effects of hydrogen peroxide (H2O2) and xanthine/xanthine oxidase (X/XO) on isolated intestinal muscle cells. We assessed cell viability with the exclusion dye trypan blue and assayed the effects of H2O2 and X/XO on the intracellular redox state with the fluorescent probe 2',7'-dichlorofluorescein. Intracellular calcium concentration was measured in cells loaded with fura 2-acetoxymethyl ester, and we recorded whole membrane currents with conventional patch-clamp methods. Cells remained viable after a 5-min exposure to H2O2 and X/XO. H2O2 and X/XO led to a significant rise of the intracellular concentration of ROS. H2O2 (270 microM to 2.7 mM) as well as X/XO (0.25-16 mU; 0.5 mM xanthine) significantly increased intracellular calcium concentrations. Depletion of intracellular calcium with ryanodine or thapsigargin did not abolish the effect of ROS on the intracellular calcium concentration. In the absence of external calcium or in the presence of the calcium channel blocker nifedipine, H2O2 and X/XO still increased the intracellular calcium level. Thus calcium influx and calcium release from internal stores contributed to this rise in cytosolic calcium. Catalase and superoxide dismutase blunted or completely abolished the changes in calcium concentration elicited by H2O2 and X/XO. Exposure to ROS resulted in a rapid decline of the membrane resistance without significant changes in voltage-sensitive ion currents. We conclude that ROS disrupt the calcium homeostasis of cells at concentrations that do not lead to immediate cell death. The resulting elevation in cytosolic free calcium will activate a variety of biochemical reactions and may thus contribute to the cytotoxicity of reactive oxygen molecules.

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47

Barber, R. G., Zoey A. Grenier i Jason L. Burkhead. "Copper Toxicity Is Not Just Oxidative Damage: Zinc Systems and Insight from Wilson Disease". Biomedicines 9, nr 3 (20.03.2021): 316. http://dx.doi.org/10.3390/biomedicines9030316.

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Essential metals such as copper (Cu) and zinc (Zn) are important cofactors in diverse cellular processes, while metal imbalance may impact or be altered by disease state. Cu is essential for aerobic life with significant functions in oxidation-reduction catalysis. This redox reactivity requires precise intracellular handling and molecular-to-organismal levels of homeostatic control. As the central organ of Cu homeostasis in vertebrates, the liver has long been associated with Cu storage disorders including Wilson Disease (WD) (heritable human Cu toxicosis), Idiopathic Copper Toxicosis and Endemic Tyrolean Infantile Cirrhosis. Cu imbalance is also associated with chronic liver diseases that arise from hepatitis viral infection or other liver injury. The labile redox characteristic of Cu is often discussed as a primary mechanism of Cu toxicity. However, work emerging largely from the study of WD models suggests that Cu toxicity may have specific biochemical consequences that are not directly attributable to redox activity. This work reviews Cu toxicity with a focus on the liver and proposes that Cu accumulation specifically impacts Zn-dependent processes. The prospect that Cu toxicity has specific biochemical impacts that are not entirely attributable to redox may promote further inquiry into Cu toxicity in WD and other Cu-associated disorders.

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Kwon, Dong H., Saboor Hekmaty i Gomattie Seecoomar. "Homeostasis of Glutathione Is Associated with Polyamine-Mediated β-Lactam Susceptibility in Acinetobacter baumannii ATCC 19606". Antimicrobial Agents and Chemotherapy 57, nr 11 (26.08.2013): 5457–61. http://dx.doi.org/10.1128/aac.00692-13.

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ABSTRACTGlutathione is a tripeptide (l-γ-glutamyl–l-cysteinyl–glycine) thiol compound existing in many bacteria and maintains a proper cellular redox state, thus protecting cells against toxic substances such as reactive oxygen species. Polyamines (spermine and spermidine) are low-molecular-weight aliphatic polycations ubiquitously presenting in all living cells and modulate many cellular functions. We previously reported that exogenous polyamines significantly enhanced β-lactam susceptibility of β-lactam-associated multidrug-resistantAcinetobacter baumannii. In this study, three genes differentially associated with the polyamine effects on β-lactam susceptibility were identified by transposon mutagenesis ofA. baumanniiATCC 19606. All three genes encoded components of membrane transport systems. Inactivation of one of the genes encoding a putative glutathione transport ATP-binding protein increased the accumulation of intracellular glutathione (∼150 to ∼200%) and significantly decreased the polyamine effects on β-lactam susceptibility inA. baumanniiATCC 19606. When the cells were grown with polyamines, the levels of intracellular glutathione inA. baumanniiATCC 19606 significantly decreased from ∼0.5 to ∼0.2 nmol, while the levels of extracellular glutathione were correspondingly increased. However, the levels of total glutathione (intra- plus extracellular) were unchanged when the cells were grown with or without polyamines. Overall, these results suggest that exogenous polyamines induce glutathione export, resulting in decreased levels of intracellular glutathione, which may produce an improper cellular redox state that is associated with the polyamine-mediated β-lactam susceptibility ofA. baumannii. This finding may provide a clue for development of new antimicrobial agents and/or novel strategies to treat multidrug-resistantA. baumannii.

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Cruz-Gil, Silvia, Lara P. Fernández, Ruth Sánchez-Martínez, Marta Gómez de Cedrón i Ana Ramírez de Molina. "Non-Coding and Regulatory RNAs as Epigenetic Remodelers of Fatty Acid Homeostasis in Cancer". Cancers 12, nr 10 (9.10.2020): 2890. http://dx.doi.org/10.3390/cancers12102890.

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Cancer cells commonly display metabolic fluctuations. Together with the Warburg effect and the increased glutaminolysis, alterations in lipid metabolism homeostasis have been recognized as a hallmark of cancer. Highly proliferative cancer cells upregulate de novo synthesis of fatty acids (FAs) which are required to support tumor progression by exerting multiple roles including structural cell membrane composition, regulators of the intracellular redox homeostasis, ATP synthesis, intracellular cell signaling molecules, and extracellular mediators of the tumor microenvironment. Epigenetic modifications have been shown to play a crucial role in human development, but also in the initiation and progression of complex diseases. The study of epigenetic processes could help to design new integral strategies for the prevention and treatment of metabolic disorders including cancer. Herein, we first describe the main altered intracellular fatty acid processes to support cancer initiation and progression. Next, we focus on the most important regulatory and non-coding RNAs (small noncoding RNA—sncRNAs—long non-coding RNAs—lncRNAs—and other regulatory RNAs) which may target the altered fatty acids pathway in cancer.

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Liu, Yang, Shaojie Zhai, Xingwu Jiang, Yanyan Liu, Kun Wang, Chaochao Wang, Meng Zhang, Xuanyong Liu i Wenbo Bu. "Intracellular Mutual Promotion of Redox Homeostasis Regulation and Iron Metabolism Disruption for Enduring Chemodynamic Therapy". Advanced Functional Materials 31, nr 17 (19.02.2021): 2010390. http://dx.doi.org/10.1002/adfm.202010390.

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