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1
Kimble, Ashley, Mary E. Robbins, and Marta Perez. "Pathogenesis of Bronchopulmonary Dysplasia: Role of Oxidative Stress from ‘Omics’ Studies." Antioxidants 11, no. 12 (December 1, 2022): 2380. http://dx.doi.org/10.3390/antiox11122380.
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Bronchopulmonary dysplasia (BPD) remains the most common respiratory complication of prematurity as younger and smaller infants are surviving beyond the immediate neonatal period. The recognition that oxidative stress (OS) plays a key role in BPD pathogenesis has been widely accepted since at least the 1980s. In this article, we examine the interplay between OS and genetic regulation and review ‘omics’ data related to OS in BPD. Data from animal models (largely models of hyperoxic lung injury) and from human studies are presented. Epigenetic and transcriptomic analyses have demonstrated several genes related to OS to be differentially expressed in murine models that mimic BPD as well as in premature infants at risk of BPD development and infants with established lung disease. Alterations in the genetic regulation of antioxidant enzymes is a common theme in these studies. Data from metabolomics and proteomics have also demonstrated the potential involvement of OS-related pathways in BPD. A limitation of many studies includes the difficulty of obtaining timely and appropriate samples from human patients. Additional ‘omics’ studies could further our understanding of the role of OS in BPD pathogenesis, which may prove beneficial for prevention and timely diagnosis, and aid in the development of targeted therapies.
2
Ozsurekci, Yasemin, and Kubra Aykac. "Oxidative Stress Related Diseases in Newborns." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/2768365.
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We review oxidative stress-related newborn disease and the mechanism of oxidative damage. In addition, we outline diagnostic and therapeutic strategies and future directions. Many reports have defined oxidative stress as an imbalance between an enhanced reactive oxygen/nitrogen species and the lack of protective ability of antioxidants. From that point of view, free radical-induced damage caused by oxidative stress seems to be a probable contributing factor to the pathogenesis of many newborn diseases, such as respiratory distress syndrome, bronchopulmonary dysplasia, periventricular leukomalacia, necrotizing enterocolitis, patent ductus arteriosus, and retinopathy of prematurity. We share the hope that the new understanding of the concept of oxidative stress and its relation to newborn diseases that has been made possible by new diagnostic techniques will throw light on the treatment of those diseases.
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Rivera, José Carlos, Rabah Dabouz, Baraa Noueihed, Samy Omri, Houda Tahiri, and Sylvain Chemtob. "Ischemic Retinopathies: Oxidative Stress and Inflammation." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/3940241.
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Ischemic retinopathies (IRs), such as retinopathy of prematurity (ROP), diabetic retinopathy (DR), and (in many cases) age-related macular degeneration (AMD), are ocular disorders characterized by an initial phase of microvascular changes that results in ischemia, followed by a second phase of abnormal neovascularization that may culminate into retinal detachment and blindness. IRs are complex retinal conditions in which several factors play a key role during the development of the different pathological stages of the disease. Increasing evidence reveals that oxidative stress and inflammatory processes are important contributors to the pathogenesis of IRs. Despite the beneficial effects of the photocoagulation and anti-VEGF therapy during neovascularization phase, the need to identify novel targets to prevent initial phases of these ocular pathologies is still needed. In this review, we provide an update on the involvement of oxidative stress and inflammation in the progression of IRs and address some therapeutic interventions by using antioxidants and anti-inflammatory agents.
4
Gitto, Eloisa, Lucia Marseglia, Sara Manti, Gabriella D’Angelo, Ignazio Barberi, Carmelo Salpietro, and Russel J. Reiter. "Protective Role of Melatonin in Neonatal Diseases." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/980374.
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Oxidative stress contributes to the severity of several newborn conditions to the extent that Saugstad coined the phrase “oxygen radical diseases of neonatology.” In order to counteract free radicals damage many strategies to augment antioxidant status in ill-term and preterm infants have been proposed and several medications have been experimented with mixed results. Several studies have tested the efficacy of melatonin to counteract oxidative damage in diseases of newborns such as chronic lung disease, perinatal brain injury, necrotizing enterocolitis, and retinopathy of prematurity, giving promising results. The peculiar perinatal susceptibility to oxidative stress indicates that prophylactic use of antioxidants as melatonin could help to prevent or at least reduce oxidative stress related diseases in newborns. However, more studies are needed to confirm these beneficial effects.
5
Wang, Jun, Mengling Li, Ziyue Geng, Saadullah Khattak, Xinying Ji, Dongdong Wu, and Yalong Dang. "Role of Oxidative Stress in Retinal Disease and the Early Intervention Strategies: A Review." Oxidative Medicine and Cellular Longevity 2022 (October 14, 2022): 1–13. http://dx.doi.org/10.1155/2022/7836828.
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The retina, owing to its cellular anatomy and physical location, is susceptible to generating reactive oxygen species (ROS), which are associated with several major retinal diseases. When ROS exceeds the body’s natural antioxidants, the retina is in a state of oxidative stress, which is recognized as the pathogenesis of retinal diseases. The early stage of the pathogenic process is an adaptive change in which oxidative stress and endogenous defense mechanisms occur. If no treatment is applied, the retinal diseases will progress to the pathological stage with neuronal and vascular dysfunction or damage and even blindness. This review summarizes the role of oxidative stress in several common retinal diseases, including retinitis pigmentosa, age-related macular degeneration, diabetic retinopathy, glaucoma, and retinopathy of prematurity. In addition, we discuss the early intervention strategies for these diseases. An outline is provided to identify potential intervention targets for further research. Early intervention for retinal diseases is necessary and urgent and may offer hope to improve patients’ quality of life through functional vision.
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Aceti, Arianna, Isadora Beghetti, Silvia Martini, Giacomo Faldella, and Luigi Corvaglia. "Oxidative Stress and Necrotizing Enterocolitis: Pathogenetic Mechanisms, Opportunities for Intervention, and Role of Human Milk." Oxidative Medicine and Cellular Longevity 2018 (July 2, 2018): 1–7. http://dx.doi.org/10.1155/2018/7397659.
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This review will examine the role of oxidative stress (OS) in the pathogenesis of necrotizing enterocolitis (NEC) and explore potential preventive and therapeutic antioxidant strategies. Preterm infants are particularly exposed to OS as a result of several perinatal stimuli and constitutive defective antioxidant defenses. For this reason, OS damage represents a contributing factor to several complications of prematurity, including necrotizing enterocolitis (NEC). Being NEC a multifactorial disease, OS may act as downstream component of the pathogenetic cascade. To counteract OS in preterm infants with NEC, several antioxidant strategies have been proposed and different antioxidant compounds have been experimented. It is well known that human milk (HM) is an important source of antioxidants. At the same time, the role of an exclusive HM diet is well recognized in the prevention of NEC. However, donor HM (DHM) processing may impair antioxidant properties. As DHM is becoming a common nutritional intervention for high risk PI, the antioxidant status of preterm and DHM and potential ways to preserve its antioxidant capacity may merit further investigation.
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Tissot van Patot, Martha C., Andrew J. Murray, Virginia Beckey, Tereza Cindrova-Davies, Jemma Johns, Lisa Zwerdlinger, Eric Jauniaux, Graham J. Burton, and Natalie J. Serkova. "Human placental metabolic adaptation to chronic hypoxia, high altitude: hypoxic preconditioning." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R166—R172. http://dx.doi.org/10.1152/ajpregu.00383.2009.
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We have previously demonstrated placentas from laboring deliveries at high altitude have lower binding of hypoxia-inducible transcription factor (HIF) to DNA than those from low altitude. It has recently been reported that labor causes oxidative stress in placentas, likely due to ischemic hypoxic insult. We hypothesized that placentas of high-altitude residents acquired resistance, in the course of their development, to oxidative stress during labor. Full-thickness placental tissue biopsies were collected from laboring vaginal and nonlaboring cesarean-section term (37–41 wk) deliveries from healthy pregnancies at sea level and at 3,100 m. After freezing in liquid nitrogen within 5 min of delivery, we quantified hydrophilic and lipid metabolites using 31P and 1H NMR metabolomics. Metabolic markers of oxidative stress, increased glycolysis, and free amino acids were present in placentas following labor at sea level, but not at 3,100 m. In contrast, at 3,100 m, the placentas were characterized by the presence of concentrations of stored energy potential (phosphocreatine), antioxidants, and low free amino acid concentrations. Placentas from pregnancies at sea level subjected to labor display evidence of oxidative stress. However, laboring placentas at 3,100 m have little or no oxidative stress at the time of delivery, suggesting greater resistance to ischemia-reperfusion. We postulate that hypoxic preconditioning might occur in placentas that develop at high altitude.
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Xia, Wei, Zhipeng Cao, Xiaoyu Zhang, and Lina Gao. "A Proteomics Study on the Mechanism of Nutmeg-Induced Hepatotoxicity." Molecules 26, no. 6 (March 20, 2021): 1748. http://dx.doi.org/10.3390/molecules26061748.
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Nutmeg is a traditional spice and medicinal plant with a variety of pharmacological activities. However, nutmeg abuse due to its hallucinogenic characteristics and poisoning cases are frequently reported. Our previous metabolomics study proved the hepatotoxicity of nutmeg and demonstrated that high-dose nutmeg can affect the synthesis and secretion of bile acids and cause oxidative stress. In order to further investigate the hepatotoxicity of nutmeg, normal saline, 1 g/kg, 4 g/kg nutmeg were administrated to male Kunming mice by intragastrical gavage for 7 days. Histopathological investigation of liver tissue, proteomics and biochemical analysis were employed to explore the mechanism of liver damage caused by nutmeg. The results showed that a high-dose (4 g/kg) of nutmeg can cause significant increased level of CYP450s and depletion of antioxidants, resulting in obvious oxidative stress damage and lipid metabolism disorders; but this change was not observed in low-dose group (1 g/kg). In addition, the increased level of malondialdehyde and decreased level of glutathione peroxidase were found after nutmeg exposure. Therefore, the present study reasonably speculates that nutmeg exposure may lead to liver injury through oxidative stress and the degree of this damage is related to the exposure dose.
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Ng, Kai Song, Sheri-Ann Tan, Chui Yin Bok, Khye Er Loh, Intan Safinar Ismail, Chen Son Yue, and Chui Fung Loke. "Metabolomic Approach for Rapid Identification of Antioxidants in Clinacanthus nutans Leaves with Liver Protective Potential." Molecules 27, no. 12 (June 7, 2022): 3650. http://dx.doi.org/10.3390/molecules27123650.
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Antioxidants are currently utilized to prevent the occurrence of liver cancer in non-alcoholic fatty liver disease (NAFLD) patients. Clinacanthus nutans possesses anti-oxidative and anti-inflammatory properties that could be an ideal therapy for liver problems. The objective of this study is to determine the potential antioxidative compounds from the C. nutans leaves (CNL) and stems (CNS). Chemical- and cell-based antioxidative assays were utilized to evaluate the bioactivities of CNS and CNL. The NMR metabolomics approach assisted in the identification of contributing phytocompounds. Based on DPPH and ABTS radical scavenging activities, CNL demonstrated stronger radical scavenging potential as compared to CNS. The leaf extract also recorded slightly higher reducing power properties. A HepG2 cell model system was used to investigate the ROS reduction potential of these extracts. It was shown that cells treated with CNL and CNS reduced innate ROS levels as compared to untreated controls. Interestingly, cells pre-treated with both extracts were also able to decrease ROS levels in cells induced with oxidative stress. CNL was again the better antioxidant. According to multivariate data analysis of the 1H NMR results, the main metabolites postulated to contribute to the antioxidant and hepatoprotective abilities of leaves were clinacoside B, clinacoside C and isoschaftoside, which warrants further investigation.
10
Wimalawansa, Sunil J. "Vitamin D Deficiency: Effects on Oxidative Stress, Epigenetics, Gene Regulation, and Aging." Biology 8, no. 2 (May 11, 2019): 30. http://dx.doi.org/10.3390/biology8020030.
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Recent advances in vitamin D research indicate that this vitamin, a secosteroid hormone, has beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)2D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)2D] are essential for human physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. Vitamin D is one of the key controllers of systemic inflammation, oxidative stress and mitochondrial respiratory function, and thus, the aging process in humans. In turn, molecular and cellular actions form 1,25(OH)2D slow down oxidative stress, cell and tissue damage, and the aging process. On the other hand, hypovitaminosis D impairs mitochondrial functions, and enhances oxidative stress and systemic inflammation. The interaction of 1,25(OH)2D with its intracellular receptors modulates vitamin D–dependent gene transcription and activation of vitamin D-responsive elements, which triggers multiple second messenger systems. Thus, it is not surprising that hypovitaminosis D increases the incidence and severity of several age-related common diseases, such as metabolic disorders that are linked to oxidative stress. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. Vitamin D adequacy leads to less oxidative stress and improves mitochondrial and endocrine functions, reducing the risks of disorders, such as autoimmunity, infections, metabolic derangements, and impairment of DNA repair; all of this aids a healthy, graceful aging process. Vitamin D is also a potent anti-oxidant that facilitates balanced mitochondrial activities, preventing oxidative stress-related protein oxidation, lipid peroxidation, and DNA damage. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunction with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentrations, likely to promise cost-effective better clinical outcomes in humans.
11
Nelson, David Roy, Ala’a Al Hrout, Amnah Salem Alzahmi, Amphun Chaiboonchoe, Amr Amin, and Kourosh Salehi-Ashtiani. "Molecular Mechanisms behind Safranal’s Toxicity to HepG2 Cells from Dual Omics." Antioxidants 11, no. 6 (June 7, 2022): 1125. http://dx.doi.org/10.3390/antiox11061125.
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The spice saffron (Crocus sativus) has anticancer activity in several human tissues, but the molecular mechanisms underlying its potential therapeutic effects are poorly understood. We investigated the impact of safranal, a small molecule secondary metabolite from saffron, on the HCC cell line HepG2 using untargeted metabolomics (HPLC–MS) and transcriptomics (RNAseq). Increases in glutathione disulfide and other biomarkers for oxidative damage contrasted with lower levels of the antioxidants biliverdin IX (139-fold decrease, p = 5.3 × 105), the ubiquinol precursor 3-4-dihydroxy-5-all-trans-decaprenylbenzoate (3-fold decrease, p = 1.9 × 10−5), and resolvin E1 (−3282-fold decrease, p = 45), which indicates sensitization to reactive oxygen species. We observed a significant increase in intracellular hypoxanthine (538-fold increase, p = 7.7 × 10−6) that may be primarily responsible for oxidative damage in HCC after safranal treatment. The accumulation of free fatty acids and other biomarkers, such as S-methyl-5′-thioadenosine, are consistent with safranal-induced mitochondrial de-uncoupling and explains the sharp increase in hypoxanthine we observed. Overall, the dual omics datasets describe routes to widespread protein destabilization and DNA damage from safranal-induced oxidative stress in HCC cells.
12
Zhu, Yueping, Qilai Xie, Jinshao Ye, Ruzhen Wang, Xudong Yin, Wenyu Xie, and Dehao Li. "Metabolic Mechanism of Bacillus sp. LM24 under Abamectin Stress." International Journal of Environmental Research and Public Health 20, no. 4 (February 9, 2023): 3068. http://dx.doi.org/10.3390/ijerph20043068.
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Abamectin (ABM) has been recently widely used in aquaculture. However, few studies have examined its metabolic mechanism and ecotoxicity in microorganisms. This study investigated the molecular metabolic mechanism and ecotoxicity of Bacillus sp. LM24 (B. sp LM24) under ABM stress using intracellular metabolomics. The differential metabolites most affected by the bacteria were lipids and lipid metabolites. The main significant metabolic pathways of B. sp LM24 in response to ABM stress were glycerolipid; glycine, serine, and threonine; and glycerophospholipid, and sphingolipid. The bacteria improved cell membrane fluidity and maintained cellular activity by enhancing the interconversion pathway of certain phospholipids and sn-3-phosphoglycerol. It obtained more extracellular oxygen and nutrients to adjust the lipid metabolism pathway, mitigate the impact of sugar metabolism, produce acetyl coenzyme A to enter the tricarboxylic acid (TCA) cycle, maintain sufficient anabolic energy, and use some amino acid precursors produced during the TCA cycle to express ABM efflux protein and degradative enzymes. It produced antioxidants, including hydroxyanigorufone, D-erythroascorbic acid 1′-a-D-xylopyranoside, and 3-methylcyclopentadecanone, to alleviate ABM-induced cellular and oxidative damage. However, prolonged stress can cause metabolic disturbances in the metabolic pathways of glycine, serine, threonine, and sphingolipid; reduce acetylcholine production; and increase quinolinic acid synthesis.
13
Poggi, Chiara, and Carlo Dani. "Antioxidant Strategies and Respiratory Disease of the Preterm Newborn: An Update." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/721043.
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Preterm newborns are challenged by an excessive oxidative burden, as a result of several perinatal stimuli, as intrauterine infections, resuscitation, mechanical ventilation, and postnatal complications, in the presence of immature antioxidant capacities. “Oxygen radical disease of neonatology” comprises a wide range of conditions sharing a common pathway of pathogenesis and includes bronchopulmonary dysplasia (BPD) and other main complications of prematurity. Antioxidant strategies may be beneficial in the prevention and treatment of oxidative stress- (OS-) related lung disease of the preterm newborn. Endotracheal supplementation or lung-targeted overexpression of superoxide dismutase was proved to reduce lung damage in several models; however, the supplementation in preterm newborn failed to reduce the risk of BPD, although long-term respiratory outcomes were improved. Also melatonin administration to small cohorts of preterm newborns suggested beneficial effects on lung OS. The possibility to identify single nucleotide polymorphism affecting the risk of BPD may help to identify specific populations with particularly high risk of OS-related diseases and may pose the basis for individually targeted treatments. Finally, surfactant replacement may lead to local anti-inflammatory and antioxidant effects, thanks to specific enzymatic and nonenzymatic antioxidants naturally present in animal surfactants.
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Gessner, Denise K., Lena M. Sandrock, Erika Most, Christian Koch, Robert Ringseis, and Klaus Eder. "Performance and Metabolic, Inflammatory, and Oxidative Stress-Related Parameters in Early Lactating Dairy Cows with High and Low Hepatic FGF21 Expression." Animals 13, no. 1 (December 29, 2022): 131. http://dx.doi.org/10.3390/ani13010131.
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Induction of FGF21 expression in the liver and a significant increase in plasma FGF21 concentration have been demonstrated in cows during early lactation, but knowledge about the function of FGF21 in dairy cows remains limited. In order to improve the understanding of the physiological role of FGF21 in dairy cows, the present study aimed to investigate differences in metabolic pathways between dairy cows with high and low hepatic expression of FGF21 at week 1 of lactation (n = 8/group) by liver transcriptomics, targeted plasma metabolomics, and analysis of inflammatory and oxidative stress-related parameters. Dry matter intake, energy balance, milk yield, and energy-corrected milk yield at days 8–14 postpartum did not differ between cows with high and low hepatic FGF21 expression. However, cows with high FGF21 expression showed an upregulation of genes involved in endoplasmic reticulum stress, inflammation, and nuclear factor E2-related factor 2 (Nrf2)-dependent cytoprotection compared to cows with low FGF21 expression at week 1 postpartum (p < 0.05). Concentrations of important antioxidants (tocopherols, β-carotene, and glutathione) in the liver and plasma, trolox equivalent antioxidant capacity in plasma, concentrations of oxidative stress-related compounds (thiobarbituric acid-reactive substances and protein carbonyls), and levels of most acute phase proteins at week 1 postpartum did not differ between cows with high or low FGF21 expression. Moreover, among a total of >200 metabolites assayed in the plasma, concentrations of only 7 metabolites were different between cows with high or low FGF21 expression (p < 0.05). Overall, the results showed that cows with high and low FGF21 hepatic expression had only moderate differences in metabolism, but FGF21 might be important in the adaptation of dairy cows to stress conditions during early lactation.
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Pfluger, Brigitte A., Hillary V. Smith, Annika M. Weber, Hend Ibrahim, Lassina Doumbia, Abdoulaye Bore, Alima Cissoko, et al. "Non-Targeted Dried Blood Spot-Based Metabolomics Analysis Showed Rice Bran Supplementation Effects Multiple Metabolic Pathways during Infant Weaning and Growth in Mali." Nutrients 14, no. 3 (January 30, 2022): 609. http://dx.doi.org/10.3390/nu14030609.
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Rice bran contains essential nutrients, antioxidants, and bioactives with anti-inflammatory and diarrheal protective properties important for infants. This 6-month randomized controlled trial investigated the effects of heat-stabilized rice bran supplementation during Malian infant weaning. Fifty healthy 6-month-old infants were randomized to a rice bran intervention (N = 25) or non-intervention control group (N = 25). Intervention infants received dose-escalating rice bran supplementation for 6 months (1–5 g/day). Monthly infant dried blood spot and anthropometric measurements were collected. Dried blood spot metabolite abundances were compared monthly according to diet for six months. Supplementation resulted in favorable weight-for-age and weight-for-length z-score changes. Non-targeted dried blood spot-based metabolomics identified 796 metabolites, of which 33% had significant fold differences between groups (7–12 months). Lipids and amino acids represented 70.6% of the metabolites identified. Rice bran supplementation during infant weaning significantly modulated the metabolites involved in antioxidant defenses and with neuroactive properties including reduced glutathione, glycine, glutamate, cysteinylglycine, tryptophan betaine, and choline. These findings support rice bran as a weaning ingredient to meet infant nutritional requirements and with the potential to reduce oxidative stress and improve cognitive outcomes. This study provides evidence for dried blood spots as a cost-effective tool to detect infant biomarkers of nutritional and metabolic status.
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Snegarova, Violeta, and Darina Naydenova. "Vitamin D: a Review of its Effects on Epigenetics and Gene Regulation." Folia Medica 62, no. 4 (December 31, 2020): 662–67. http://dx.doi.org/10.3897/folmed.62.e50204.
Full textAbstract:
Vitamin D is a secosteroid hormone with known beneficial effects on several body systems other than the musculoskeletal system. Both 25 dihydroxy vitamin D [25(OH)2D] and its active hormonal form, 1,25-dihydroxyvitamin D [1,25(OH)2D] are essential for hu-man physiological functions, including damping down inflammation and the excessive intracellular oxidative stresses. In the present study we set out to review all available literature on vitamin D and the role it plays in epigenetics and gene regulation. We searched the PubMed/Medline electronic database for studies published in the English language up to January 2020. The Medical Subject Headings (MeSH) database was searched with the keywords ‘vitamin D’, ‘DNA methylation’, ‘nutritional supplements’, ‘epigenome’ and ‘pregnancy’. Observational studies, supplementation studies, and meta-analyses dealing with the effect of vitamin D on epigenetics and gene regula-tion were included in the review. The obtained information from the databases such as PubMed, Google Scholar, and ResearchGate was analysed and summarized. We found that hypovitaminosis D increases the incidence and severity of several age-related common diseases such as the oxidative stress-associated metabolic disorders. These include obesity, insulin resistance, type 2 diabetes, hypertension, pregnancy complications, memory disorders, osteoporosis, autoimmune diseases, certain cancers, and systemic inflammatory diseases. New understandings of vitamin D-related advances in metabolomics, transcriptomics, epigenetics, in relation to its ability to control oxidative stress in conjunc-tion with micronutrients, vitamins, and antioxidants, following normalization of serum 25(OH)D and tissue 1,25(OH)2D concentra-tions, are likely to promise better cost-effective clinical outcomes in humans. There is a strong reciprocity between the vitamin D system and epigenetic mechanisms. The vitamin D system is, on the one hand regu-lated by epigenetic mechanisms and, on the other hand, is involved in regulating epigenetic events.
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Ganguly, Samit, David Finkelstein, Timothy I. Shaw, Ryan D. Michalek, Kimberly M. Zorn, Sean Ekins, Kazuto Yasuda, et al. "Metabolomic and transcriptomic analysis reveals endogenous substrates and metabolic adaptation in rats lacking Abcg2 and Abcb1a transporters." PLOS ONE 16, no. 7 (July 13, 2021): e0253852. http://dx.doi.org/10.1371/journal.pone.0253852.
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Abcg2/Bcrp and Abcb1a/Pgp are xenobiotic efflux transporters limiting substrate permeability in the gastrointestinal system and brain, and increasing renal and hepatic drug clearance. The systemic impact of Bcrp and Pgp ablation on metabolic homeostasis of endogenous substrates is incompletely understood. We performed untargeted metabolomics of cerebrospinal fluid (CSF) and plasma, transcriptomics of brain, liver and kidney from male Sprague Dawley rats (WT) and Bcrp/Pgp double knock-out (dKO) rats, and integrated metabolomic/transcriptomic analysis to identify putative substrates and perturbations in canonical metabolic pathways. A predictive Bayesian machine learning model was used to predict in silico those metabolites with greater substrate-like features for either transporters. The CSF and plasma levels of 169 metabolites, nutrients, signaling molecules, antioxidants and lipids were significantly altered in dKO rats, compared to WT rats. These metabolite changes suggested alterations in histidine, branched chain amino acid, purine and pyrimidine metabolism in the dKO rats. Levels of methylated and sulfated metabolites and some primary bile acids were increased in dKO CSF or plasma. Elevated uric acid levels appeared to be a primary driver of changes in purine and pyrimidine biosynthesis. Alterations in Bcrp/Pgp dKO CSF levels of antioxidants, precursors of neurotransmitters, and uric acid suggests the transporters may contribute to the regulation of a healthy central nervous system in rats. Microbiome-generated metabolites were found to be elevated in dKO rat plasma and CSF. The altered dKO metabolome appeared to cause compensatory transcriptional change in urate biosynthesis and response to lipopolysaccharide in brain, oxidation-reduction processes and response to oxidative stress and porphyrin biosynthesis in kidney, and circadian rhythm genes in liver. These findings present insight into endogenous functions of Bcrp and Pgp, the impact that transporter substrates, inhibitors or polymorphisms may have on metabolism, how transporter inhibition could rewire drug sensitivity indirectly through metabolic changes, and identify functional Bcrp biomarkers.
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Ma, Zhou, Chen, Urriola, Shurson, Ruan, and Chen. "Metabolomic Evaluation of Scenedesmus sp. as a Feed Ingredient Revealed Dose-Dependent Effects on Redox Balance, Intermediary and Microbial Metabolism in a Mouse Model." Nutrients 11, no. 9 (August 21, 2019): 1971. http://dx.doi.org/10.3390/nu11091971.
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Scenedesmus is a common green algae genus with high biomass productivity, and has been widely used in biofuel production and waste water management. However, the suitability and metabolic consequences of using Scenedesmus as an animal feed ingredient have not been examined in detail. In this study, the influences of consuming Scenedesmus on the metabolic status of young mice were investigated through growth performance, blood chemistry, and liquid chromatography-mass spectrometry (LC-MS)-based metabolomics. Compared to the control diet, feeding a diet containing 5% Scenedesmus improved growth performance while the diet containing 20% Scenedesmus suppressed it. Among common macronutrients-derived blood biochemicals, serum triacylglycerols and cholesterol levels were dramatically decreased by feeding the 20% Scenedesmus diet. Metabolomic analysis of liver, serum, feces, and urine samples indicated that Scenedesmus feeding greatly affected the metabolites associated with amino acid, lipid, purine, microbial metabolism, and the endogenous antioxidant system. The growth promotion effect of feeding the 5% Scenedesmus diet was associated with elevated concentrations of antioxidants, an expanded purine nucleotide cycle, and modified microbial metabolism, while the growth suppression effect of feeding the 20% Scenedesmus diet was correlated to oxidative stress, disrupted urea cycle, upregulated fatty acid oxidation, and an imbalanced lipidome. These correlations among Scenedesmus dietary inclusion rate, individual metabolite markers, and growth performance suggest the need to define the dietary inclusion rate threshold for using Scenedesmus and other microalgae supplements as feed ingredients, and also warrant further mechanistic investigations on the biological processes connecting specific constituents of Scenedesmus with the metabolic effects observed in this study.
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Perkovic, Matea Nikolac, Morana Jaganjac, Lidija Milkovic, Tea Horvat, David Rojo, Kamelija Zarkovic, Marijana Ćorić, et al. "Relationship between 4-Hydroxynonenal (4-HNE) as Systemic Biomarker of Lipid Peroxidation and Metabolomic Profiling of Patients with Prostate Cancer." Biomolecules 13, no. 1 (January 10, 2023): 145. http://dx.doi.org/10.3390/biom13010145.
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An oxidative degradation product of the polyunsaturated fatty acids, 4-hydroxynonenal (4-HNE), is of particular interest in cancer research due to its concentration-dependent pleiotropic activities affecting cellular antioxidants, metabolism, and growth control. Although an increase in oxidative stress and lipid peroxidation was already associated with prostate cancer progression a few decades ago, the knowledge of the involvement of 4-HNE in prostate cancer tumorigenesis is limited. This study investigated the appearance of 4-HNE-protein adducts in prostate cancer tissue by immunohistochemistry using a genuine 4-HNE monoclonal antibody. Plasma samples of the same patients and samples of the healthy controls were also analyzed for the presence of 4-HNE-protein adducts, followed by metabolic profiling using LC-ESI-QTOF-MS and GC-EI-Q-MS. Finally, the analysis of the metabolic pathways affected by 4-HNE was performed. The obtained results revealed the absence of 4-HNE-protein adducts in prostate carcinoma tissue but increased 4-HNE-protein levels in the plasma of these patients. Metabolomics revealed a positive association of different long-chain and medium-chain fatty acids with the presence of prostate cancer. Furthermore, while linoleic acid positively correlated with the levels of 4-HNE-protein adducts in the blood of healthy men, no correlation was obtained for cancer patients indicating altered lipid metabolism in this case. The metabolic pathway of unsaturated fatty acids biosynthesis emerged as significantly affected by 4-HNE. Overall, this is the first study linking 4-HNE adduction to plasma proteins with specific alterations in the plasma metabolome of prostate cancer patients. This study revealed that increased 4-HNE plasma protein adducts could modulate the unsaturated fatty acids biosynthesis pathway. It is yet to be determined if this is a direct result of 4-HNE or whether they are produced by the same underlying mechanisms. Further mechanistic studies are needed to grasp the biological significance of the observed changes in prostate cancer tumorigenesis.
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Syusyuka, V. G., N. G. Kolokot, and I. F. Belenichev. "Estimation of efficiency of complex cytoprotective therapy of pregnant women with fetal growth delay." HEALTH OF WOMAN, no. 9-10(155-156) (December 30, 2020): 83–90. http://dx.doi.org/10.15574/hw.2020.155-156.83.
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The objective: estimate efficiency and influence of complex, cytoprotective therapy of pregnant women with fetal growth delay on biochemical indexes and results of delivery. Materials and methods. 93 women with monocyesis at term of 28-34 gestation weeks took part in the research. Group І includes 30 pregnant women with fetal growth delay (FGD). The pregnant women of the present group were prescribed with complex, cytoprotective therapy. It includes prescription of thiotriazolin in complex with L-arginine and diosmin. Group ІІ is presented by 33 pregnant women with FGD whose management of pregnancy and delivery is provided by valid orders of Ministry of Healthcare of Ukraine. Group ІІІ (the control one) consists of 30 pregnant women without FGD. Research of protein oxidative modification (POM) markers and level of stable nitrogen oxide metabolites (NO) were estimated in blood serum with spectrophotometric method. Reduced glutathione (GSH) was determined with calculation of its level according to the calibration curve. Results. Primary estimation of their content showed statistically valid (p < 0.05) lower GSH and NO in comparison of indexes of pregnant women without FGD (ІІІ group) with indexes of pregnant women with FGD (both І and ІІ groups). This fact indicates decrease of antioxidant protection and deficit of the main vessel dilator in the present group. Further estimation of biochemical indexes in dynamics of pregnancy permitted to determine considerable progress of imbalance between oxidants and antioxidants and absence of significant changes of NO level among pregnant women of II group. In pregnant women of I group who got the proposed complex cytoprotective therapy, on contrary, statistically valid (p < 0.05) decrease of POM indexes together with increase of GSH and NO level that indicates its positive influence were found. By means of analysis of special features of the pregnancy course in research group there was stated that the rate of habitual pregnancy non-carrying (HPN) in group II made 39.4% and considerably exceeded relevant indexes of І (20.0%) and ІІІ (16.7%) groups. Hypertensive disorders during pregnancy and labour are diagnosed only in pregnant women of І (6.7%) and ІІ (9.1%) groups. Average index of giving birth in І and ІІІ groups made 38.5±0.6 weeks and 39.4 ± 0.5 weeks correspondingly and in group ІІ it was lower 37.2±0.6 weeks. Index of preterm delivery (PD) rate in І group made 3.3% and was 6 times lower than appropriate index of ІІ group (21.2%). PD rate was absent in ІІІ group. Rate of the fetus distress in ІІ group (18.2%) was 2.7 times higher than the relevant index of І group (6.7%) and in ІІІ group it made 3.3%. Condition of newborns in research groups was estimated under Apgar scale. Both at the 1-st and 5-th minute the general index under appropriate scale was statistically valid (p < 0.05) and lower than in ІІ group as compared to indexes of І and ІІІ groups. During description of perinatal complications there was stated considerable percentage of neonatal encephalopathy and jaundice in ІІ group, namely 33.3% and 36.4% correspondingly. In І group their rate made 10.0% and 3.3%, correspondingly. In structure of perinatal pathology prematurity was in 21.2% of newborns of ІІ group that is 6 times higher than appropriate index of І group (3.3%). Mentioned complications were not determined in ІІІ group. In calculation under weight and height parameters of newborns the rate of FGD in ІІ group was the highest and made 88.6%. Mentioned index in І and ІІІ groups made 60.0% and 10.0%, correspondingly. Conclusion. The proposed complex cytoprotective therapy including combined use of thiotriazolin, L-arginine and diosmin (that considerably increases anti-ischemic, antioxidant and endothelium protective action of complex therapy) in women with fetal growth delay has the positive effect on oxidative-reductive hemeostasis and thiol-disulfide balance of mother-placenta-fetus system. Obstetric and perinatal results of delivery in the present group of pregnant women are characterized by statistically valid (р < 0.05) prevalence of estimation indexes under Apgar scale and correspondingly processes of adaptation as well as results of anthropomorphic measurements of newborns, their weight and height parameters and lower rate of neonatal encephalopathy and delivery of premature babies. Keywords: pregnancy, fetus growth inhibition, protein oxidative modification, antioxidant defense system, oxidative stress, obstetric and perinatal complications, cytoprotective therapy.
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Kurosawa, Ryo, Ryota Sugimoto, Hiroe Imai, Kohei Atsuji, Koji Yamada, Yusuke Kawano, Iwao Ohtsu, and Kengo Suzuki. "Impact of spaceflight and artificial gravity on sulfur metabolism in mouse liver: sulfur metabolomic and transcriptomic analysis." Scientific Reports 11, no. 1 (November 8, 2021). http://dx.doi.org/10.1038/s41598-021-01129-1.
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AbstractSpaceflight induces hepatic damage, partially owing to oxidative stress caused by the space environment such as microgravity and space radiation. We examined the roles of anti-oxidative sulfur-containing compounds on hepatic damage after spaceflight. We analyzed the livers of mice on board the International Space Station for 30 days. During spaceflight, half of the mice were exposed to artificial earth gravity (1 g) using centrifugation cages. Sulfur-metabolomics of the livers of mice after spaceflight revealed a decrease in sulfur antioxidants (ergothioneine, glutathione, cysteine, taurine, thiamine, etc.) and their intermediates (cysteine sulfonic acid, hercynine, N-acethylserine, serine, etc.) compared to the controls on the ground. Furthermore, RNA-sequencing showed upregulation of gene sets related to oxidative stress and sulfur metabolism, and downregulation of gene sets related to glutathione reducibility in the livers of mice after spaceflight, compared to controls on the ground. These changes were partially mitigated by exposure to 1 g centrifugation. For the first time, we observed a decrease in sulfur antioxidants based on a comprehensive analysis of the livers of mice after spaceflight. Our data suggest that a decrease in sulfur-containing compounds owing to both microgravity and other spaceflight environments (radiation and stressors) contributes to liver damage after spaceflight.
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Jindal, Sunita, Pavel Kerchev, Miroslav Berka, Martin Černý, Halidev Krishna Botta, Ashverya Laxmi, and Břetislav Brzobohatý. "Type-A response regulators negatively mediate heat stress response by altering redox homeostasis in Arabidopsis." Frontiers in Plant Science 13 (September 23, 2022). http://dx.doi.org/10.3389/fpls.2022.968139.
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Besides the long-standing role of cytokinins (CKs) as growth regulators, their current positioning at the interface of development and stress responses is coming into recognition. The current evidence suggests the notion that CKs are involved in heat stress response (HSR), however, the role of CK signaling components is still elusive. In this study, we have identified a role of the CK signaling components type-A Arabidopsis response regulators (ARRs) in HSR in Arabidopsis. The mutants of multiple type-A ARR genes exhibit improved basal and acquired thermotolerance and, altered response to oxidative stress in our physiological analyses. Through proteomics profiling, we show that the type-A arr mutants experience a ‘stress-primed’ state enabling them to respond more efficiently upon exposure to real stress stimuli. A substantial number of proteins that are involved in the heat-acclimatization process such as the proteins related to cellular redox status and heat shock, are already altered in the type-A arr mutants without a prior exposure to stress conditions. The metabolomics analyses further reveal that the mutants accumulate higher amounts of α-and γ-tocopherols, which are important antioxidants for protection against oxidative damage. Collectively, our results suggest that the type-A ARRs play an important role in heat stress response by affecting the redox homeostasis in Arabidopsis.
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Zhuan, Qingrui, Jun Li, Xingzhu Du, Luyao Zhang, Lin Meng, Yuwen Luo, Dan Zhou, et al. "Antioxidant procyanidin B2 protects oocytes against cryoinjuries via mitochondria regulated cortical tension." Journal of Animal Science and Biotechnology 13, no. 1 (August 16, 2022). http://dx.doi.org/10.1186/s40104-022-00742-y.
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Abstract Background Irreversible cryodamage caused by oocyte vitrification limited its wild application in female fertility preservation. Antioxidants were always used to antagonist the oxidative stress caused by vitrification. However, the comprehensive mechanism underlying the protective role of antioxidants has not been studied. Procyanidin B2 (PCB2) is a potent natural antioxidant and its functions in response to vitrification are still unknown. In this study, the effects of PCB2 on vitrified-thawed oocytes and subsequent embryo development were explored, and the mechanisms underlying the protective role of PCB2 were systematically elucidated. Results Vitrification induced a marked decline in oocyte quality, while PCB2 could improve oocyte viability and further development after parthenogenetic activation. A subsequent study indicated that PCB2 effectively attenuated vitrification-induced oxidative stress, rescued mitochondrial dysfunction, and improved cell viability. Moreover, PCB2 also acts as a cortical tension regulator apart from strong antioxidant properties. Increased cortical tension caused by PCB2 would maintain normal spindle morphology and promote migration, ensure correct meiosis progression and finally reduce the aneuploidy rate in vitrified oocytes. Further study reveals that ATP biosynthesis plays a crucial role in cortical tension regulation, and PCB2 effectively increased the cortical tension through the electron transfer chain pathway. Additionally, PCB2 would elevate the cortical tension in embryo cells at morula and blastocyst stages and further improve blastocyst quality. What’s more, targeted metabolomics shows that PCB2 has a beneficial effect on blastocyst formation by mediating saccharides and amino acids metabolism. Conclusions Antioxidant PCB2 exhibits multi-protective roles in response to vitrification stimuli through mitochondria-mediated cortical tension regulation.
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Fatima, Arooj. "Malondialdehyde (MDA) Total Antioxidant Capacity and Vitamin E Levels in Preterm and Term Infants." International Journal of Current Science Research and Review 05, no. 04 (April 12, 2022). http://dx.doi.org/10.47191/ijcsrr/v5-i4-17.
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Introduction: Oxygen radical injury is thought to be one of the common mechanisms for several diseases in premature infants. Lipid peroxidation plays a vital role in the pathogenesis of many neonatal complications. Broncho pulmonary dysplasia, Intraventricular hemorrhage and Retinopathy of Prematurity are due to excessive production of oxygen free radicals. Objectives: The main objective of the study is to find the Malondialdehyde (MDA), total antioxidant capacity and Vitamin E levels in preterm and term infants. Material and methods: We aimed to determine the levels of Malondialdehyde (MDA), Total antioxidant capacity and vitamin E in cord blood of term and preterm infants. To determine the oxidative stress and antioxidants in cord blood of term and preterm infants that may have clinical implications. In the present study we determine MDA, Total antioxidant capacity and vitamin E levels in the umbilical cord blood of term (n=50) and preterm (n=50) infants by manual method. Blood samples were collected during delivery. MDA is high in preterm infants compared to term infants. Results: Total antioxidant capacity and Vitamin E levels are high in term infants compared to preterm infants. Therefore it is possible to postulate that preterm infants are more susceptible to oxidative stress than term infants. Conclusion: It is concluded that Preterm neonates are exposed to increased oxidant stress at birth and are susceptible to anti-oxidant deficiencies.
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Zhong, Zhi-Hong, Zhi-Cheng Li, Han Li, Qing-Kai Guo, Chen-Xi Wang, Ji-Zhen Cao, and An-Xing Li. "Glutathione metabolism in Cryptocaryon irritans involved in defense against oxidative stress induced by zinc ions." Parasites & Vectors 15, no. 1 (September 7, 2022). http://dx.doi.org/10.1186/s13071-022-05390-9.
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Abstract Background Cryptocaryon irritans is a fatal parasite for marine teleosts and causes severe economic loss for aquaculture. Galvanized materials have shown efficacy in controlling this parasite infestation through the release of zinc ions to induce oxidative stress. Methods In this study, the resistance mechanism in C. irritans against oxidative stress induced by zinc ions was investigated. Untargeted metabolomics analysis was used to determine metabolic regulation in C. irritans in response to zinc ion treatment by the immersion of protomonts in ZnSO4 solution at a sublethal dose (20 μmol). Eight differential metabolites were selected to assess the efficacy of defense against zinc ion stimulation in protomonts of C. irritans. Furthermore, the mRNA relative levels of glutathione metabolism-associated enzymes were measured in protomonts following treatment with ZnSO4 solution at sublethal dose. Results The results showed that zinc ion exposure disrupted amino acid metabolism, carbohydrate metabolism, lipid metabolism, and nucleotide metabolism in C. irritans. Four antioxidants, namely ascorbate, S-hexyl-glutathione, syringic acid, and ubiquinone-1, were significantly increased in the Zn group (P < 0.01), while the glutathione metabolism pathway was enhanced. The encystment rate of C. irritans was significantly higher in the ascorbate and methionine treatment (P < 0.05) groups. Additionally, at 24 h post-zinc ion exposure, the relative mRNA level of glutathione reductase (GR) was increased significantly (P < 0.01). On the contrary, the relative mRNA levels of glutathione S-transferase (GT) and phospholipid-hydroperoxide glutathione peroxidase (GPx) were significantly decreased (P < 0.05), thus indicating that the generation of reduced glutathione was enhanced. Conclusions These results revealed that glutathione metabolism in C. irritans contributes to oxidative stress resistance from zinc ions, and could be a potential drug target for controlling C. irritans infection. Graphical Abstract
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Han, Weijuan, Kun Cao, Songfeng Diao, Peng Sun, Huawei Li, Yini Mai, Yujing Suo, and Jianmin Fu. "Characterization of browning during CO2 deastringency treatment in astringent persimmon fruit." Journal of Food Measurement and Characterization, February 25, 2022. http://dx.doi.org/10.1007/s11694-022-01298-1.
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AbstractDeastringency treatment with CO2 is an effective and convenient method for improving the marketability of persimmon fruit. However, the main persimmon cultivars in China turn brown very quickly following exposure to a high-CO2 atmosphere, causing significant economic loss. However, the mechanisms of persimmon browning under CO2 treatment remain largely unknown. In this study, we evaluated components and enzymes related to persimmon fruit browning. The results revealed that astringency was alleviated by simultaneous reduction of soluble tannin content and accumulation of insoluble tannin. During persimmon browning, fruit firmness, total phenolic content, and phenylalanine ammonia lyase (PAL) activity decreased significantly, whereas malondialdehyde (MDA), superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), and polyphenol oxidase (PPO) activity increased significantly, suggesting that reactive oxygen species (ROS)-scavenging enzymes and non-enzymatic antioxidants cannot effectively maintain redox reaction balance to protect cell membranes from oxidative damage during CO2 treatment. An untargeted metabolomics analysis identified 19 polyhydroxyphenols that were downregulated in CO2-treated fruit, suggesting that phenolics may act as a substrate for persimmon browning. We also identified 11 metabolites associated with abiotic stress. Together, these results study provide valuable information on the mechanism of persimmon fruit browning induced by CO2 treatment and will contribute to the ongoing development of the persimmon fruit industry.
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Dong, Mingyuan, Honghan Liu, Tianjiao Cao, Lanzhou Li, Zhen Sun, Ye Qiu, and Di Wang. "Huoxiang Zhengqi alleviates azoxymethane/dextran sulfate sodium-induced colitis-associated cancer by regulating Nrf2/NF-κB/NLRP3 signaling." Frontiers in Pharmacology 13 (October 21, 2022). http://dx.doi.org/10.3389/fphar.2022.1002269.
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Colitis-associated cancer (CAC) is a subtype of inflammatory bowel disease (IBD)-associated colorectal cancer. Huoxiang Zhengqi (HXZQ) is a classical Chinese herbal medicine and has been used to treat intestinal disorders, however, anti-CAC effects and underlying mechanisms of HXZQ have not been reported. An azoxymethane/dextran sulfate sodium-induced CAC mice model was used to investigate the anti-CAC effect of HXZQ. HXZQ significantly reduced colonic inflammation, suppressed the size and number of tumors, and reduced the levels of pro-inflammatory cytokines (interleukin [IL]-1α, IL-1β, IL-6, IL-17A, IL-21, IL-23, granulocyte macrophage-colony stimulating factor, and tumor necrosis factor-α) and oxidative stress markers (reactive oxygen species and malondialdehyde), and increased the levels of anti-inflammatory cytokines (IL-10 and IL-27) in CAC mice. Intestinal microbiota and serum metabolomics analyses indicated that HXZQ altered the gut microbial composition and the abundance of 29 serum metabolites in CAC mice. Additionally, HXZQ activated the nuclear factor-erythroid factor 2-related factor 2 (Nrf2) signaling pathway and increased the levels of antioxidants such as catalase (CAT), heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductases-1 (NQO-1), and superoxide dismutase-1 (SOD-1). HXZQ inhibited the activation of the nuclear factor kappa-B (NF-κB) signaling pathway and decreased the expression of NLR family pyrin domain containing 3 (NLRP3) by inhibiting the phosphorylation of inhibitor of nuclear factor kappa-B (IκB), inhibitor of nuclear factor kappa-B kinase (IKK), and NF-κB. In conclusion, HXZQ alleviated CAC in mice by modulating the intestinal microbiota and metabolism, activating Nrf2-mediated antioxidant response, and inhibiting NF-κB-mediated NLRP3 inflammasome activation against inflammation. The present data provide a reference for the use of HXZQ as a therapeutic or combination agent for clinical CAC treatment.
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Anesti, Ourania, Nafsika Papaioannou, Catherine Gabriel, Achilleas Karakoltzidis, Vazha Dzhedzheia, Ioannis Petridis, Antonios Stratidakis, et al. "An exposome connectivity paradigm for the mechanistic assessment of the effects of prenatal and early life exposure to metals on neurodevelopment." Frontiers in Public Health 10 (January 9, 2023). http://dx.doi.org/10.3389/fpubh.2022.871218.
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The exposome paradigm through an integrated approach to investigating the impact of perinatal exposure to metals on child neurodevelopment in two cohorts carried out in Slovenia (PHIME cohort) and Greece (HERACLES cohort) respectively, is presented herein. Heavy metals are well-known neurotoxicants with well-established links to impaired neurodevelopment. The links between in utero and early-life exposure to metals, metabolic pathway dysregulation, and neurodevelopmental disorders were drawn through urinary and plasma untargeted metabolomics analysis, followed by the combined application of in silico and biostatistical methods. Heavy metal prenatal and postnatal exposure was evaluated, including parameters indirectly related to exposure and health adversities, such as sociodemographic and anthropometric parameters and dietary factors. The primary outcome of the study was that the identified perturbations related to the TCA cycle are mainly associated with impaired mitochondrial respiration, which is detrimental to cellular homeostasis and functionality; this is further potentiated by the capacity of heavy metals to induce oxidative stress. Insufficient production of energy from the mitochondria during the perinatal period is associated with developmental disorders in children. The HERACLES cohort included more detailed data regarding diet and sociodemographic status of the studied population, allowing the identification of a broader spectrum of effect modifiers, such as the beneficial role of a diet rich in antioxidants such as lycopene and ω-3 fatty acids, the negative effect the consumption of food items such as pork and chicken meat has or the multiple impacts of fish consumption. Beyond diet, several other factors have been proven influential for child neurodevelopment, such as the proximity to pollution sources (e.g., waste treatment site) and the broader living environment, including socioeconomic and demographic characteristics. Overall, our results demonstrate the utility of exposome-wide association studies (EWAS) toward understanding the relationships among the multiple factors that determine human exposure and the underlying biology, reflected as omics markers of effect on neurodevelopment during childhood.