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Journal articles on the topic 'Intracellular accumulation'

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Author: Grafiati

Published: 7 July 2024

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1

Atabayeva, S. D., S. Sh Asrandina, R. A. Alybaeva, and S. A. Shoinbekova. "Intracellular localization, accumulation and distribution of heavy metals in plants." International Journal of Biology and Chemistry 8, no. 2 (2015): 9–12. http://dx.doi.org/10.26577/2218-7979-2015-8-2-9-12.

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Melnichenko, A., M. Iltchuk, T. Fatkhudinov, G. Bolshakova, R. Wetzker, and A. Orekhov. "Intracellular Accumulation Of Ldl Associates." Atherosclerosis 287 (August 2019): e233. http://dx.doi.org/10.1016/j.atherosclerosis.2019.06.717.

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3

Vingtdeux, Valérie, Malika Hamdane, Séverine Bégard, Anne Loyens, André Delacourte, Jean-Claude Beauvillain, Luc Buée, Philippe Marambaud, and Nicolas Sergeant. "Intracellular pH regulates amyloid precursor protein intracellular domain accumulation." Neurobiology of Disease 25, no. 3 (March 2007): 686–96. http://dx.doi.org/10.1016/j.nbd.2006.09.019.

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4

Garringer, Holly J., Neeraja Sammeta, Adrian Oblak, Bernardino Ghetti, and Ruben Vidal. "Amyloid and intracellular accumulation of BRI2." Neurobiology of Aging 52 (April 2017): 90–97. http://dx.doi.org/10.1016/j.neurobiolaging.2016.12.018.

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5

Ford, Jennifer, David Cornforth, Patrick G. Hoggard, Zoe Cuthbertson, E. Rhiannon Meaden, Ian Williams, Margaret Johnson, et al. "Intracellular and Plasma Pharmacokinetics of Nelfinavir and M8 in HIV-Infected Patients: Relationship with P-Glycoprotein Expression." Antiviral Therapy 9, no. 1 (January 2004): 77–84. http://dx.doi.org/10.1177/135965350400900101.

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One of the targets of antiretroviral therapy is within cells infected with HIV. In order to improve therapeutic efficacy, it is therefore important that the intracellular pharmacokinetics of drugs, such as nelfinavir mesylate and its active metabolite M8, are studied in addition to plasma pharmacokinetics. Previously, the intracellular accumulation of protease inhibitors has been reported in vivo, displaying the following hierarchy: nelfinavir > saquinavir > ritonavir > indinavir. Multidrug resistance transporters, such as P-glycoprotein (P-gp), may result in a lower intracellular concentration of drug via an efflux mechanism, thus contributing to sanctuary site formation. The objective of this study was to determine concentrations of nelfinavir and M8 in plasma and peripheral blood mononuclear cells from HIV-infected patients, and to ascertain the relationship between intracellular accumulation and lymphocyte P-gp expression. Venous blood samples from 12 HIV-infected patients (viral load <50 copies/ml) receiving nelfinavir (1250 mg twice daily) and dual nucleoside reverse transcriptase inhibitor therapy were collected over a full dosage interval (0, 2, 4, 8 and 12 h). Plasma and intracellular (cell-associated) drug concentrations were measured by HPLC-MS/MS. Drug exposure in plasma and cells was expressed as the area under the concentration–time curve (AUC0-12h), derived from non-compartmental modelling. The ratio of intracellular AUC0-12h/total plasma AUC0-12h was calculated to determine cellular drug accumulation. P-gp expression on lymphocytes was determined by flow cytometry. The median (range) AUC0-12h of nelfinavir in plasma and cellular compartments was 21.8 mg.h.l-1 (5.64–50.8) and 104.6 mg.h.l-1 (23.1–265.7), respectively. Corresponding values for M8 in plasma and cells were 6.60 mg.h.l–1 (2.16–17.3) and 19.6 mg.h.l–1 (5.14–60.8). A ratio of plasma M8/plasma nelfinavir (AUC0–12h) and intracellular M8/intracellular nelfinavir (AUC0–12h) gave median values of 0.32 and 0.17, respectively. The cellular accumulations [median; (range)] of nelfinavir and M8 were 5.30 (2.28–16.2) and 2.32 (1.01–10.7), respectively. A significant correlation between plasma and intracellular nelfinavir minimum concentration (Cmin) (r2=0.34; P=0.049), but not between plasma and intracellular M8 Cmin was observed. C0h concentrations were higher than C12h for both nelfinavir and M8. No relationship was observed between nelfinavir or M8 accumulation and lymphocyte cell surface expression of P-gp. This study illustrates that intracellular concentrations were higher than plasma concentrations for both nelfinavir and M8, suggesting lymphocyte accumulation. The mechanism of differential intracellular accumulation of nelfinavir and M8 remains to be elucidated. It may be that affinities for influx transporters or fundamental drug characteristics play a major role in the greater accumulation of nelfinavir than M8.

6

Nguyen, Hien Thi Thu, Rikke Kristiansen, Mette Vestergaard, Reinhard Wimmer, and Per Halkjær Nielsen. "Intracellular Accumulation of Glycine in Polyphosphate-Accumulating Organisms in Activated Sludge, a Novel Storage Mechanism under Dynamic Anaerobic-Aerobic Conditions." Applied and Environmental Microbiology 81, no. 14 (May 8, 2015): 4809–18. http://dx.doi.org/10.1128/aem.01012-15.

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ABSTRACTDynamic anaerobic-aerobic feast-famine conditions are applied to wastewater treatment plants to select polyphosphate-accumulating organisms to carry out enhanced biological phosphorus removal. Acetate is a well-known substrate to stimulate this process, and here we show that different amino acids also are suitable substrates, with glycine as the most promising.13C-labeled glycine and nuclear magnetic resonance (NMR) were applied to investigate uptake and potential storage products when activated sludge was fed with glycine under anaerobic conditions. Glycine was consumed by the biomass, and the majority was stored intracellularly as free glycine and fermentation products. Subsequently, in the aerobic phase without addition of external substrate, the stored glycine was consumed. The uptake of glycine and oxidation of intracellular metabolites took place along with a release and uptake of orthophosphate, respectively. Fluorescencein situhybridization combined with microautoradiography using3H-labeled glycine revealed uncultured actinobacterialTetrasphaeraas a dominant glycine consumer. Experiments withTetrasphaera elongataas representative of unculturedTetrasphaerashowed that under anaerobic conditions it was able to take up labeled glycine and accumulate this and other labeled metabolites to an intracellular concentration of approximately 4 mM. All components were consumed under subsequent aerobic conditions. Intracellular accumulation of amino acids seems to be a novel storage strategy for polyphosphate-accumulating bacteria under dynamic anaerobic-aerobic feast-famine conditions.

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Corti, S., J. Chevalier, and A. Cremieux. "Intracellular accumulation of norfloxacin in Mycobacterium smegmatis." Antimicrobial Agents and Chemotherapy 39, no. 11 (November 1, 1995): 2466–71. http://dx.doi.org/10.1128/aac.39.11.2466.

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8

Polti, Marta A., María Julia Amoroso, and Carlos M. Abate. "Intracellular chromium accumulation by Streptomyces sp. MC1." Water, Air, & Soil Pollution 214, no. 1-4 (March 31, 2010): 49–57. http://dx.doi.org/10.1007/s11270-010-0401-5.

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9

Tang, Youcai, and Anping Chen. "Curcumin Protects Hepatic Stellate Cells against Leptin-Induced Activation in Vitro by Accumulating Intracellular Lipids." Endocrinology 151, no. 9 (July 21, 2010): 4168–77. http://dx.doi.org/10.1210/en.2010-0191.

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Obesity and type II diabetes mellitus are often associated with hyperleptinemia and commonly accompanied by nonalcoholic steatohepatitis, which could cause hepatic fibrosis. During hepatic fibrogenesis, the major effectors hepatic stellate cells (HSCs) become active, coupling with depletion of cellular lipid droplets and downexpression of genes relevant to lipid accumulation. Accumulating evidence supports the proposal that recovering the accumulation of lipids would inhibit HSC activation. We recently reported that leptin stimulated HSC activation, which was eliminated by curcumin, a phytochemical from turmeric. The current study was designed to explore the underlying mechanisms, focusing on their effects on the level of intracellular lipids. We hypothesized that one of the mechanisms by which leptin stimulated HSC activation was to stimulate the depletion of intracellular lipids, which could be abrogated by curcumin by inducing expression of genes relevant to lipid accumulation. In this report, we observed that leptin dose dependently reduced levels of intracellular fatty acids and triglycerides in passaged HSCs, which were eliminated by curcumin. The phytochemical abrogated the impact of leptin on inhibiting the activity of AMP-activated protein kinase (AMPK) in HSCs in vitro. The activation of AMPK resulted in inducing expression of genes relevant to lipid accumulation and increasing intracellular lipids in HSCs in vitro. In summary, curcumin eliminated stimulatory effects of leptin on HSC activation and increased AMPK activity, leading to inducing expression of genes relevant to lipid accumulation and elevating the level of intracellular lipids. These results provide novel insights into mechanisms of curcumin in inhibiting leptin-induced HSC activation.

10

Khoo, Saye H., Patrick G. Hoggard, Ian Williams, E. Rhiannon Meaden, Philippa Newton, Edmund G. Wilkins, Alan Smith, et al. "Intracellular Accumulation of Human Immunodeficiency Virus Protease Inhibitors." Antimicrobial Agents and Chemotherapy 46, no. 10 (October 2002): 3228–35. http://dx.doi.org/10.1128/aac.46.10.3228-3235.2002.

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ABSTRACT Intracellular accumulation of the protease inhibitors (PIs) saquinavir (SQV), ritonavir (RTV), and indinavir (IDV) was determined in 50 human immunodeficiency virus-positive patients. Following extraction, PIs were quantified by mass spectrometry. Paired plasma and intracellular samples were collected over a full dosing interval from patients (13 on SQV, 6 on RTV, 8 on IDV, 16 on SQV plus RTV, 7 on IDV plus RTV) with a plasma viral load of <400 copies/ml. Data were expressed as intracellular/plasma drug concentration ratios. A hierarchy of intracellular accumulation was demonstrated by the following medians: 9.45 for SQV > 1.00 for RTV > 0.51 for IDV. Coadministration of RTV did not boost ratios of SQV or IDV within the cell or in plasma, although absolute plasma and intracellular SQV concentrations were increased by RTV. Seven individuals receiving SQV in hard-gel capsule form (median, 32 months) had higher intracellular/plasma drug ratios than all other patients receiving SQV (median, 17.62 versus 4.83; P = 0.04), despite consistently low plasma SQV concentrations. How this occurs may provide insight into the mechanisms that limit adequate drug penetration into sanctuary sites.

11

Takano, Tomomi, Yumeho Wakayama, and Tomoyoshi Doki. "Endocytic Pathway of Feline Coronavirus for Cell Entry: Differences in Serotype-Dependent Viral Entry Pathway." Pathogens 8, no. 4 (December 16, 2019): 300. http://dx.doi.org/10.3390/pathogens8040300.

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Feline coronavirus (FCoV) is a pathogen causing a lethal infectious disease in cats, feline infectious peritonitis. It has two serotypes (type I FCoV and type II FCoV). According to our previous study, type I FCoV infection is inhibited by compounds inducing intracellular cholesterol accumulation, whereas type II FCoV infection is not inhibited. Intracellular cholesterol accumulation was reported to disrupt late endosome function. Based on these findings, types I and II FCoV are considered to enter the cytosol through late and early endosomes, respectively. We investigated whether the antiviral activities of a late endosome trafficking inhibitor and cholesterol-accumulating agents are different between the FCoV serotypes. The late endosome trafficking inhibitor did not inhibit type II FCoV infection, but it inhibited type I FCoV infection. Type I FCoV infection was inhibited by cholesterol-accumulating triazoles, but not by non-cholesterol-accumulating triazoles. These phenomena were observed in both feline cell lines and feline primary macrophages. This study provides additional information on the differences in intracellular reproductive cycle between type I and type II FCoV.

12

Foster, Karen A., and Janet D. Robishaw. "Effect of calcium and cAMP on Goα expression in neonatal rat cardiac myocytes." American Journal of Physiology-Heart and Circulatory Physiology 261, no. 4 (October 1, 1991): 15–20. http://dx.doi.org/10.1152/ajpheart.1991.261.4.15.

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Culturing neonatal rat cardiac myocytes in 50 mM KCl inhibits the accumulation of Go that occurs when myocytes are placed in culture. The mechanism by which high extracellular K+ inhibits Go accumulation in myocytes was investigated by measurement of the concentration of intracellular Ca2+ ([Ca2+]) and adenosine 3',5'-cyclic monophosphate concentration ([cAMP]) of control and K+-depolarized myocytes. Although intracellular [Ca2++] in K+-depolarized myocytes was twofold higher than basal intracellular [Ca2+] in control cells, the mean intracellular [Ca2+] in contracting control myocytes was comparable to that of K+-depolarized myocytes. Furthermore, myocytes cultured in low Ca2+ plus high K+ exhibited an inhibition of Go accumulation, even though intracellular [Ca2+] was 10-fold lower than that of cells cultured in normal Ca2+ plus high K+. In addition, intracellular [cAMP] of K+-depolarized myocytes was comparable to that of control cells. Moreover, dibutyryl cAMP inhibited Go accumulation in myocytes to the same extent as high K+, even though intracellular [cAMP] differed 10-fold. Thus neither intracellular Ca2+ nor cAMP appear to mediate the inhibitory effect of high K+ on Go accumulation. However, cAMP has an inhibitory effect on Goα expression that is independent of K+. dibutyryl cAMP; fura-2; immunoblotting

13

Tabira, T. "Significance of intracellular Ab42 accumulation in alzheimer's disease." Frontiers in Bioscience 7, no. 1-3 (2002): a44. http://dx.doi.org/10.2741/tabira.

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14

Krivohlavek, Adela, Željka Kuharić, Ana Marija Marjanović Čermak, Sandra Šikić, Ivan Pavičić, and Ana-Marija Domijan. "Assessment of intracellular accumulation of cadmium and thallium." Journal of Pharmacological and Toxicological Methods 110 (July 2021): 107087. http://dx.doi.org/10.1016/j.vascn.2021.107087.

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15

D'Amore, T., C. J. Panchal, and G. G. Stewart. "Intracellular ethanol accumulation in Saccharomyces cerevisiae during fermentation." Applied and Environmental Microbiology 54, no. 1 (1988): 110–14. http://dx.doi.org/10.1128/aem.54.1.110-114.1988.

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16

Gladue, R. P., and M. E. Snider. "Intracellular Accumulation of Azithromycin by Cultured Human Fibroblasts." Antimicrobial Agents and Chemotherapy 34, no. 10 (October 1, 1990): 2041. http://dx.doi.org/10.1128/aac.34.10.2041.

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17

Gladue, R. P., and M. E. Snider. "Intracellular accumulation of azithromycin by cultured human fibroblasts." Antimicrobial Agents and Chemotherapy 34, no. 6 (June 1, 1990): 1056–60. http://dx.doi.org/10.1128/aac.34.6.1056.

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18

HINTZE, V., A. STEPLEWSKI, and A. FERTALA. "Intracellular accumulation of mutant collagen leads to apoptosis." Matrix Biology 25 (November 2006): S74. http://dx.doi.org/10.1016/j.matbio.2006.08.203.

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19

Perkins, J., and G. M. Gadd. "Caesium toxicity, accumulation and intracellular localization in yeasts." Mycological Research 97, no. 6 (June 1993): 717–24. http://dx.doi.org/10.1016/s0953-7562(09)80153-6.

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20

Fan, H. J., I. Paternotte, M. Vermander, K. Li, M. Beaujean, B. Scorneaux, P. Dumont, et al. "Ester prodrugs of ampicillin tailored for intracellular accumulation." Bioorganic & Medicinal Chemistry Letters 7, no. 24 (December 1997): 3107–12. http://dx.doi.org/10.1016/s0960-894x(97)10146-9.

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21

Lambert, Catherine, Heloisa Beraldo, Nicole Lievre, Arlette Garnier-Suillerot, Pierre Dorlet, and Milena Salerno. "Bis(thiosemicarbazone) copper complexes: mechanism of intracellular accumulation." JBIC Journal of Biological Inorganic Chemistry 18, no. 1 (October 27, 2012): 59–69. http://dx.doi.org/10.1007/s00775-012-0949-1.

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22

Wolf, Peter, Yvonne Winhofer, Christian-Heinz Anderwald, Martin Krššák, and Michael Krebs. "Intracellular lipid accumulation and shift during diabetes progression." Wiener Medizinische Wochenschrift 164, no. 15-16 (July 22, 2014): 320–29. http://dx.doi.org/10.1007/s10354-014-0292-y.

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23

Panasenko, O. M., T. V. Vol'nova, O. A. Azizova, and Yu A. Vladimirov. "Lipid peroxidation promotes intracellular cholesterol accumulation in atherosclerosis." Bulletin of Experimental Biology and Medicine 106, no. 3 (September 1988): 1232–36. http://dx.doi.org/10.1007/bf00834481.

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24

Hasegawa, Junichi, Mariko Tsuboi, Kohshi Narasaki, Shozo Hirai, Takahiro Nawada, Hiroshi Kotake, and Hiroto Mashiba. "Quinidine enhances intracellular Ca2+ accumulation during rapid stimulation." General Pharmacology: The Vascular System 26, no. 5 (September 1995): 971–76. http://dx.doi.org/10.1016/0306-3623(94)00297-z.

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25

Stanley, G. A., and N. B. Pamment. "Transport and intracellular accumulation of acetaldehyde insaccharomyces cerevisiae." Biotechnology and Bioengineering 42, no. 1 (June 5, 1993): 24–29. http://dx.doi.org/10.1002/bit.260420104.

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26

Kubekina, M. V., N. G. Nikiforov, V. P. Karagodin, I. A. Sobenin, and A. N. Orekhov. "Analysis of macrophage transcriptome in atherogenesis." Russian Journal of Cardiology, no. 2 (March 7, 2019): 92–98. http://dx.doi.org/10.15829/1560-4071-2019-2-92-98.

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The accumulation of cholesterol under the influence of modified low density lipoprotein is a key cause of atherogenesis. It is known that atherosclerosis is accompanied by chronic local inflammation. Monocytes/macrophages, main cells of the innate immunity, may not only capturing and accumulating lipids in the vascular wall, but also secreting signaling molecules that affect the functions of other cells. An atherosclerotic lesion is characterized by the inability to complete the inflammatory response, as a result of which the inflammation becomes chronic. Intracellular lipid accumulation is a necessary condition for the initiation of atherogenesis, but it is not known whether it is sufficient. Analysis of the transcriptome allowed us to characterize the state of macrophages loaded with lipids. Studies presented in this review show that the reaction of innate immunity contributes to the accumulation of intracellular lipids and aggravates it.

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Ritchie, Helen, and Nuala Booth. "The Distribution of the Secreted and Intracellular Forms of Plasminogen Activator Inhibitor 2 (PAI-2) in Human Peripheral Blood Monocytes Is Modulated by Serum." Thrombosis and Haemostasis 79, no. 04 (1998): 813–17. http://dx.doi.org/10.1055/s-0037-1615070.

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SummaryPlasminogen activator inhibitor 2 (PAI-2) is produced by activated monocytes in two forms, intracellular and secreted. We have studied the distribution of these two forms in unstimulated human peripheral blood monocytes and after stimulation by thrombin. Fetal calf serum (FCS) in the culture medium was absolutely necessary for accumulation of intracellular PAI-2; but not for synthesis and secretion. Even at a concentration as low as 0.1%, FCS restored accumulation of intra-cellular PAI-2. Increasing concentrations of FCS resulted in an increase in the ratio of intracellular to secreted PAI-2. The factor that promoted accumulation of intracellular PAI-2 was not a platelet product. Failure of monocytes to accumulate PAI-2 did not reflect leakage due to cell death, as assessed by LDH in culture supernatants. We propose that accumulation of intracellular PAI-2 is not simply due to poor secretion, but is an active process that is modulated by factor(s) found in serum.

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Nobre, M. Fernanda, and Milton S. da Costa. "Factors favouring the accumulation of arabinitol in the yeast Debaryomyces hansenii." Canadian Journal of Microbiology 31, no. 5 (May 1, 1985): 467–71. http://dx.doi.org/10.1139/m85-087.

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Culture conditions which lead to the intracellular accumulation of arabinitol were investigated in Debaryomyces hansenii. Arabinitol, detected in very low concentrations during the exponential phase of growth, accumulated during the stationary phase of growth in yeast extract – peptone – 1% (w/v) glucose medium. This polyol was retained intracellularly even after depletion of exogenous glucose, but was rapidly depleted during regrowth in fresh glucose medium. The accumulation of arabinitol was also favoured in media containing 1% (w/v) D-fructose, sucrose, L-arabinose, glycerol, and sodium acetate. High mannitol levels accumulated in stationary phase cells derived from growth in 1% (w/v) D-mannitol, and in these cultures only traces of arabinitol were detectable. Intracellular mannitol was also retained after the extracellular mannitol had been consumed, and was rapidly depleted during regrowth in glucose medium. Arabinitol did not accumulate in basal medium with no added carbon source, nor in media with nonmetabolizable carbon sources (D-arabinose or D-ribose). On the other hand, arabinitol accumulation was independent of the initial glucose concentration between 1% (w/v) and about 9% (w/v).

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Tamura, Yoshifumi, Saori Kakehi, and Kageumi Takeno. "Intracellular lipid accumulation and insulin sensitivity in muscle and liver: Fighting against “intracellular obesity”." Journal of Physical Fitness and Sports Medicine 3, no. 5 (2014): 501–5. http://dx.doi.org/10.7600/jpfsm.3.501.

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Pilliod, Julie, Alexandre Desjardins, Camille Pernègre, Hélène Jamann, Catherine Larochelle, Edward A. Fon, and Nicole Leclerc. "Clearance of intracellular tau protein from neuronal cells via VAMP8-induced secretion." Journal of Biological Chemistry 295, no. 51 (October 22, 2020): 17827–41. http://dx.doi.org/10.1074/jbc.ra120.013553.

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In Alzheimer's disease (AD), tau, a microtubule-associated protein (MAP), becomes hyperphosphorylated, aggregates, and accumulates in the somato-dendritic compartment of neurons. In parallel to its intracellular accumulation in AD, tau is also released in the extracellular space, as revealed by its increased presence in cerebrospinal fluid (CSF). Consistent with this, recent studies, including ours, have reported that neurons secrete tau, and several therapeutic strategies aim to prevent the intracellular tau accumulation. Previously, we reported that late endosomes were implicated in tau secretion. Here, we explore the possibility of preventing intracellular tau accumulation by increasing tau secretion. Using neuronal models, we investigated whether overexpression of the vesicle-associated membrane protein 8 (VAMP8), an R-SNARE found on late endosomes, could increase tau secretion. The overexpression of VAMP8 significantly increased tau secretion, decreasing its intracellular levels in the neuroblastoma (N2a) cell line. Increased tau secretion by VAMP8 was also observed in murine hippocampal slices. The intracellular reduction of tau by VAMP8 overexpression correlated to a decrease of acetylated tubulin induced by tau overexpression in N2a cells. VAMP8 staining was preferentially found on late endosomes in N2a cells. Using total internal reflection fluorescence (TIRF) microscopy, the fusion of VAMP8-positive vesicles with the plasma membrane was correlated to the depletion of tau in the cytoplasm. Finally, overexpression of VAMP8 reduced the intracellular accumulation of tau mutants linked to frontotemporal dementia with parkinsonism and α-synuclein by increasing their secretion. Collectively, the present data indicate that VAMP8 could be used to increase tau and α-synuclein clearance to prevent their intracellular accumulation.

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Matz, Paul G., Anders Lewén, and Pak H. Chan. "Neuronal, but Not Microglial, Accumulation of Extravasated Serum Proteins after Intracerebral Hemolysate Exposure is Accompanied by Cytochrome c Release and DNA Fragmentation." Journal of Cerebral Blood Flow & Metabolism 21, no. 8 (August 2001): 921–28. http://dx.doi.org/10.1097/00004647-200108000-00004.

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Vasogenic edema after oxidative injury has been accompanied by intracellular accumulation of serum proteins and nuclear damage. This study sought to determine whether serum protein accumulation, along with other markers of brain injury, was present after exposure to intracerebral hemolysate, an oxidant model of intracerebral hemorrhage (ICH). Saline (n = 24) or hemolysate (n = 30) was injected into the caudate-putamen of adult Sprague-Dawley rats. Compared with saline, hemolysate deposition was associated with intracellular accumulation of serum proteins as evidenced by Evans blue uptake in neurons and microglia at 4 and 24 hours. Intracellular Evans blue colocalized with DNA fragmentation detected by nick end-labeling and whose presence was confirmed by gel electrophoresis. Immunoblots of cytosolic fractions confirmed cytochrome c release. Immunostaining established colocalization of cytosolic cytochrome c and intracellular Evans blue at 4 hours. At 24 hours, cytosolic cytochrome c was evident in astrocytes surrounding Evans blue-positive cells. Immunoblot analysis and immunostaining revealed HSP70 induction at 24 hours in regions adjacent to intracellular serum accumulation. Neuronal accumulation of extravasated serum proteins in this model of ICH was associated with cytochrome c release, DNA fragmentation, and cell death. Stress protein induction in adjacent regions suggested that vasogenic edema might have exacerbated cellular dysfunction and cell death after ICH.

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Goodkin, H. P. "Status Epilepticus Increases the Intracellular Accumulation of GABAA Receptors." Journal of Neuroscience 25, no. 23 (June 8, 2005): 5511–20. http://dx.doi.org/10.1523/jneurosci.0900-05.2005.

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Carini, Rita, Maria Grazia De Cesaris, Giorgio Bellomo, and Emanuele Albano. "INTRACELLULAR Na+ ACCUMULATION AND HEPATOCYTE INJURY DURING COLD STORAGE." Transplantation 68, no. 2 (July 1999): 294–97. http://dx.doi.org/10.1097/00007890-199907270-00023.

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MARTÍNEZ, ROSA, ROSAURA NAVARRO, CÉSAR MARTÍN, IGOR AURREKOETXEA, M. LUISA HERNÁNDEZ, MERCEDES LACORT, JOSÉ IGNACIO RUIZ-SANZ, and M. BEGOÑA RUIZ-LARREA. "Intracellular Diacylglycerol Accumulation Induced by Doxorubicin in Rat Hepatocytes." Annals of the New York Academy of Sciences 973, no. 1 (November 2002): 52–56. http://dx.doi.org/10.1111/j.1749-6632.2002.tb04605.x.

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Perkins, Joy, and Geoffrey M. Gadd. "Accumulation and intracellular compartmentation of lithium ions inSaccharomyces cerevisiae." FEMS Microbiology Letters 107, no. 2-3 (March 1993): 255–60. http://dx.doi.org/10.1111/j.1574-6968.1993.tb06039.x.

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Jeannot, Valérie, Jean-Marie Salmon, Michel Deumié, and Pierre Viallet. "Intracellular Accumulation of Rhodamine 110 in Single Living Cells." Journal of Histochemistry & Cytochemistry 45, no. 3 (March 1997): 403–12. http://dx.doi.org/10.1177/002215549704500308.

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To gain a better understanding of the internalization of rhodamines, vital staining of living cells in situ by two different rhodamines, R110 and R123, was studied by microfluorometry. These dyes differ strongly in their lipophilic properties because of differences in charge distribution. Microspectrofluorometry was used to study the fluorescence emission spectra of R110-loaded cells to determine reliable loading conditions. Cell uptake and cell efflux studies of R110 were performed by numerical microfluorescence imaging. A slower uptake was observed for R110 (14 hr) vs R123 (2 hr), but the R110 efflux was much more rapid (30 min) than that of R123 (<24 hr). Although it appeared in the R110 and R123 co-localization study that R110 was able to accumulate in mitochondria, labeling with R110 was lower than with R123. Our results indicate that, rhodamine 110 in its acid cationic form is able to cross the plasma and mitochondrial membrane and to accumulate in cell compartments as does the cationic rhodamine 123. However, because of its acido-basic properties, R110 should be able to decrease the pH of cell compartments, depending on their ability to regulate pH. In such a model, mitochondrial pH should be more greatly decreased than cytosolic pH, leading to a lower mitochondrial accumulation of R110 than of R123. Surprisingly, these effects, which should affect the energetic state of mitochondria, do not influence cell growth, because no cytotoxic effect was observed. (J Histochem Cytochem 45:403–412, 1997)

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Pascual, Alvaro, M. Carmen Conejo, Isabel Garcia, and Evelio J. Perea. "Factors affecting the intracellular accumulation and activity of azithromycin." Journal of Antimicrobial Chemotherapy 35, no. 1 (1995): 85–93. http://dx.doi.org/10.1093/jac/35.1.85.

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Iwamoto, Koji, and Yoshihiro Shiraiwa. "Characterization of Intracellular Iodine Accumulation by Iodine-Tolerant Microalgae." Procedia Environmental Sciences 15 (2012): 34–42. http://dx.doi.org/10.1016/j.proenv.2012.05.007.

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Simchowitz, L., O. W. Woltersdorf, and E. J. Cragoe. "Intracellular accumulation of potent amiloride analogues by human neutrophils." Journal of Biological Chemistry 262, no. 33 (November 1987): 15875–85. http://dx.doi.org/10.1016/s0021-9258(18)47670-3.

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Shoji, Mikio, Noboru Iwakami, Sousuke Takeuchi, Masaaki Waragai, Misao Suzuki, Ichiro Kanazawa, Carol F. Lippa, Satoshi Ono, and Hitoshi Okazawa. "JNK activation is associated with intracellular β-amyloid accumulation." Molecular Brain Research 85, no. 1-2 (December 2000): 221–33. http://dx.doi.org/10.1016/s0169-328x(00)00245-x.

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Choi, Ilho, Yumi Lee, Joong-Yeol Park, Youngsup Song, Eun-Ju Chang, and Sang-Wook Kang. "Radicicol induces intracellular accumulation of glycan-deficient clusterin variant." Biochemical and Biophysical Research Communications 458, no. 3 (March 2015): 555–60. http://dx.doi.org/10.1016/j.bbrc.2015.02.005.

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Oddi, S., F. Fezza, N. Pasquariello, C. De Simone, C. Rapino, E. Dainese, A. Finazzi-Agrò, and M. Maccarrone. "Evidence for the intracellular accumulation of anandamide in adiposomes." Cellular and Molecular Life Sciences 65, no. 5 (January 24, 2008): 840–50. http://dx.doi.org/10.1007/s00018-008-7494-7.

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Lönnroth, Peter, J. Islwyn Davies, and Ulf Smith. "Bacitracin enhances intracellular accumulation of insulin in rat adipocytes." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 845, no. 2 (May 1985): 272–75. http://dx.doi.org/10.1016/0167-4889(85)90187-9.

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Galluzzi, Lorenzo, Sabrina Marsili, Ilio Vitale, Laura Senovilla, Judith Michels, Pauline Garcia, Erika Vacchelli, Etienne Chatelut, Maria Castedo, and Guido Kroemer. "Vitamin B6 metabolism influences the intracellular accumulation of cisplatin." Cell Cycle 12, no. 3 (February 2013): 417–21. http://dx.doi.org/10.4161/cc.23275.

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Kellner-Weibel, G., W. G. Jerome, D. M. Small, G. J. Warner, J. K. Stoltenborg, M. A. Kearney, M. H. Corjay, M. C. Phillips, and G. H. Rothblat. "Effects of Intracellular Free Cholesterol Accumulation on Macrophage Viability." Arteriosclerosis, Thrombosis, and Vascular Biology 18, no. 3 (March 1998): 423–31. http://dx.doi.org/10.1161/01.atv.18.3.423.

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Tsukahara, Tamotsu, and Hisao Haniu. "Nanoparticle-mediated intracellular lipid accumulation during C2C12 cell differentiation." Biochemical and Biophysical Research Communications 406, no. 4 (March 2011): 558–63. http://dx.doi.org/10.1016/j.bbrc.2011.02.090.

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Bjors, Jenny, Camilla Nilsberth, Jan Naslund, and Lars Lannfelt. "Accumulation of intracellular amyloid ß peptide in Alzheimer's disease." Neurobiology of Aging 21 (May 2000): 200. http://dx.doi.org/10.1016/s0197-4580(00)82240-x.

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Vogt, Thomas, Paul-Gerhard Gülz, and Hans Reznik. "UV Radiation Dependent Flavonoid Accumulation of Cistus laurifolius L." Zeitschrift für Naturforschung C 46, no. 1-2 (February 1, 1991): 37–42. http://dx.doi.org/10.1515/znc-1991-1-207.

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Abstract:

Abstract Epicuticular and in tracellular flavonoids of Cistus laurifolius grown with and without UV radiation in a phytotron as well as under natural garden conditions in the field were studied. The amount of intracellular flavonoid glycosides of leaves receiving UV -A radiation was two fold higher than that measured in the absence of UV -A radiation , whether grown in the phytotron or in the field. Exposure of previously protected leaves to UV -A radiation increased the intracellular flavonoid glycoside content to that of unprotected leaves. The qualitative composition of intracellular flavonoid glycosides showed a reduced amount of quercetin-3-galactoside to the myricetin monosides when the leaves were grown without UV-A radiation in the field and in the phytotron . Epicuticular flavonoid aglycones were not influenced by UV radiation significantly.

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Sikes, Patricia J., Piyu Zhao, David L. Maass, and Jureta W. Horton. "Time course of myocardial sodium accumulation after burn trauma: a 31P- and 23Na-NMR study." Journal of Applied Physiology 91, no. 6 (December 1, 2001): 2695–702. http://dx.doi.org/10.1152/jappl.2001.91.6.2695.

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Abstract:

In this study,23Na- and 31P- nuclear magnetic resonance (NMR) spectra were examined in perfused rat hearts harvested 1, 2, 4, and 24 h after 40% total body surface area burn trauma and lactated Ringer resuscitation, 4 ml · kg−1 · %−1 burn.23Na-NMR spectroscopy monitored myocardial intracellular Na+ using the paramagnetic shift reagent thulium 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetra(methylenephosphonic acid). Left ventricular function, cardiac high-energy phosphates (ATP/PCr), and myocyte intracellular pH were studied by using31P NMR spectroscopy to examine the hypothesis that burn-mediated acidification of cardiomyocytes contributes to subsequent Na+ accumulation by this cell population. Intracellular Na+ accumulation was confirmed by sodium-binding benzofuran isophthalate loading and fluorescence spectroscopy in cardiomyocytes isolated 1, 2, 4, 8, 12, 18, and 24 h postburn. This myocyte Na+ accumulation as early as 2 h postburn occurred despite no changes in cardiac ATP/PCr and intracellular pH. Left ventricular function progressively decreased after burn trauma. Cardiomyocyte Na+ accumulation paralleled cardiac contractile dysfunction, suggesting that myocardial Na+overload contributes, in part, to the progressive postburn decrease in ventricular performance.

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Park, Myung-Hwan, Chae-Hong Park, Yeon Bo Sim, and Soon-Jin Hwang. "Response of Scenedesmus quadricauda (Chlorophyceae) to Salt Stress Considering Nutrient Enrichment and Intracellular Proline Accumulation." International Journal of Environmental Research and Public Health 17, no. 10 (May 21, 2020): 3624. http://dx.doi.org/10.3390/ijerph17103624.

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Abstract:

Aquatic organisms are exposed to a wide range of salinity, which could critically affect their survival and growth. However, their survival and growth response to salinity stress remain unclear. This study evaluates the growth response and intracellular proline accumulation of green algae, Scenedesmus quadricauda, isolated from brackish water, against dissolved salts stress with N and P enrichment. We tested a hypothesis that nutrient enrichment can relieve the dissolved salts stress of algae by accumulating intracellular proline, thereby improving survival and growth. Four levels of salinity (0, 3, 6, 12 psu) were experimentally manipulated with four levels of nutrient stoichiometry (N:P ratio = 2, 5, 10, 20) at constant N (1 mgN/L) or P levels (0.05 and 0.5 mgP/L). In each set of experiments, growth rate and intracellular proline content were measured in triplicate. The highest level of salinity inhibited the growth rate of S. quadricauda, regardless of the nutrient levels. However, with nutrient enrichment, the alga showed tolerance to dissolved salts, reflecting intracellular proline synthesis. Proline accumulation was most prominent at the highest salinity level, and its maximum value appeared at the highest N:P ratio (i.e., highest N level) in all salinity treatments, regardless of P levels. Therefore, the effects of P and N on algal response to salt stress differ.