Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury

Wu, Yiming; Taylor, B. M.; Sun, Frank F.

doi:10.1152/ajpcell.1996.270.1.c115

Cited by 23 publications

(3 citation statements)

References 24 publications

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“…Therefore, it appears that human skeletal muscle may respond to inflammation by increasing its antioxidant reserve. Similar changes have been observed in a variety of experimental models which, like inflammation, increase oxidative stress [31,47,50].…”

Section: Discussionsupporting

confidence: 75%

Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions

et al. 1999

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This study investigated the effects of chronic muscle inflammation on indices of antioxidant status and muscle injury after eccentric exercise. Eight subjects each performed 70 maximal voluntary eccentric muscle actions on an isokinetic dynamometer, using the knee extensors of a single leg. Venous blood samples were collected into serum and EDTA tubes 5 and 3 days before exercise, immediately before exercise, and then again on days 3, 4, 5, 6, 7, 10 and 12 after the bout. Needle biopsies were taken from the vastus lateralis of six subjects, a week before exercise (baseline), and again on days 4 and 7 post-exercise. The concentrations of malondialdehyde in plasma and muscle were used as markers of lipid peroxidation. Creatine kinase activity, beta-glucuronidase activity and total antioxidant capacity were determined in serum. In muscle, aqueous and bound total antioxidant capacity, the aqueous sulphydryl concentration, and beta-glucuronidase and glucose-6-phosphate dehydrogenase activity were determined. No changes were detected in serum total antioxidant capacity, serum creatine kinase and beta-glucuronidase after the baseline biopsy. After exercise serum creatine kinase and beta-glucuronidase were elevated although other serum measures were unchanged. In muscle, aqueous and bound total antioxidant capacity, sulphydryls, glucose-6-phosphate dehydrogenase and beta-glucuronidase were all elevated. Despite evidence of inflammation in this study, muscle antioxidant status was not compromised, and malondialdehyde was unaltered in muscle and plasma. Therefore, this study provides no evidence that chronic muscle inflammation compromises antioxidant status or increases lipid peroxidation.

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Section: Discussionsupporting

confidence: 75%

Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions

et al. 1999

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“…In fact, it is known that ROS-induced chronic production of irreversibly oxidized proteins reduces cell growth and can even be lethal. 18 The question is how these nonenzymatic modifications have the requisite specificity to alter cellular function in such specific ways as to produce a disease state.…”

Section: Introductionmentioning

confidence: 99%

“…The fact that nature has evolved systems to eliminate nonenzymatically modified proteins when possible and the association of diseases with aberrations in the protein repair mechanism lead to the conclusion that failure to prevent the production and accumulation of nonspecifically modified proteins can put biological systems at risk, at least in the case of oxidized proteins. In fact, it is known that ROS-induced chronic production of irreversibly oxidized proteins reduces cell growth and can even be lethal . The question is how these nonenzymatic modifications have the requisite specificity to alter cellular function in such specific ways as to produce a disease state.…”

Section: Introductionmentioning

confidence: 99%

Creation of Allotypic Active Sites during Oxidative Stress

Mirzaei

Regnier

2006

J. Proteome Res.

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Oxidative stress is a factor in a series of diseases and aging, primarily through irreversible oxidative modification of proteins. A major question is how nonenzymatic oxidation has the specificity to impact cellular regulation. Here, we report the degree to which in vivo protein oxidation to the ketone and aldehyde level is random using yeast as a simple model system and hydrogen peroxide as an environmental oxidative stress agent. Among 415 affinity-selected proteins identified throughout the matrix of stressed cells, oxidation sites were found in 87, predominantly on lysine, arginine, proline, histidine, threonine, and methionine residues. In almost all cases, one to two specific oxidation sites on the exterior of proteins were identified using MS-derived sequence and publicly available 3-D structural data. This suggests that, when regulation or disease progression is mediated by protein oxidation, specific new "allotypic active sites" are being created in proteins that trigger the process.

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Metabolic inhibition increases glutamate susceptibility on a PC12 cell line

1998

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The effect of energetic metabolism compromise, obtained by chemical induction of hypoglycaemia (glucose deprivation), hypoxia (mitochondrial respiratory chain inhibition), and ischaemia (hypoglycaemia plus hypoxia), on glutamate toxicity was analyzed on PC12 cells. The respiratory status of these cells, measured by the MTT [3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide] assay, was significantly decreased after metabolic inhibition induced by ischaemia, but it was not affected by both hypoglycaemia and hypoxia. Under hypoglycaemia, but not under hypoxia, ATP levels were significantly reduced (from 12.67+/-0.48 to 5.38+/-1.41 nmol/mg protein). However, ischaemic-like conditions greatly potentiated the decline of ATP levels (95% decrease) observed after hypoglycaemia. The influence of metabolic inhibition on glutamate-induced cytotoxicity was also analyzed. When the cells were preincubated under conditions that deplete ATP (hypoglycaemia and ischaemia), the inhibition of MTT reduction, measured after glutamate incubation, was potentiated. This effect could be reverted when vitamin E and idebenone were present during the induction of metabolic inhibition. The ATP levels above which glutamate susceptibility was enhanced were also determined. These results indicate that glutamate toxicity on PC12 cells, which occurs by a mechanism independent of N-methyl-D-aspartate (NMDA) receptor activation, can be enhanced by the depletion of intracellular ATP upon metabolic stress; it is dependent on the extent of ATP depletion and seems to involve the generation of free radicals. It can be concluded that under ischaemic conditions, the deleterious effects of glutamate can be potentiated by the energetic compromise associated with this pathologic situation.

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Alterations in reactive oxygen, pH, and calcium in astrocytoma cells during lethal injury

Cited by 23 publications

References 24 publications

Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions

Changes in indices of antioxidant status, lipid peroxidation and inflammation in human skeletal muscle after eccentric muscle actions

Creation of Allotypic Active Sites during Oxidative Stress

Metabolic inhibition increases glutamate susceptibility on a PC12 cell line

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