Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heat shock protein (HSP) expression is an adaptive mechanism against the disruption of cell homeostasis during exercise. Several antioxidant supplementation strategies have been used to enhance tissue protection. In this study, we examined the effects of a redox modulator, alpha-lipoic acid (LA) on HSP responses in six standardbred trotters following intense aerobic exercise. DL-LA supplementation (25 mg kg(-1) d(-1)) for five weeks increased the resting levels of HSP90 (1.02+/-0.155 in control and 1.26+/-0.090 after supplementation in arbitrary units) and the recovery levels of inducible HSP70 (0.89+/-0.056 in control and 1.05+/-0.089 after supplementation in arbitrary units) in skeletal muscle. Furthermore, LA increased skeletal muscle citrate synthase activity at rest and lowered the blood lactate concentration during exercise without any changes in the heart rate. LA had no effect on concentrations of HSP60, HSP25 or GRP75 in skeletal muscle. LA decreased the exercise-induced increases in plasma aspartate aminotransferase and creatine kinase concentrations during recovery. Our results suggest that LA supplementation may enhance tissue protection and increase oxidative capacity of the muscle in horse.
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PMID:alpha-Lipoic acid supplementation enhances heat shock protein production and decreases post exercise lactic acid concentrations in exercised standardbred trotters. 1942 59

It has been reported that over-expression of GRP75 can protect cells under different types of stress. In this study, we investigated the protective effect of GRP75 on the liver both in vivo and in vitro. To evaluate the effect of GRP75 over-expression on oxidative damage in the liver in vitro, cell viability and the mitochondrial function of GRP75-overexpressing HL-7702 cells and control transfected cells were monitored during H(2)O(2) treatment. In vivo, liver fibrosis was induced in rats by carbon tetrachloride (CCl(4)) injection for 8 weeks. The GRP75-overexpressing vector was randomly injected into rats before fibrosis was established to study the inhibitory effect of GRP75 on hepatic fibrosis. Liver injury and mitochondrial function were assessed. On H(2)O(2) treatment, GRP75-overexpressing HL-7702 cells exhibited more moderate cell damage than control HL-7702 cells. Both groups of cells showed a decrease in ATP following an early increase on H(2)O(2) treatment, and the mitochondrial membrane potential also decreased similarly in these two groups of cells. Control HL-7702 cells showed an immediate and rapid increase in reactive oxygen species accumulation after the onset of H(2)O(2) treatment, and this accumulation was slowed and reduced in GRP75-overexpressing cells. Western blotting revealed that cytochrome c was greater in control HL-7702 cells than in GRP75-overexpressing HL-7702 cells. Compared with the CCl(4)-only rats, serum alanine transaminase and aspartate aminotransferase were significantly lower in CCl(4)-treated rats transfected with the GRP75 vector (P < 0.01). ATP concentrations decreased in both groups of rats treated with CCl(4), but were higher in the GRP75-overexpressing CCl(4)-treated group than in CCl(4)-only rats. Cytochrome c expression was lower in GRP75-overexpressing rats than in CCl(4)-only rats.
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PMID:Over-expression of GRP75 inhibits liver injury induced by oxidative damage. 2328 70