Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glyoxals are reactive alpha-oxoaldehydes that are formed endogenously from sugars, the levels of which are increased in various pathological conditions associated with hyperglycaemia and thiamine deficiency. However, the molecular cytotoxic mechanisms of glyoxal are not known. Results presented here and in the other studies cited provide a glimpse into the cytotoxicity mechanisms involved and their pathological implications. We found that glyoxal (10 microM) markedly increased the susceptibility of hepatocyte glutathione (GSH) to oxidation by hydrogen peroxide (H(2)O(2)) and markedly increased cytotoxicity by compromising the cellular antioxidant enzyme system. At higher concentrations, glyoxal was cytotoxic towards hepatocytes, which can be attributed to GSH depletion, oxidative stress and mitochondrial toxicity. Aminoguanidine or penicillamine protected the hepatocytes. Glyoxal cytotoxicity was prevented by increasing glyoxal metabolism with thiamine or NAD(P)H generators, and was increased in GSH- or thiamine-deficient hepatocytes. It was also found that feeding rats reduced thiamine levels in a diet high in simple sugars increased the number of aberrant crypt foci/colon in the absence of clinical evidence of beriberi. This was associated with decreased plasma thiamine and low erythrocyte transketolase activity. Western diets, which are frequently poor in thiamine and high in sugars, could result in increased levels of endogenous glyoxals, which in turn may lead to a predisposition to AGE (advanced glycation end-product)-related pathologies and neoplastic conditions.
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PMID:Toxicity of glyoxals--role of oxidative stress, metabolic detoxification and thiamine deficiency. 1464 Oct 70

The purpose of the study was to investigate the effect of aminoguanidine (AG) on visual evoked potentials (VEPs), thiobarbituric acid reactive substances (TBARS), the activities of Cu, Zn superoxide dismutase (Cu,Zn-SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and nitrite/nitrate levels. Forty healthy male Wistar rats, aged 3 months, were divided into four equal groups: Control (C), the group treated with aminoguanidine (A), the group exposed to restraint stress (S), the group exposed to restraint stress and treated with aminoguanidine (AS). Chronic restraint stress was applied for 21 days (1 h/day) and aminoguanidine (50 mg/kg/day) was injected intraperitoneally to the A and AS groups for the same period. Aminoguanidine treatment significantly decreased retina and brain TBARS levels in rats exposed to restraint stress compared to rats exposed to restraint stress alone. Aminoguanidine treatment produced a significant decrease in brain and retina nitrite and nitrate levels with respect to the control groups. Aminoguanidine increased all antioxidant enzyme activities in both brain and retina in rats exposed to restraint stress compared to rats exposed to restraint stress alone. All VEP components were significantly decreased in AG treated rats exposed to restraint stress compared to rats exposed to restraint stress alone. Our study clearly showed that AG has the potential to prevent changes caused by stress.
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PMID:Effect of aminoguanidine on visual evoked potentials (VEPs), antioxidant status and lipid peroxidation in rats exposed to chronic restraint stress. 1799 25