ABSTRACT
Inactivation of methionine synthase (MS) by nitrous oxide (N2O) administration to animals and man has been postulated to be mediated by hydroxyl radical (OH). An alternate mechanism has been proposed which involves superoxide radical (O2.-) originating from N2O in the inactivation of MS by OH that may arise from O2.- through Fenton/Haber-Weiss reaction. Rats inhaling a mixture of N2O:O2 (1:1) for 5 hr showed inactivation of MS in liver to nearly 90% which could not be reversed by prior administration of either dimethyl sulfoxide (DMSO) or sodium benzoate. Pretreatment of rats with superoxide dismutase (SOD) at two doses, 0.1 mg and 3.5 mg/100 g body weight, retarded the in vivo inactivation of MS by N2O, to 76% and 47% respectively. In vitro inactivation of MS with N2O could not be retarded by DMSO or Na-benzoate, or either exogenous SOD or catalase.
Subject(s)
5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase/antagonists & inhibitors , Anesthetics, Inhalation/toxicity , Nitrous Oxide/toxicity , Superoxides/metabolism , Animals , Free Radical Scavengers , Male , Rats , Rats, WistarABSTRACT
The antioxidative defence capacity was assessed in tissues from different groups of rats at 3, 12 and 24 months of age. It was observed that the levels of antioxidants, vitamin E and ascorbic acid decreased in serum without any changes in liver; whereas reduced glutathione showed lower levels in both serum and liver with advancing age. Antioxidative enzymes such as superoxide dismutase and catalase activities did not indicate appreciable changes in hepatic mitochondria, but were observed to point out divergent trends in post-mitochondrial supernatants, superoxide dismutase showed reduced activities and catalase activities enhanced with age.
Subject(s)
Aging/metabolism , Oxygen/metabolism , Peroxidases/metabolism , Aging/blood , Animals , Antioxidants/metabolism , Ascorbic Acid/metabolism , Catalase/metabolism , Free Radicals , Glutathione/metabolism , Liver/metabolism , Male , Rats , Rats, Inbred Strains , Superoxide Dismutase/metabolism , Vitamin E/metabolismABSTRACT
The effects of feeding vitamin E-deficient diets to rats for one year were investigated to analyse the relationship of the vitamin with other antioxidants and some antioxidative enzymes. Long-term vitamin E deficiency lowered the levels of antioxidants like vitamin E, ascorbic acid and glutathione (GSH) in all tissues analysed and thus increasing the extent of tissue peroxidisability. Vitamin E deficiency had also influenced the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase, the enzymes that are involved in detoxification mechanisms of products arising from free radical metabolism.
Subject(s)
Glutathione Reductase/metabolism , Peroxidases/metabolism , Superoxide Dismutase/metabolism , Vitamin E Deficiency/metabolism , Vitamin E/physiology , Animals , Ascorbic Acid/metabolism , Body Weight , Brain/metabolism , Glutathione/metabolism , Lipid Peroxidation , Liver/metabolism , Male , Muscles/metabolism , Rats , Rats, Inbred Strains , Vitamin E/metabolism , Vitamin E Deficiency/enzymologyABSTRACT
Weanling male Wistar strain rats were administered, through the drinking water, nitrite (0.2%) and dimethylamine (DMA) (0.2%), either singly or in combination for 9 months. Some animals also received 0.5% butylated hydroxytoluene (BHT) in the diet. Nitrite, as well as DMA, caused higher in vitro lipoperoxidation, free lysosomal enzyme activities and cytosolic superoxide dismutase activity in liver. Some of these increases viz., the enzyme activities in liver, were counteracted to a significant extent in the rats receiving a dietary supplement of BHT. The results indicate that nitrite and DMA may induce toxicity through some free radical reactions and that BHT can provide some protection.
