Evidence for the occurrence of selenium-independent glutathione peroxidase activity in rat liver microsomes
ABSTRACT Rat liver microsomes exhibit selenium-independent glutathione peroxidase activity which is associated with glutathione S-transferase activity. The peroxidase activity is not due to contamination with either soluble selenium-dependent or selenium-independent glutathione peroxidase activities of the cytosol. N-Ethylmaleimide treatment which stimulates rat liver microsomal glutathione transferase activity concomitantly stimulates the glutathione peroxidase activity. In contrast, N-ethylmaleimide depresses both enzyme activities of the cytosol. A protein exhibiting both glutathione peroxidase and glutathione transferase activity was isolated from the microsomes and purified to homogeneity by DEAE cellulose ion-exchange and S-hexylglutathione Sepharose 6B affinity chromatography.
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ABSTRACT: In rat liver, in addition to their intrinsic transferase activity, alpha-class GSTs have Se-independent glutathione peroxidase activity toward fatty acid hydroperoxides, cumene hydroperoxide and phospholipids hydroperoxides but not toward H(2)O(2.) We have previously shown that hepatic GST activity by these isoenzymes is significantly increased 24h after cadmium or manganese administration (Casalino et al., 2004). Here it is reported that Se-independent glutathione peroxidase activity by alpha-class GSTs is also stimulated in the liver of intoxicated rats. The stimulation is associated with a higher level of alpha-class GST proteins, whose induction is blocked by actinomycin D co-administration. The observed Se-independent glutathione peroxidase activity is due to alpha-class GST isoenzymes, as indicated by the studies with diethyldithiocarbamate which, at any concentration, equally inhibits both GST and Se-independent glutathione peroxidase and is an uncompetitive inhibitor of both enzymes. As for liver Se-GSPx, it is not at all affected under these toxic conditions. For comparison, we have evaluated the status of another important antioxidant enzyme, NAD(P)H:quinone reductase, 24h after cadmium or manganese administration. NQO1 too results strongly stimulated in the liver of the intoxicated rats. In these animals, a higher expression of Nrf2 protein is observed, actively translocated from the cytoplasm to the nucleus. The results with the transcription inhibitor, actinomycin D, and the effects on Nrf2 protein are the first clear indication that acute manganese intoxication, similarly to that of cadmium and other heavy metals, increases both the hepatic level of Nrf2 and its transfer from the cytoplasm to the nucleus where it actively regulates the induction of phase II enzymes.Toxicology 08/2007; 237(1-3):24-34. · 4.02 Impact Factor
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ABSTRACT: Chronic alcohol consumption causes severe hepatic oxidative damage, particularly to old subjects by decreasing various antioxidant enzymes. In this study, we test the hypothesis that exercise training can protect the aging liver against alcohol-induced oxidative damage. Two different age groups of Wistar albino rats (3 months young, n=24; 18 months old, n=24) were evenly divided into four groups: control (Con), exercise trained (Tr, 23 m/min 30 min/day, 5 days/week for 2 months), ethanol drinking/treated (Et, 2.0 g/kg b.w. orally), and exercise training plus ethanol drinking/treated (Tr+Et). We found significantly (P<.001) lowered hepatic antioxidant enzymes including superoxide dismutase, catalase, selenium (Se)-dependent glutathione peroxidase (Se-GSH-Px), Se-non-dependent glutathione peroxidase (non-Se-GSH-Px), glutathione reductase, and glutathione S-transferase activities in aged rats compared with young. Age-related decrease in antioxidant enzyme status was further exacerbated with ethanol drinking, which indicates liver in aged rats is more susceptible to oxidative damage because of decreased free radical scavenging system in aged/old ethanol-drinking rats. However, the decrease in liver antioxidant enzymes status with ethanol consumption was ameliorated by 2 months exercise training in old and young rats. These results demonstrate that age-associated decrease in hepatic free radical scavenging system exacerbated by ethanol drinking. For the first time, we found that this deterioration was significantly reversed by exercise training in aging liver, thus protects against alcohol-induced oxidative damage.Alcohol (Fayetteville, N.Y.) 09/2010; 44(6):523-9. · 2.41 Impact Factor
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ABSTRACT: A comparative study was performed to evaluate the immunostimulatory effect of yeast and yeast-derived glucan in white prawn Fenneropenaeus indicus (sub-adults of ∼20 gm). Feed with a whole cell biomass of marine yeast Candida sake S165 (CSY) at a concentration of 10% (w/w) and another feed with 0.2% glucan of C. sake S165 (CSG) were used in the study. Fenneropenaeus indicus were fed with these diets for 40 days and subsequently challenged with the white spot syndrome virus (WSSV). Haematological parameters such as the total haemocyte count, phenoloxidase activity, superoxide anion (O2−) level, haemolymph peroxidase level and post-challenge survival against WSSV infection were determined to assess the immune status. In the present experiment, a higher immunity index and post-challenge survival were recorded in shrimps fed with the whole cell yeast diet. The better immunostimulatory performance of the whole cell yeast diet compared with the glucan diet could be attributed to the cellular constituents of yeast including the cell wall glucan, nucleotides, carotenoid pigments and vitamins. Here we observed that whole cell yeast performed better as an immunostimulant than the extracted cell wall glucans. Therefore, the use of yeast biomass in diets, rather than the yeast cell wall extract, glucan, would confer better protection against microbial infection besides reducing the cost of shrimp production.Aquaculture Research 06/2009; 40(15):1723 - 1730. · 1.42 Impact Factor