[Relation of bile hydrogen peroxide level and liver super oxide dismutase activity in selenium-deficient rats].
نویسندگان
چکیده
The relationship of hydrogen peroxide (H2O2) levels in bile with liver SOD and GSH-Px activity in selenium (Se)-deficient rats is discussed. Normal rats and 7 groups of rats fed a Se-deficient diet with different feeding periods were examined. H2O2 levels in bile were measured using the spin-trapping method with electron spin resonance (ESR). Bile H2O2 levels in the initial stage (20-60 min from start of the cannulation) of measurement were increased depending on the length of the feeding period with the Se-deficient diet and absence of Se. Bile H2O2 levels in the later stage (60-120 min) of measurement first increased with the length of feeding with the Se-deficient diet and then decreased with longer feeding periods. Bile H2O2 levels immediately after the operation were relatively low in almost all cases. The operation may result in oxidative stress to generate H2O2. Liver GSH-Px activity decreased depending on the length of the feeding period with the Se-deficient diet and existence of Se. Liver SOD activity increased in Se-deficient groups. It is suggested that the H2O2 levels in bile are related to decreased GSH-Px activity, SOD activity, and also the oxidative stress caused by surgery. Therefore the H2O2 levels in bile can be used as an index of sensitivity to oxidative stress. Although severe oxidative stress may decrease SOD activity, Se deficiency can induce liver SOD activity.
منابع مشابه
Evaluation of in vivo oxidative stress in liver of selenium-deficient rat
Hepatic endogenous hydrogen peroxide (H2O2) in bile of selenium (Se)-deficient rats was measured using electron spin resonance (ESR) spin-trapping technique. The level of hepatic H2O2 increased as the glutathione peroxidase (GSH-Px) activity decreased. In vivo reducing capacity was evaluated in the Se-deficient rats with low frequency (300MHz) in vivo ESR. The in vivo reducing capacity was sign...
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عنوان ژورنال:
- Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan
دوره 122 6 شماره
صفحات -
تاریخ انتشار 2002