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Previous studies have implied a relationship between Se-deficiency and oxidative stress. In the present study, the occurrence of oxidative stress due to Se-deficiency was investigated by evaluating the age dependence of growth and indices of oxidative damage for the liver of Se-deficient (SeD) rats. The ratios of liver weight to body weight of the SeD rats were greater than those of the normal rats. The values of AST and ALT (clinical indices of liver damage) were higher in the SeD rats than the normal ones especially in the young (6-12 weeks of age). The TBARS level of the 4-week-old SeD group were higher than the normal group while the level decreased with age. Conversely, the TBARS level of the normal group gradually increased and became higher than SeD group in older rats (12-20 weeks of age). Vitamin E rather than vitamin C may be consumed during oxidative stress due to Se-deficiency. Damage induced by Se-deficiency may be related to growth and the mechanisms of this damage may alter with age.

The amounts of selenium (Se), iron (Fe), and zinc (Zn) in the liver, kidney, and spleen as a function of age of rats measured using instrumental neutron activation analysis were compared between Se-deficient (SeD) rats and normal rats. The SeD model rats can live for more than 50 weeks. The effect of Se-deficinecy in rats might be weak, compared to the marked malfunction of GSH-Px. The SeD rats can be considered as a model of non-lethal chronic oxidative stress. Fluctuations of Fe and Zn in the liver of Se-deficient rats were observed. The amount of redox-relating minerals, such as Fe and Zn, in SeD rat organs is changeable depending on the age.

The relationship of hydrogen peroxide (H 2 O 2 ) levels in bile with liver SOD and GSH Px activity in selenium (Se)-deˆcient rats is discussed. Normal rats and 7 groups of rats fed a Se-deˆcient diet with diŠerent feeding periods were examined. H 2 O 2 levels in bile were measured using the spin-trapping method with electron spin resonance (ESR). Bile H 2 O 2 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-deˆcient diet and absence of Se. Bile H 2 O 2 levels in the later stage (60 120 min) of measurementˆrst increased with the length of feeding with the Se-deˆcient diet and then decreased with longer feeding periods. Bile H 2 O 2 levels immediately after the operation were relatively low in almost all cases. The operation may result in oxidative stress to generate H 2 O 2 . Liver GSH Px activity decreased depending on the length of the feeding period with the Se-deˆcient diet and existence of Se. Liver SOD activity increased in Se-deˆcient groups. It is suggested that the H 2 O 2 levels in bile are related to decreased GSH Px activity, SOD activity, and also the oxidative stress caused by surgery. Therefore the H 2 O 2 levels in bile can be used as an index of sensitivity to oxidative stress. Although severe oxidative stress may decrease SOD activity, Se deˆciency can induce liver SOD activity.Key words-oxidative stress; X band ESR; Fenton's reaction; spin trapping; hydroxyl radical; glutathione peroxidase

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