Abstract
The antioxidant defense alteration in young and old senescence accelerated mice (SAM) was studied by examining superoxide dismutase (SOD) activity, thiobarbituric acid (TBA) reactivity, and reduced glutathione (GSH) level in brain and liver tissues. The changes were compared with those in age-paired ddY mice, a strain exhibiting normal aging. SAM mice showed an age-dependent increase in SOD activity in liver, and an age-dependent increase in TBA reactivity in both the brain and the liver; they also showed an age-dependent decrease in the GSH level in the brain and the liver. When compared with ddY mice, SAM mice showed a higher SOD activity in the brain (at both 3 and 11 months old), a lower GSH level in the liver (at 3 months old), and a higher TBA reactivity in the liver (at 3 months old). These findings suggest that the mechanism of senescence acceleration in SAM mice is to some extent related to free radical damage.
Published Version
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