Liu J, Mori A
Department of Neuroscience, Okayama University Medical School, Japan.
Mech Ageing Dev. 1993 Oct 1;71(1-2):23-30. doi: 10.1016/0047-6374(93)90032-m.
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.
通过检测年轻和老年衰老加速小鼠（SAM）脑和肝组织中的超氧化物歧化酶（SOD）活性、硫代巴比妥酸（TBA）反应性以及还原型谷胱甘肽（GSH）水平，研究其抗氧化防御的变化。将这些变化与年龄匹配的ddY小鼠（一种表现出正常衰老的品系）的变化进行比较。SAM小鼠肝脏中的SOD活性随年龄增长而增加，脑和肝脏中的TBA反应性随年龄增长而增加；它们脑和肝脏中的GSH水平也随年龄增长而降低。与ddY小鼠相比，SAM小鼠脑内的SOD活性更高（3个月和11个月时均如此），肝脏中的GSH水平更低（3个月时），肝脏中的TBA反应性更高（3个月时）。这些发现表明，SAM小鼠衰老加速的机制在一定程度上与自由基损伤有关。
