Oxidative status in senescence-accelerated mice.
The lipid peroxidation and activities of antioxidant enzymes were examined in the livers of two substrains of senescence-accelerated mice (SAM): senescence-resistant SAM-R/1 and senescence-prone SAM-P/1. Fluorescent age pigment and conjugated diene levels in both substrains increased gradually with age, but we found higher levels in SAM-P/1 at all ages tested. Differences in the levels of lipid peroxidation products became more marked with age. Among the enzymes studied, only mitochondrial superoxide dismutase (SOD) in SAM-P/1 showed decreased activity in all age groups. The specific mitochondrial SOD in that case was Cu,Zn-SOD. The amount of Cu,Zn-SOD in mitochondrial fractions of SAM-P/1 was only half that of SAM-R/1, whereas there were no apparent differences in the mRNA levels of both SAM groups. Our study indicates that impaired transport of Cu,Zn-SOD into mitochondria after cytosolic synthesis reduces defense against oxidative stress. That reduction may be one of the factors contributing to accelerated senescence in the SAM-P/1.
Park
J W
JW
Department of Pharmacology, Seoul National University College of Medicine, Chongno-gu, Korea.
Choi
C H
CH
Kim
M S
MS
Chung
M H
MH
D000375:Aging / Q000378:metabolism*; D000818:Animals; D015152:Blotting, Northern; D002374:Catalase / Q000378:metabolism; D003600:Cytosol / Q000201:enzymology; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D015151:Immunoblotting; D015227:Lipid Peroxidation; D008099:Liver / Q000201:enzymology*; D008543:Melanins; D051379:Mice; D008815:Mice, Inbred Strains; D008930:Mitochondria, Liver / Q000201:enzymology; D018384:Oxidative Stress; D010860:Pigments, Biological / Q000032:analysis; D013482:Superoxide Dismutase / Q000378:metabolism
D008543:Melanins; D010860:Pigments, Biological; C030524:fluorescent age pigment; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase