| Co-Investigator(Kenkyū-buntansha) |
DOBASHI Kazushige Yamanashi Medical College, Pediatrics, Instructor, 医学部, 助手
AIHARA Masao Yamanashi Medical College, Pediatrics, Instructor, 医学部, 助手 (30242639)
UCHIDA Norihiko Yamanashi Medical College, Pediatrics, Assistant, 医学部, 医員
OHTA Masanori Yamanashi Medical College, Pediatrics, Instructor, 医学部, 助手 (80233146)
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| Research Abstract |
Cellular glutathione peroxidase (GPX) was purified from rat liver to homogeniety (2000 folds), and polyclonal antibody against GPX was raised by immunizing rabbits. Immunogold labeling study revealed that almost all compartments of rat hepatocyte were labeled. The labeling density was highest in the mitochondria, second highest in the nuclei, and very low in the peroxisomes and lysosomes. Immunohistochemically, GPX distributed widely in various tissues. There was a general trend toward richness of GPX in epithelia and metabolically active sites. GPX occurred earliest in the fetal rat heart, second earliest in the liver, then the gastrointestinal tract and lung, and latest in the kidneys. Thus, developmental profile of GPX was essentially similar to those of SODs. Serum antioxidant activity (AOA) was low in human neonates and increased gradually during the first 3 months of life. The AOA was higher in infants older than 4 months of age than in adults. Ceruloplasmin, transferrin and albumin changed in a similar manner to that of AOA.It appears that preventive antioxidant activity is immature in the neonetal and early infantile period, and that this defect is compensated by the increased radical scavenging activity. In insulin-dependent diabetic children, serum AOA was decreased in relation to poor glycemic control. Total radical scavenging activity was also decreased mainly due to the decreased contribution of unidentified chain-breaking antioxidants, suggesting that a defective serum antioxidant status contributes to the increased oxidative stress in the patients. In diabetic rats, serum preventive antioxidants, but not radical scavengers, were markedly decreased. In patients with end-stage chronic renal failure, serum AOA was markedly decreased, and this may contribute to the putative accelerated development of atherosclerosis in the patients. High concentration of glucose enhanced H2O2-induced lipid peroxidation in human red blood cell membrane via, at least, two
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