title: [Homeostasis of antioxidant status in hemodialysis patients].
abstract: Oxidative stress, which occurs when there is excessive free-radical production or low antioxidant levels, makes significant contributions to pathogenesis in many human diseases. Cardiovascular disease is the major cause of mortality in patients receiving hemodialysis. For these patients, oxidative stress and increased lipid peroxidation may contribute to increased risk of atherosclerosis. The aim of this study was to determine if hemodialysis patients were associated with disturbance of homeostasis of antioxidant status. In this experiment, total antioxidant status of serum is measured by its ability to inhibit generation of free radicals from 2,2'-amino-di-[3-ethylbenzthiazole sulphonate] by metmyoglobin and hydrogen peroxide. Status of radical scavengers, such as serum total protein, albumin, uric acid and total bilirubin, was also measured. Blood were collected from three different episodes of hemodialysis. In the first group (n = 29), blood were collected before and after hemodialysis. In the second group (n = 29), blood were collected after dialysis and before next hemodialysis. In the third group (n = 8), blood were collected before hemodialysis. After last hemodialysis, patients started ingesting vitamin C and blood were collected before next hemodialysis. There was a marked reduction of total antioxidant status after hemodialysis in the first group. There was a marked increase in total antioxidant status before next hemodialysis in the second group. High doses of vitamin C caused increase in total antioxidant status in the third group. In conclusion, disturbance of homeostasis of total antioxidant status were observed in patients receiving hemodialysis. This may play a role in the pathogenesis in these groups.
authors.affiliation: Department of Laboratory Medicine, National Defense Medical College, Tokorozawa.
authors.forename: K
authors.initials: K
authors.lastname: Saionji
authors.forename: T
authors.initials: T
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Higurashi
authors.forename: K
authors.initials: K
authors.lastname: Iizuka
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000378:metabolism*; D001161:Arteriosclerosis / Q000209:etiology; D001205:Ascorbic Acid / Q000494:pharmacology; D002318:Cardiovascular Diseases / Q000209:etiology; D005260:Female; D016166:Free Radical Scavengers / Q000097:blood*; D006706:Homeostasis; D006801:Humans; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D006435:Renal Dialysis / Q000009:adverse effects*; D012306:Risk
chemical_list: D000975:Antioxidants; D016166:Free Radical Scavengers; D001205:Ascorbic Acid