title: Role of oxygen radicals in adriamycin-induced nephrosis.
abstract: The mechanism of cellular processes responsible for proteinuria induced by adriamycin (ADR) remains unclear. In this study, we examined whether oxygen radicals contribute to the development of proteinuria in ADR-induced nephrosis. The peak concentration of malondialdehyde (MDA) of kidney was found on 8th day after ADR treatment in rats. ADR-treated rats received either superoxide dismutase (SOD, scavenger of O2-, catalase (CAT, scavenger of . H2O2) or dimethyl sulfoxide (DMSO, scavenger of OH). The SOD, CAT or DMSO treated groups had a significant suppression of urinary protein excretion, serum and renal MDA compared to ADR control group. There were also less severe renal morphologic changes in the former three groups vs the ADR controls. These data provide indirect evidence that oxygen radicals generated by ADR are important mediators of ADR-induced proteinuria.
authors.affiliation: Department of Pediatrics, First Affiliated Hospital of Nanjing Medical College.
authors.forename: S H
authors.initials: SH
authors.lastname: Wu
authors.forename: Y C
authors.initials: YC
authors.lastname: Yang
authors.forename: Z M
authors.initials: ZM
authors.lastname: Wang
mesh_terms: D000818:Animals; D004317:Doxorubicin; D005609:Free Radicals; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009401:Nephrosis / Q000139:chemically induced / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000494:pharmacology
chemical_list: D005609:Free Radicals; D008315:Malondialdehyde; D004317:Doxorubicin; D013482:Superoxide Dismutase; D010100:Oxygen