THE EFFECTS OF VITAMIN-E ON TISSUE OXIDATION IN NEPHROTOXIC (ANTIGLOMERULAR BASEMENT-MEMBRANE) NEPHRITIS

被引:17
作者
ENDREFFY, E
TURI, S
LASZIK, Z
BERECZKI, C
KASA, K
机构
[1] Department of Pacdiatrics, Albert Szent-Györgyi University Medical School, Szeged, H-6725
[2] Department of Pathology, Albert Szent-Györgyi University Medical School, Szeged, H-6725
关键词
NEPHROTOXIC (ANTIGLOMERULAR BASEMENT MEMBRANE) NEPHRITIS; TISSUE OXIDATION;
D O I
10.1007/BF00867490
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The effects of vitamin E on tissue oxidation, kidney function and morphology were studied in rats with nephrotoxic nephritis (NTN). Thirty-six nephritic animals received no treatment (group 1), while 36 were treated with vitamin E (group 2). Twenty-four hours after the administration of anti-glomerular basement membrane antibody, sulfhydryl-containing renal protein was significantly lower in group 1 than in group 2 (0.70 +/- 0.16 and 1.08 +/- 0.06 mmol/100 g kidney tissue, respectively), suggesting a free oxygen radical scavenging effect of vitamin E in group 2. The difference was similar on day 14. The creatinine clearance was significantly lower in group 1 than in group 2 on day 1 (40 +/- 30 and 204 +/- 60-mu-l/min per 100 g body weight, respectively). The protein excretion was initially high in both groups, but a significant decrease was detected in group 2 relative to group 1 on day 14 (25 +/- 18 and 92 +/- 38 mg/24 h, respectively). The morphological changes were less severe in group 2. Vitamin E treatment did not alter any of the above values significantly in healthy animals. The release of oxygen free radicals in NTN might play an important role in the pathogenesis, which can be influenced by free radical scavengers through changes in kidney function and morphology.
引用
收藏
页码:312 / 317
页数:6
相关论文
共 30 条
[1]  
Couser W.G., Baker P.J., Adler S., Complement and the direct mediation of immune glomerular injury: a new perspective, Kidney International, 28, pp. 879-890, (1985)
[2]  
Thoon N.M., Holdsworth S.R., Glasgow E.F., Atkins R.C., The macrophage in the development of experimental crescentic glomerulonephritis, Am J Pathol, 94, pp. 223-235, (1979)
[3]  
Fantone J.C., Ward P.A., Role of oxygen derived free radicals and metabolites in leukocyte dependent inflammatory reactions, Am J Pathol, 107, pp. 395-418, (1982)
[4]  
Roos D., Weenig R.S., Voetman A.A., Protection of human neutrophils against oxidation damage, Agents Actions, 10, pp. 528-535, (1980)
[5]  
Sacks T., Moldow C.F., Craddock P.R., Bowers J.K., Jacob H.S., Oxygen radical mediated endothelial cell damage by complement stimulated granulocytes: an in vitro model of immune vascular damage, J Clin Invest, 61, pp. 1161-1167, (1978)
[6]  
McCormick J.R., Harkin M.M., Johnson K.J., Ward P.A., Suppression by superoxide dismutase of immune-complex-induced pulmonary alveolitis and dermal inflammation, Am J Pathol, 102, pp. 55-61, (1981)
[7]  
Petrone W.F., English D.K., Wong K., McCord J.M., Free radicals and inflammation: the superoxide-dependent activation of a neutrophil chemotactic factor in plasma, Proc Natl Acad Sci USA, 77, pp. 1159-1163, (1980)
[8]  
Weis S.J., Neutrophil generated hydroxyl radicals destroy RBC targets (abstract), Clin Res, 27, (1979)
[9]  
Rehan A., Johnson K.J., Wiggins R.C., Kunkel R.G., Ward P.A., Evidence for the role of oxygen radicals in acute nephrotoxic nephritis, Lab Invest, 51, pp. 396-403, (1984)
[10]  
Rehan A., Wiggins R.C., Kunkel R.G., Till G.D., Johnson K.J., Glomerular injury and proteinuria in rats after intrarenal injection of cobra venom factor. Evidence for the role of neutrophil-derived oxygen free radicals, Am J Pathol, 123, pp. 57-66, (1986)