) LPS( پلاسما و عليه موش صحرايي ناشي از ليپوپلي ساكاريد E تغييرات ويتامين

Changes of Plasma and Renal Vitamin E Levels in LPS-Treated Rats

Gram-negative bacterial lipopolysaccharide (LPS) release and subsequent septic shock is a major cause of death in the Intensive Care Unit. LPS is reported to increase nitric oxide (NO) production and oxygen-derived free radicals (OFR) formation. Vitamin E, the most important fat soluble antioxidant, protects cells against oxidative stress. This study was designed to evaluate the role of inducible nitric oxide synthase (iNOS) activity and OFR prodoction in LPS-induced renal failure. Measurement of vitamin E used as a marker of tissue oxidative stress. LPS was used to induce renal failure, L-N6 (1-Imino ethyl-lysine) ,L-NIL) to inhibit iNOS activity and dimethylthiourea (DMTU, a well known OFR scavenger) to prevent oxidative stress. Four groups of 8 rats were studied. One group received LPS, while a second group received LPS+ L-NIL. A third group received LPS+DMTU and a saline group served as a control . To evaluate renal function plasma creatinine and BUN were estimated . HPLC and UV detection were used to measure plasma and tissue vitamin E contents. LPS markedly decreased vitamin E contents of renal plasma and tissue. Administration of L-NIL and DMTU prevented this reduction. Inhibition of iNOS activity by L-NIL and prevention of OFR production by DMTU attenuated renal dysfunction, suggesting involvement of an over production of NO and OFR in LPS-induced renal injury.