Role of nitric oxide in lipopolysaccharide-induced oxidant stress in the rat kidney.
Role of nitric oxide in lipopolysaccharide-induced oxidant stress in the rat kidney.
复制标题
一氧化氮在脂多糖诱导的大鼠肾脏氧化应激中的作用。
DOI：
10.1016/s0006-2952(99)00324-x
复制
发表时间：
2000
影响因子：
5.8
通讯作者：
Mayeux,PR
中科院分区：
文献类型：
--
作者：
Zhang,C;Walker,LM;Mayeux,PR
Lipopolysaccharide (LPS)-induced renal oxidant injury and the role of nitric oxide (NO) were evaluated using the inducible nitric oxide synthase (iNOS) inhibitor l-iminoethyl-lysine (l-NIL). One group of male rats received LPS (Salmonella minnesota; 2 mg/kg, i.v.). A second group received LPS plus l-NIL (3 mg/kg, i.p.). A third group received saline i.v. At 6 hr, iNOS protein was induced in the kidney cortex, and plasma nitrate/nitrite levels were increased from 4 ± 2 nmol/mL in the Saline group to 431 ± 23 nmol/mL in the LPS group. The value for the LPS + l-NIL group was reduced significantly to 42 ± 9 nmol/mL. LPS increased blood urea nitrogen levels from 13 ± 1 to 47 ± 3 mg/dL. LPS + l-NIL reduced these levels significantly to 29 ± 2 mg/dL. Plasma creatinine levels were unchanged in all groups. Tissue lipid peroxidation products in the kidney were increased from 0.16 ± 0.01 nmol/mg in the Saline group to 0.30 ± 0.03 nmol/mg in the LPS group. LPS + l-NIL reduced the values significantly to 0.22 ± 0.02 nmol/mg. Intracellular glutathione levels were decreased in the kidneys from 1.32 ± 0.1 nmol/mg in the Saline group to 0.66 ± 0.08 nmol/mg in the LPS group. LPS + l-NIL increased the levels significantly to 0.99 ± 0.13 nmol/mg. LPS increased the 3-nitrotyrosine-protein adducts in renal tubules as detected by immunohistochemistry, indicating the generation of peroxynitrite. l-NIL decreased adduct formation. These data indicated that LPS-induced NO generation resulted in peroxynitrite formation and oxidant stress in the kidney and that inhibitors of iNOS may offer protection against LPS-induced renal toxicity.
登录
查看更多内容
过氧化氢酶对内毒素诱导的未麻醉绵羊急性肺损伤的影响。
DOI：
10.1164/ajrccm/137.2.420
发表时间：
1988
期刊：
The American review of respiratory disease
影响因子：
--
作者：
Milligan,SA;Hoeffel,JM;Goldstein,IM;Flick,MR
通讯作者：
Flick,MR
影响因子：
19.6
作者：
J. Morrissey;R. McCracken;H. Kaneto;M. Vehaskari;D. Montani;S. Klahr
通讯作者：
J. Morrissey;R. McCracken;H. Kaneto;M. Vehaskari;D. Montani;S. Klahr
DOI：
10.1164/ajrccm/151.4.1250
发表时间：
1995-04
影响因子：
24.7
作者：
N. Kooy;J. Royall;Y. Ye;D. R. Kelly;J. Beckman
通讯作者：
N. Kooy;J. Royall;Y. Ye;D. R. Kelly;J. Beckman
感染性休克的病理生理学和治疗。
DOI：
10.1001/jama.1991.03470040112032
发表时间：
1991
期刊：
JAMA
影响因子：
--
作者：
E. Rackow;M. Astiz
通讯作者：
M. Astiz
一氧化氮在内毒素休克中的保护和病理作用。
影响因子：
10.8
作者：
C. Wright;D. Rees;S. Moncada
通讯作者：
S. Moncada