|
|
| |
| Articles
by
Ugur Atik |
Total Records (
1 ) for
Ugur Atik |
|
 |
| |
|
| |
Bahar Tunctan
,
Belma Korkmaz
,
Hatice Yyldyrym
,
Lulufer Tamer
,
Ugur Atik
and
C. Kemal Buharalyoglu
|
| |
Overproduction of reactive oxygen and nitrogen species leads to oxidative
stress and decreased total antioxidant capacity, which is responsible for high
mortality from several diseases such as endotoxic shock. Nitric oxide (NO) produced
by inducible NO synthase (iNOS) during endotoxemia is the major cause of vascular
hyporeactivity, hypotension and multiple organ failure. In this study, we investigated
whether increased production of NO contributes to renal oxidative stress in
endotoxemic rat. Saline (4 mL kg-1, i.p.), endotoxin (Escherichia coli lipopolysaccharide,
O111:B4; 10 mg kg-1, i.p.) and/or selective iNOS inhibitor (1,3-PBIT; 10 mg
kg-1, i.p.) were administered to conscious male Wistar rats and mean arterial
blood pressure was recorded at 1, 2, 3 and 4 hr after injection. Nitrite and
malondialdehyde (MDA) levels and myeloperoxidase (MPO) activity were measured
in the sera and/or kidney homogenates at the end of the experiments. Administration
of endotoxin caused hypotension associated with increased systemic and renal
nitrite production. 1,3-PBIT prevented these effects of endotoxin at 1 hr after
injection of endotoxin. Renal MPO activity was decreased by endotoxin which
was not changed by 1,3-PBIT. Endotoxin caused a decrease in MDA levels in the
renal tissue, which was prevented by 1,3-PBIT. These data suggest that overproduction
of NO by iNOS during endotoxemia decreases renal oxidative stress and that inhibition
of iNOS restores total renal antioxidant capacity. |
|
|
|
|
| |
|
