@article {10.3844/ajidsp.2005.111.115,
article_type = {journal},
title = {Increased Production of Nitric Oxide Contributes to Renal Oxidative Stress in Endotoxemic Rat},
author = {Tunçtan, Bahar and Korkmaz, Belma and Yıldırım, Hatice and Tamer, Lülüfer and Atik, Uğur and Buharalıoğlu, C. Kemal},
volume = {1},
number = {2},
year = {2005},
month = {Jun},
pages = {111-115},
doi = {10.3844/ajidsp.2005.111.115},
url = {https://thescipub.com/abstract/ajidsp.2005.111.115},
abstract = {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 kgˉ1, i.p.), endotoxin (Escherichia coli lipopolysaccharide, O111:B4; 10 mg kgˉ1, i.p.) and/or selective iNOS inhibitor (1,3-PBIT; 10 mg kgˉ1, 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.},
journal = {American Journal of Infectious Diseases},
publisher = {Science Publications}
}