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Received October 16, 2006
Revised December 13, 2006
Accepted after revision February 16, 2007
1 Department of Physiology, College of Medicine, National Taiwan University, Taipei 100, Taiwan
2 School of Medicine, Fu-Jen Catholic University, Hsinchuang 242, Taiwan
3 Department of Medical Research, National Taiwan University College of Medicine and National Taiwan U
* To whom correspondence should be addressed. E-mail: chfochen{at}ha.mc.ntu.edu.tw.
Chronic hypoxic preconditioning (CH) reduces superoxide-induced renal dysfunction via the upregulation of superoxide dismutase (SOD) activity and contents. Endotoxemia declines renal antioxidant status. We hypothesize that CH might protect the kidney from subsequent endotoxemia-induced oxidative injury. Endotoxemia was induced by intraperitoneal injection of lipopolysaccharide (LPS, 4 mg kg-1) in rats kept at sea level (SL) and rats with CH in an altitude chamber (5500 m for 15 h day-1) for 4 weeks. LPS enhanced xanthine oxidase (XO) and gp91phox (catalytic subunit of NADPH oxidase) expression associated with burst amount of superoxide production from the SL kidney surface and renal venous blood detected by lucigenin-enhanced chemiluminescence. LPS induced a morphologic-independent renal dysfunction in baseline and acute saline loading stages and increased renal IL-1b protein and urinary protein concentration in the SL rats. After 4 weeks¡¦ induction, CH significantly increased Cu/ZnSOD, MnSOD, and catalase expression (16¡Ó17%, 128¡Ó35%, and 48¡Ó21% respectively) in renal cortex and depressed renal cortex XO (44¡Ó16%) and renal cortex (20¡Ó9%) and medulla (28¡Ó11%) gp91phox when compared to SL rats. The combined effect of enhanced antioxidant proteins and depressed oxidative proteins significantly reduced LPS-enhanced superoxide production, renal XO and gp91phox expression, renal IL-1b production, and urinary protein level. CH also ameliorated LPS-induced renal dysfunction in the baseline and acute saline loading periods. We conclude that CH treatment enhanced intrarenal antioxidant /oxidative protein ratio to overcome endotoxemia-induced reactive oxygen species formation and inflammatory cytokine release.
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