Renal oxidative stress

Jahangir T et al (2006) Farnesol prevents Fe-NTA-mediated renal oxidative stress and early tumour promotion markers in rats. Hum Exp Toxicol 25(5) 235-242... 

ATTENUATION OF RENAL OXIDATIVE STRESS WITH GARLIC OIL... 

Iqbal, M. and Athar, M., Attenuation of iron-nitrilotriacetate (Fe-nta)-mediated renal oxidative stress, toxicity and hyperproliferative response by the prophylactic treatment of rats with garlic oil, Food Chem. Toxicol., 36, 485M95, 1998. 

Gonzalez-Correa, XA., De la Cruz, XR, Martiu-Aurioles, E., Lopez-Egea, M.A., Ortiz, R, De la Cuesta, F.S. Effects of S-adenosyl-L-methionine on hepatic and renal oxidative stress in an experimental model of acute biliary obstruction in rats. Hepatology 1997 26 121-127... 

ChanderV, Chopra K. Nifedipine attenuates changes in nitric oxide levels, renal oxidative stress, and nephrotoxicity induced by cyclosporine. Ren Fail 2005 27 441-450. 

The data indicate that zinc-induced metallothionein binds mercury in the renal cortex and shifts the distribution of mercury from its site of toxicity at the epithelial cells of the proximal tubules. Thus, the renal content of mercury is increased, yet less is available to cause toxicity. In contrast, the renal toxicity of mercuric chloride is exacerbated in zinc-deficient animals (Fukino et al. 1992). In the zinc-deficient state, less mercury accumulates in the kidneys, but the toxicity is greater. The mechanism of the protection appears to involve more than simply a redistribution of renal mercury, because in the absence of mercury exposure, zinc deficiency increases renal oxidative stress (increased lipid peroxidation, decreased reduced ascorbate). When mercury exposure occurs, the oxidative stress is compounded (increased lipid peroxidation and decreased glutathione and glutathione peroxidase). Thus, zinc appears to affect the biochemical protective mechanisms in the kidneys as well. 

Goligorsky, M.S., Morgan, M.A., Suh, H., Safirstein, R and Johnson, R (1992). Mild oxidative stress, cellular mode of mitogenic effect. Renal Failure 14, 385-389. 

R. Rodrigo and G. Rivera, Renal damage mediated by oxidative stress a hypothesis of protective effects of red wine. Free Rad. Biol. Med. 33, 409—422 (2002). 

Tanaka, T., Akatsuka, S., Ozeki, M., Shirase, T., Hiai, H., and S. Toyokuni, 2004, Redox regulation of annexin 2 and its implications for oxidative stress-induced renal carcinogenesis and metastasis. Oncogene. 13 23(22) 3980-9. 

Urine samples were taken from a urinary catheter from living-related and cadaveric renal transplant donors at the time of procurement surgery. TAC was found to be significantly lower in urine from poor cadaveric donors when compared with either good cadaveric or living donors. Therefore, TAC of urine may be a good marker of preoperative oxidant stress in the kidney and may have a predictive value with respect to the clinical outcome of transplantation (S17). Patients with acute renal failure showed higher urine TAC (K5). 

Increase in TAC is not always a good prognostic it may simply indicate an initial response to oxidative stress, as with concentrations of individual antioxidants and activities of antioxidant enzymes, or when it is due to disturbances in uric acid metabolism. Because uric acid is the main determinant of TAC of blood plasma, TAC increases in situations when the concentration of urate is increased, for example, in metabolic disorders and kidney failure. TAC is increased in urine from renal transplant recipients with delayed graft function (SI6). Ischemia of small intestine leads to an increase in TAC of rat blood serum, which is maximal (almost twofold) immediately after termination of 45-min ischemia (S22). TAC of blood plasma of rats poisoned with a high dose of carbon tetrachloride (1200 mg/kg, intraperitoneal injection, measurement 16 hr after injection) was significantly (over twofold) increased (Kl). These apparently paradoxical effects can be explained, however, by release of antioxidants from cells undergoing necrosis. Increase in TAC after intensive physical exercise also may be a marker of tissue... 

TAC of blood plasma in rats fed an ethanol-supplemented diet increases, although ethanol is known to induce oxidative stress. The effect is due to ethanol-induced purine degradation and increase in the level of uric acid (G2). TAC of blood plasma in critically ill patients with renal dysfunction is augmented, again due to increase in uric acid level (Ml). Caloric restriction, a procedure known to improve the redox status and prolong the life span of mammals, decreases TAC of rat serum (C12). 

Shoskes, D. A., Shahed, A. R., Kim, S., Gritsch, H. A., Danovitch, G., and Wilkinson, A., Oxidant stress and antioxidant capacity in urine of renal transplant recipients predict early graft function. Transplant. Proc. 33, 984 (2001). 

Shoskes, D. A., Webster, R., and Shahed, A., Oxidant stress in cadaveric and living kidney donors as markers of renal injury Utility of total antioxidant capacity and isoprostane levels in urine. Transplant. Proc. 32, 804-805 (2000). 

It remains to be clarified why patients with renal hypouricemia frequently develop acute renal failure. The following hypothesis has been proposed. Oxidative stress is essential for the onset of ischemic acute renal failure. In the kidney, uric acid acts as a protective mechanism against oxidative stress. However, in patients with renal hypouricemia, a decrease in uric acid may allow exposure of the kidney to oxidative stress, causing ALPE [152,153]. 

We selected one renal hypouricemia patient with a history of ALPE and one healthy adult (control) without a history of ALPE, and measured creatinine clearance, FEUA, and oxidative stress markers (urinary 8-isoprostane and NOx) after anaerobic and aerobic exercise load tests (a 400-m race, 16 min on a treadmill, Bruce method, 13.5metabolic equivalents (METs)) (Fig. 67). In the hypouricemia patient, (a) exercise reduced creatinine clearance (Fig. 68), (b) FEUA increased 5h after the exercise load test (Fig. 69), (c) the urinary 8-isoprostane level increased slightly 6-25h after the exercise load test, although there were no marked differences compared with the control values (Fig. 70), and (d) the urinary NOx level increased 2 and 5h after the exercise load test (Fig. 71). Thus, we found that exercise reduced creatinine clearance in the renal hypouricemia patient with a history of ALPE, but there was no marked influence of oxidative stress. 

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