Potential sources of oxidative stress that induce postexercise proteinuria in rats

Abstract

Exercise-induced proteinuria is a common consequence of physical activity and is caused predominantly by alterations in renal hemodynamics. Although it has been shown that exercise-induced oxidative stress can also contribute to the occurrence of postexercise proteinuria, the sources of reactive oxygen species that promote it are unknown. We investigated the enzymes nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) as possible sources of oxidative stress in postexercise proteinuria. First, we evaluated the effect of blocking the NADPH oxidase enzyme on postexercise proteinuria. We found a significant increase in urinary protein level, kidney thiobarbituric acid-reactive substances (TBARS), and protein carbonyl content after exhaustive exercise, and NADPH oxidase activity was induced by exercise. Rats that were treated with an NADPH oxidase inhibitor for 4 days before exhaustive exercise showed no increase in kidney TBARS or protein carbonyl derivative level and no proteinuria or NADPH oxidase activation. In the next set of experiments, we investigated the effect of XO blockage on postexercise proteinuria. Oxypurinol, an XO inhibitor was administered to rats for 3 days before exercise. Although XO inhibition significantly decreased kidney TBARS levels and protein carbonyl content in exercised rats, the inhibition did not prevent exercise-induced proteinuria. However, plasma and kidney XO activity was not induced by exercise, but rather it was suppressed under oxypurinol treatment. These results suggest that increased NADPH oxidase activity induced by exhaustive exercise is an important source of elevated oxidative, stress during exercise, which contributes to the occurrence of postexercise proteinuria.

Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats

“…Similarly, TBARS, a well-known biomarker of lipid peroxidation and oxidative stress (3), is known to increase both at plasma and tissue levels after an exhaustive exercise bout (29,45). In this study, the TBARS increase induced by the exhaustive exercise protocol was significantly reduced by SF treatment, evidencing a protection of muscle tissue against exhaustive exerciseinduced oxidative stress.…”

The Renin–Angiotensin System, Not the Kinin–Kallikrein System, Affects Post-Exercise Proteinuria

“…The main mechanisms involved in post-exercise proteinuria (i.e., saturation in tubular protein reabsorption and increase the nephrons’ glomerular permeability) are not well explained. In addition to these mechanisms, oxidant stress also induces post-exercise proteinuria, as revealed in our previous studies [19-21]. Renal haemodynamic alterations occurring during exercise may cause post-exercise proteinuria.…”

ffect of Purple Sweet Potato (Ipomoea Batatas L.) on Reducing Renal Tissue Damage of House Mice (Mus Musculus L.) After Excessive Physical Exercise

“…Oxidative stress as the result of the exercise may cause muscle damage and interfere some tissues including heart, kidney, liver, brain, and erythrocytes. The source of oxidative stress that works in kidney may be based on two enzyme systems that are leukocytes activation (system of NADPH oxidize enzyme) and process of ischemic-reperfusion (system of xantin oxidize enzymes) that are source of ROS produced by extramuscular tissues during exercise (Kocer et al, 2008). ROS is identified as the cause of cell injury possibility in may diseases.…”

“…The process of ischemia-reperfusion and leucocytes activation through oxidase NADPH system may cause oxidative stress to kidney during and after exercise. Both mechanisms are extremely responsible for the emergence of oxidative stress inside the organ and extramuscular tissue after physical exercise (Kocer et al, 2008).…”