XXXX as a potential strategy to attenuate the oxidative stress induced by uremic serum in the vascular system.

@entity1 @entity9492 @entity462 @entity137 @entity5507 @entity26 @entity2041 @entity898 @entity740 @entity2197 @entity1434 @entity35 @entity65
AIMS: @entity740 ( @entity740 ) progression is accompanied by systemic oxidative stress, which contributes to an increase in the risk of @entity65 ( @entity65 ). @entity898 (NAC) is among the most studied antioxidants, but its therapeutic benefits in @entity740 -associated CVD remain controversial. Here, we investigated whether NAC could inhibit the oxidative stress induced by @entity5507 in vitro and in vivo. MAIN METHODS: Endothelial and smooth muscle cells were challenged with @entity1 uremic or non-uremic sera, and the effects of a pre-treatment with 2mM NAC were evaluated. Reactive @entity26 species (ROS) production, protein oxidation and total @entity2041 / @entity9492 (tGSH/ @entity9492 ) ratios were measured. Five-sixths nephrectomized or sham-operated @entity35 were orally treated (in the drinking water) with 60mg/kg/day NAC or not treated for 53days. Plasma @entity462 / @entity1434 reduction potential Eh(Cyss/2Cys) was determined as a novel marker of the systemic oxidative stress. KEY FINDINGS: NAC inhibited all the determined oxidative stress parameters, likely by increasing the t @entity2197 / @entity9492 ratio, in both cell lines exposed to uremic serum. Orally administered NAC attenuated the systemic oxidative stress in uremic @entity35 . SIGNIFICANCE: The present results indicate that NAC, by preventing @entity2197 depletion in vascular cells exposed to uremic serum and by attenuating the systemic oxidative stress during @entity740 progression, emerges as a potential strategy to prevent the oxidative stress induced by @entity137 in the vascular system.
