Durante Paula, Romero Freddy, Pérez Mariela, Chávez Maribel, Parra Gustavo
Centro de Investigaciones Biomédicas, IVIC-Zulia, Maracaibo, Venezuela.
Toxicol Ind Health. 2010 Apr;26(3):163-74. doi: 10.1177/0748233710362377. Epub 2010 Feb 22.
Oxidative stress is an important mechanism in mercury poisoning. We studied the effect of uric acid, a natural and potent reactive oxygen species and peroxynitrite scavenger, in HgCl( 2)-induced nephrotoxicity. Rats were injected with a unique dose of HgCl(2) (2.5 mg/kg body weight, subcutaneously) and then vehicle (for 3 days, twice daily) or HgCl(2) (unique dose) and intraperitoneal uric acid suspension (250 mg/kg body weight, twice daily, for 3 days), and then killed at 24, 48 and 72 hours after HgCl(2) administration (n = 5 for each group). At the end of the experimental study, kidneys and blood samples were taken. Tissues were prepared and examined under light microscopy. Uric acid significantly prevented the increase in plasma levels of creatinine and blood urea nitrogen (BUN); it helped maintain systemic nitrate/nitrite concentration and total antioxidant capacity. Uric acid attenuated the increase of renal lipid peroxidation and it markedly diminished nitrotyrosine signal and histopathological changes as early as 24 hours after HgCl(2) administration. Uric acid did not prevent a decrease in beta-actin signal caused by mercuric chloride, but it promoted a faster recovery when compared to the HgCl(2) alone group. Our results indicate that UA could play a beneficial role against HgCl(2) toxicity by preventing systemic and renal oxidative stress and tissue damage.
氧化应激是汞中毒的重要机制。我们研究了尿酸（一种天然且强效的活性氧和过氧亚硝酸盐清除剂）对氯化汞诱导的肾毒性的影响。给大鼠皮下注射单次剂量的氯化汞（2.5毫克/千克体重），然后分别给予赋形剂（持续3天，每日两次）或氯化汞（单次剂量）及腹腔内尿酸悬浮液（250毫克/千克体重，每日两次，持续3天），在给予氯化汞后24、48和72小时处死大鼠（每组n = 5）。在实验研究结束时，采集肾脏和血液样本。制备组织并在光学显微镜下检查。尿酸显著阻止了血浆肌酐和血尿素氮（BUN）水平的升高；有助于维持全身硝酸盐/亚硝酸盐浓度和总抗氧化能力。尿酸减轻了肾脏脂质过氧化的增加，并且早在给予氯化汞后24小时就显著减少了硝基酪氨酸信号和组织病理学变化。尿酸未能阻止氯化汞引起的β-肌动蛋白信号降低，但与单独使用氯化汞组相比，它促进了更快的恢复。我们的结果表明，尿酸可通过预防全身和肾脏氧化应激及组织损伤，对氯化汞毒性发挥有益作用。
