Brandão R, Santos F W, Farina M, Zeni G, Bohrer D, Rocha J B T, Nogueira C W
Departamento de Quimica, Centro de Ciencias Naturais e Exatas, Universidade Federal de Santa Maria, 97105-900, Santa Maria, RS, Brazil.
Cell Biol Toxicol. 2006 Nov;22(6):429-38. doi: 10.1007/s10565-006-0119-8. Epub 2006 Sep 11.
Acute effects of mercury on mouse blood, kidneys, and liver were evaluated. Mice received a single dose of mercuric chloride (HgCl2, 4.6 mg/kg, subcutaneously) for three consecutive days. We investigated the possible beneficial effects of antioxidant therapy (N-acetylcysteine (NAC) and diphenyl diselenide (PhSe)2) compared with the sodium salt of 2,3-dimercapto-1-propanesulfonic acid (DMPS), an effective chelating agent in HgCl2 exposure in mice. We also verified whether metallothionein (MT) induction might be involved in a possible mechanism of protection against HgCl2 poisoning and whether different treatments would modify MT levels and other toxicological parameters. The results demonstrated that HgCl2 exposure significantly inhibited delta-aminolevulinate dehydratase (delta-ALA-D) activity in liver and only DMPS treatment prevented the inhibitory effect. Mercuric chloride caused an increase in renal non-protein thiol groups (NPSH) and none of the treatments modified renal NPSH levels. Urea concentration was increased after HgCl2 exposure. NAC plus (PhSe)2 was partially effective in protecting against the effects of mercury. DMPS and (PhSe)2 were effective in restoring the increment in urea concentration caused by mercury. Thiobarbituric acid-reactive substances (TBARS), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) activities and ascorbic acid levels were not modified after mercury exposure. Mercuric chloride poisoning caused an increase in hepatic and renal MT levels and antioxidant treatments did not modify this parameter. Our data indicated a lack of therapeutic effect of the antioxidants tested.
评估了汞对小鼠血液、肾脏和肝脏的急性影响。小鼠连续三天接受单剂量的氯化汞（HgCl2，4.6毫克/千克，皮下注射）。我们研究了抗氧化疗法（N-乙酰半胱氨酸（NAC）和二苯基二硒化物（PhSe）2）与2,3-二巯基-1-丙磺酸钠（DMPS）相比可能的有益效果，DMPS是一种在小鼠HgCl2暴露中有效的螯合剂。我们还验证了金属硫蛋白（MT）的诱导是否可能参与预防HgCl2中毒的潜在机制，以及不同的治疗方法是否会改变MT水平和其他毒理学参数。结果表明，HgCl2暴露显著抑制了肝脏中的δ-氨基乙酰丙酸脱水酶（δ-ALA-D）活性，只有DMPS治疗可预防这种抑制作用。氯化汞导致肾脏非蛋白硫醇基团（NPSH）增加，且没有任何一种治疗方法改变肾脏NPSH水平。HgCl2暴露后尿素浓度升高。NAC加（PhSe）2在预防汞的影响方面部分有效。DMPS和（PhSe）2在恢复汞引起的尿素浓度升高方面有效。汞暴露后，硫代巴比妥酸反应性物质（TBARS）、天冬氨酸转氨酶（AST）和丙氨酸转氨酶（ALT）活性以及抗坏血酸水平未发生改变。氯化汞中毒导致肝脏和肾脏MT水平升高，抗氧化治疗未改变该参数。我们的数据表明所测试的抗氧化剂缺乏治疗效果。
