Programa de Pós-Graduação em Ciências Biomédicas, Centro Universitário Hermínio Ometto, UNIARARAS, Avenida Dr. Maximiliano Barutto, no 500, Jd. Universitário, CEP 13607-339 Araras, São Paulo, Brazil.
Ecotoxicol Environ Saf. 2012 Apr;78:170-7. doi: 10.1016/j.ecoenv.2011.11.020. Epub 2011 Dec 5.
Risk assessments suggest that intermediate and long-term exposure to triazine herbicides and its metabolites through water can cause severe damage to human health. The objective of this study was to investigate the possible effects of atrazine on Wistar rats submitted to subacute treatment. For this purpose, the activity of catalase and alanine aminotransferase was quantified, and the effect of the herbicide on cell membranes was examined based on the measurement of lipid peroxidation and consequent formation of malondialdehyde and on the mRNA expression of antioxidant enzymes (Mn-superoxide dismutase [SOD] and GSTM1) and connexins. In addition, we evaluated histopathological alterations in the liver, cellular expression of SOD and glutathione (GST), activation of heat shock proteins (HSPs) by immunohistochemistry, and the induction of apoptosis. The genotoxic potential of the herbicide was investigated by the micronucleus test in bone marrow smears. Adult male Wistar rats were treated with an aqueous solution of atrazine at a concentration of 400mg/kg/day, by gavage, for 14 consecutive days. Control groups were also included. The results showed an increase of catalase levels and maintenance of the expression of antioxidant enzymes (SOD and GST). In addition, lipid peroxidation, hepatic tissue degeneration, activation of HSP90, increased levels of connexin mRNA, and genotoxicity were observed. In conclusion, atrazine induced early hepatic oxidative stress that triggered defense mechanisms to maintain the morphophysiological integrity of the liver. Further studies are needed to better understand the effects of this herbicide on human health.
风险评估表明，通过水接触到的三嗪类除草剂及其代谢物，可能会对人类健康造成严重损害。本研究的目的是调查莠去津对亚急性处理的 Wistar 大鼠可能产生的影响。为此，我们定量了过氧化氢酶和丙氨酸氨基转移酶的活性，并基于脂质过氧化作用的测量，评估了除草剂对细胞膜的影响，该作用导致丙二醛的形成，同时还检测了抗氧化酶（Mn-超氧化物歧化酶[SOD]和 GSTM1）和连接蛋白的 mRNA 表达。此外，我们还评估了肝脏的组织病理学变化、SOD 和谷胱甘肽（GST）的细胞表达、热休克蛋白（HSPs）的免疫组织化学激活以及细胞凋亡的诱导。通过骨髓涂片的微核试验研究了除草剂的遗传毒性。雄性 Wistar 大鼠连续 14 天通过灌胃给予莠去津浓度为 400mg/kg/天的水溶液进行处理，同时设立了对照组。结果表明，过氧化氢酶水平升高，抗氧化酶（SOD 和 GST）的表达得以维持。此外，还观察到了脂质过氧化作用、肝组织变性、HSP90 的激活、连接蛋白 mRNA 水平升高和遗传毒性。综上所述，莠去津诱导了早期肝氧化应激，从而触发了防御机制，以维持肝脏的形态和生理学完整性。需要进一步的研究来更好地了解这种除草剂对人类健康的影响。
