1 Department of Biological Sciences, Covenant University, Sango Ota-Idiroko Road, Ogun State, Nigeria.
2 Department of Pure and Applied Zoology, College of Bioscience, Federal University of Agriculture, Abeokuta, Nigeria.
Int J Toxicol. 2018 Jul/Aug;37(4):285-295. doi: 10.1177/1091581818779553. Epub 2018 Jun 11.
There have been major concerns that the nephrotoxicity of commercial formulations of Roundup herbicide is due to the active ingredient glyphosate. We therefore investigated and compared the mechanisms underlining the nephrotoxicity of Roundup herbicide and glyphosate alone in rat. Fifty-six adult male rats randomized into 7 groups of 8 rats per group were exposed to Roundup formulation and glyphosate alone daily by gavage at 3.6, 50.4, and 248.4 mg/kg body weight (bw) of glyphosate concentrations for 12 weeks with distilled water administered to the control group. Kidney biomarker (serum urea and creatinine, plasma cystatin-C, and neutrophil gelatinase-associated lipocalin), oxidative stress indices in the kidney tissue, activities of kidney membrane-bound enzymes (Mg-adenosine triphosphatase [ATPase], Ca-ATPase, Na/K-ATPase, and total ATPase), and histopathological changes in the kidney were monitored. Glyphosate concentration in the kidney was quantified by high-performance liquid chromatography with ultraviolet detection. Significant ( P < 0.05) alterations in the levels of the kidney biomarker, oxidative stress markers, and membrane-bound enzymes were observed in the rats exposed to Roundup compared to the rats exposed to glyphosate alone. Rats exposed to Roundup accumulated more glyphosate residue in their kidney tissue. Severe histopathological lesions were only seen in the kidneys of rats exposed to Roundup. The nephrotoxicity observed cannot be due to the active ingredient in the Roundup formulation, as glyphosate alone has virtually no effect on the renal function of the exposed animals. Therefore, the general claim attributing nephrotoxicity of a glyphosate-based herbicide to its active ingredient should be discouraged.
人们一直高度关注商业配方的农达除草剂的肾毒性是由于其有效成分草甘膦。因此，我们研究并比较了农达除草剂和草甘膦单独对大鼠的肾毒性机制。56 只成年雄性大鼠随机分为 7 组，每组 8 只大鼠，通过灌胃暴露于农达配方和草甘膦中，草甘膦浓度分别为 3.6、50.4 和 248.4mg/kg 体重，对照组给予蒸馏水。监测肾脏生物标志物（血清尿素和肌酐、血浆胱抑素-C 和中性粒细胞明胶酶相关脂质运载蛋白）、肾脏组织中的氧化应激指标、肾脏膜结合酶（Mg-三磷酸腺苷酶[ATPase]、Ca-ATPase、Na/K-ATPase 和总 ATPase）的活性以及肾脏的组织病理学变化。采用高效液相色谱法结合紫外检测定量测定肾脏中的草甘膦浓度。与单独暴露于草甘膦的大鼠相比，暴露于农达的大鼠的肾脏生物标志物、氧化应激标志物和膜结合酶的水平发生了显著（P<0.05）的改变。暴露于农达的大鼠在其肾脏组织中积累了更多的草甘膦残留。只有暴露于农达的大鼠的肾脏出现严重的组织病理学损伤。观察到的肾毒性不能归因于农达配方中的有效成分，因为草甘膦单独对暴露动物的肾功能几乎没有影响。因此，不应鼓励将基于草甘膦的除草剂的肾毒性归因于其有效成分的普遍说法。
