Rani Nisha, Alam Mohammad Mumtaz, Parvez Suhel
Department of Toxicology, School of Chemical & Life Sciences, Jamia Hamdard, New Delhi, India.
Department of Pharmaceutical Chemistry, School of Pharmaceutical Education & Research, Jamia Hamdard, New Delhi, India.
Front Toxicol. 2025 Jul 1;7:1578230. doi: 10.3389/ftox.2025.1578230. eCollection 2025.
Pesticide-related environmental contamination poses a growing global concern, threatening human health, wildlife, and ecosystems. Glyphosate (N-phosphonomethyl-glycine, GLY), a widely used organophosphorus herbicide, has been associated with neurotoxic effects. This study investigates the potential neurodegenerative impact of glyphosate using a Caenorhabditis elegans Alzheimer's disease (AD) model.
Transgenic strain CL4176, which expresses human amyloid-beta (Aβ1-42) upon temperature induction, was exposed to various concentrations of glyphosate (12, 15, 18.5, 20, and 25 mg/L) for 24 hours. Behavioral assays (body bends, head thrashes, body length, and pharyngeal pumping), oxidative stress markers (catalase activity), and Aβ protein expression were evaluated.
Glyphosate exposure induced a concentration-dependent decline in locomotor and feeding behaviors. Catalase activity was significantly reduced, indicating elevated oxidative stress. Additionally, a marked increase in Aβ1-42 protein expression was observed in glyphosate-treated CL4176 worms.
These findings suggest that glyphosate exacerbates Aβ toxicity and induces AD-like phenotypes in the model through behavioral impairment, oxidative stress, and increased Aβ accumulation. Glyphosate's potential contribution to neurodegenerative processes warrants further investigation.
与农药相关的环境污染日益引起全球关注，威胁着人类健康、野生动物和生态系统。草甘膦（N-膦酰甲基甘氨酸，GLY）是一种广泛使用的有机磷除草剂，已被证实与神经毒性作用有关。本研究使用秀丽隐杆线虫阿尔茨海默病（AD）模型，探究草甘膦潜在的神经退行性影响。
将温度诱导时表达人淀粉样β蛋白（Aβ1-42）的转基因品系CL4176暴露于不同浓度（12、15、18.5、20和25mg/L）的草甘膦中24小时。评估行为学指标（身体弯曲、头部摆动、体长和咽部抽动）、氧化应激标志物（过氧化氢酶活性）以及Aβ蛋白表达。
草甘膦暴露导致运动和摄食行为呈浓度依赖性下降。过氧化氢酶活性显著降低，表明氧化应激增加。此外，在经草甘膦处理的CL4176线虫中观察到Aβ1-42蛋白表达显著增加。
这些发现表明，草甘膦通过行为损伤、氧化应激和Aβ积累增加，加剧了Aβ毒性，并在该模型中诱导出类似AD的表型。草甘膦对神经退行性过程的潜在影响值得进一步研究。
