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Neurotoxic mechanisms of glyphosate exposure

神经毒性 海马体 胶质纤维酸性蛋白 星形胶质细胞 大脑皮层 化学 海马结构 谷氨酸受体 皮质(解剖学) 药理学 内分泌学 内科学 生物化学 心理学 生物 医学 毒性 神经科学 中枢神经系统 免疫组织化学 受体
作者
Christian Limberger,Ana Cristina Roginski,Alexandre Umpierrez Amaral,Gianina Teribele Venturin,Moaçir Wajner,Jaderson Costa DaCosta,Eduardo R. Zimmer,Diogo O. Souza,Débora Guerini de Souza
出处
期刊:Alzheimers & Dementia [Wiley]
卷期号:18 (S3) 被引量:1
标识
DOI:10.1002/alz.068335
摘要

Abstract Background Human exposure to pesticides is increasing, especially glyphosate‐based herbicides (GBH). Thus, it is of great interest to characterize whether glyphosate (Gly) exerts neurotoxic effects. Besides Gly, GBH formulations contain adjuvants, mainly POEA, a surfactant. We hypothesize adjuvants may enhance glyphosate neurotoxicity. Therefore, we aimed at investigating the neurotoxic properties of Gly and its adjuvants. Method Gly, POEA, Gly+POEA, and GBH were orally administered into male Wistar rats (90‐day‐old, n = 30) for 28 days (5 mg/kg/day). Controls received vehicle. Then, we assessed the working memory via Y‐maze test, glial fibrillary acidic protein (GFAP), inducible nitric oxide synthase (iNOS), and glutamate transporter 1 (GLT‐1) immunocontent in cortex and hippocampus via Western blot, mitochondrial respiration via high‐resolution respirometry in cortex and brain metabolism via FDG‐PET (pons as reference region). Result GFAP and iNOS in the cortex were higher in Gly (p= 0.0053 and p=0.0012, respectively) compared to GBH (Figures A, B), whereas GLT‐1 was higher in the GBH (p=0.0004), compared to Gly (Figure C). Hippocampus showed no changes in GFAP, iNOS, and GLT‐1 expression in any group. The POEA group showed impaired working memory in the Y‐maze test (p=0.005) (Figure D). The respiratory control ratio was affected in the cortices of POEA (p=0.0212) and Gly+POEA (p=0.0281) groups (Figure E). Brain metabolism was not altered in cortical and hippocampal regions. However, the striatum presented hypermetabolism in POEA (p=0.0492) group (Figure F). Conclusion Environmental factors may contribute to the onset of neurodegenerative diseases in later life, including AD. Our preliminary results reveal individual toxic effects of Gly, POEA, and GBH, highlighting the overlooked role that adjuvants may have in herbicides toxicity. It seems that different subsets of reactive astrocytes result from each treatment. Mitochondrial uncoupling and striatum hypermetabolism may underlie working memory deficits. The study of potential pathways of neurotoxicity is fundamental for translational findings since the general population is chronically exposed to low doses of complex glyphosate formulations.

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