Izumi Yukitoshi, O'Dell Kazuko A, Zorumski Charles F
Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, USA.
Taylor Family Institute for Innovative Psychiatric Research, Washington University School of Medicine, St. Louis, MO, USA.
Neural Regen Res. 2024 Oct 1;19(10):2212-2218. doi: 10.4103/1673-5374.391331. Epub 2023 Dec 21.
Glyphosate-based herbicides are widely used around the world, making it likely that most humans have significant exposure. Because of habitual exposure, there are concerns about toxicity including neurotoxicity that could result in neurological, psychiatric, or cognitive impairment. We recently found that a single injection of glyphosate inhibits long-term potentiation, a cellular model of learning and memory, in rat hippocampal slices dissected 1 day after injection, indicating that glyphosate-based herbicides can alter cognitive function. Glyphosate-based herbicides could adversely affect cognitive function either indirectly and/or directly. Indirectly, glyphosate could affect gut microbiota, and if dysbiosis results in endotoxemia (leaky gut), infiltrated bacterial by-products such as lipopolysaccharides could activate pro-inflammatory cascades. Glyphosate can also directly trigger pro-inflammatory cascades. Indeed, we observed that acute glyphosate exposure inhibits long-term potentiation in rat hippocampal slices. Interestingly, direct inhibition of long-term potentiation by glyphosate appears to be similar to that of lipopolysaccharides. There are several possible measures to control dysbiosis and neuroinflammation caused by glyphosate. Dietary intake of polyphenols, such as quercetin, which overcome the inhibitory effect of glyphosate on long-term potentiation, could be one effective strategy. The aim of this narrative review is to discuss possible mechanisms underlying neurotoxicity following glyphosate exposure as a means to identify potential treatments.
草甘膦基除草剂在全球广泛使用，这使得大多数人很可能都有大量接触。由于习惯性接触，人们担心其毒性，包括可能导致神经、精神或认知障碍的神经毒性。我们最近发现，单次注射草甘膦会抑制注射后1天解剖的大鼠海马切片中的长时程增强，这是一种学习和记忆的细胞模型，表明草甘膦基除草剂会改变认知功能。草甘膦基除草剂可能通过间接和/或直接方式对认知功能产生不利影响。间接而言，草甘膦可能会影响肠道微生物群，如果生态失调导致内毒素血症（肠道渗漏），诸如脂多糖等渗入的细菌副产物可能会激活促炎级联反应。草甘膦还可直接触发促炎级联反应。实际上，我们观察到急性接触草甘膦会抑制大鼠海马切片中的长时程增强。有趣的是，草甘膦对长时程增强的直接抑制作用似乎与脂多糖的作用相似。有几种可能的措施来控制由草甘膦引起的生态失调和神经炎症。饮食中摄入多酚，如槲皮素，可克服草甘膦对长时程增强的抑制作用，这可能是一种有效的策略。本叙述性综述的目的是讨论草甘膦接触后神经毒性的潜在机制，以此作为确定潜在治疗方法的一种手段。
