关键词: Aflatoxin B1 Glial cell Molecular mechanism Neurotoxicity T-2 toxin

Mesh : Aflatoxin B1 / toxicity T-2 Toxin / toxicity Humans Animals Blood-Brain Barrier / metabolism drug effects Oxidative Stress / drug effects Mycotoxins / toxicity Reactive Oxygen Species / metabolism

来  源:   DOI:10.1016/j.envpol.2024.124359

Abstract:
Aflatoxin B1 (AFB1) and T-2 toxin are commonly found in animal feed and stored grain, posing a serious threat to human and animal health. Mycotoxins can penetrate brain tissue by compromising the blood-brain barrier, triggering oxidative stress and neuroinflammation, and leading to oxidative damage and apoptosis of brain cells. The potential neurotoxic mechanisms of AFB1 and T-2 toxin were discussed by summarizing the relevant research reports from the past ten years. AFB1 and T-2 toxin cause neuronal damage in the cerebral cortex and hippocampus, leading to synaptic transmission dysfunction, ultimately impairing the nervous system function of the body. The toxic mechanism is related to excessive reactive oxygen species (ROS), oxidative stress, mitochondrial dysfunction, apoptosis, autophagy, and an exaggerated inflammatory response. After passing through the blood-brain barrier, toxins can directly affect glial cells, alter the activation state of microglia and astrocytes, thereby promoting brain inflammation, disrupting the blood-brain barrier, and influencing the synaptic transmission process. We discussed the diverse effects of various concentrations of toxins and different modes of exposure on neurotoxicity. In addition, toxins can also cross the placental barrier, causing neurotoxic symptoms in offspring, as demonstrated in various species. Our goal is to uncover the underlying mechanisms of the neurotoxicity of AFB1 and T-2 toxin and to provide insights for future research, including investigating the impact of mycotoxins on interactions between microglia and astrocytes.
摘要:
黄曲霉毒素B1(AFB1)和T-2毒素常见于动物饲料和储存谷物中,严重威胁人类和动物的健康。霉菌毒素可以通过破坏血脑屏障穿透脑组织,引发氧化应激和神经炎症,并导致脑细胞的氧化损伤和凋亡。通过总结近十年来的相关研究报道,探讨了AFB1和T-2毒素的潜在神经毒性机制。AFB1和T-2毒素引起大脑皮层和海马神经元损伤,导致突触传递功能障碍,最终损害身体的神经系统功能。毒性机制与过量的活性氧(ROS)有关,氧化应激,线粒体功能障碍,凋亡,自噬,和夸大的炎症反应。穿过血脑屏障后,毒素可以直接影响神经胶质细胞,改变小胶质细胞和星形胶质细胞的激活状态,从而促进大脑炎症,破坏血脑屏障,影响突触传递过程。我们讨论了各种毒素浓度和不同暴露方式对神经毒性的不同影响。此外,毒素也可以穿过胎盘屏障,在后代中引起神经毒性症状,正如在各种物种中所证明的那样。我们的目标是揭示AFB1和T-2毒素的神经毒性的潜在机制,并为未来的研究提供见解。包括研究霉菌毒素对小胶质细胞和星形胶质细胞之间相互作用的影响。
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