Department of Clinical Pharmacology, School of Pharmacy, China Medical University, Shenyang, Liaoning 110122, China.
Department of Drug Control, Criminal Investigation Police University of China, Shenyang, Liaoning 110854, China.
Oxid Med Cell Longev. 2020 Nov 27;2020:8874304. doi: 10.1155/2020/8874304. eCollection 2020.
Methamphetamine is a derivative of amphetamines, a highly addictive central stimulant with multiple systemic toxicity including the brain, heart, liver, lung, and spleen. It has adverse effects such as apoptosis and breakdown of the blood-brain barrier. Methamphetamine is a fatal and toxic chemical substance, and its lethal mechanism has been widely studied in recent years. The possible mechanism is that methamphetamine can cause cardiotoxicity and neurotoxicity mainly by inducing oxidative stress so as to generate heat, eliminate people's hunger and thirst, and maintain a state of excitement so that people can continue to exercise. According to many research, there is no doubt that methamphetamine triggers neurotoxicity by inducing reactive oxygen species (ROS) production and redox imbalance. This review summarized the mechanisms of methamphetamine-induced neurotoxicity including apoptosis and blood-brain barrier breakdown through oxidative stress and analyzed several possible antioxidative mechanisms of tert-butylhydroquinone (TBHQ) which is a kind of food additive with antioxidative effects. As a nuclear factor E2-related factor 2 (Nrf2) agonist, TBHQ may inhibit neurotoxicity caused by oxidative stress through the following three mechanisms: the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system, the astrocytes activation, and the glutathione pathway. The mechanism about methamphetamine's toxic effects and its antioxidative therapeutic drugs would become a research hotspot in this field and has very important research significance.
甲基苯丙胺是苯丙胺的衍生物,是一种高度成瘾的中枢兴奋剂,具有多种全身毒性,包括大脑、心脏、肝脏、肺和脾脏。它会引起细胞凋亡和血脑屏障破裂等不良反应。甲基苯丙胺是一种致命和有毒的化学物质,近年来其致死机制已得到广泛研究。其可能的机制是,甲基苯丙胺主要通过诱导氧化应激引起心脏毒性和神经毒性,从而产生热量,消除人的饥饿感和口渴感,并保持兴奋状态,使人能够继续运动。根据许多研究,毫无疑问,甲基苯丙胺通过诱导活性氧(ROS)的产生和氧化还原失衡引发神经毒性。本综述通过氧化应激总结了甲基苯丙胺诱导的神经毒性(包括细胞凋亡和血脑屏障破裂)的机制,并分析了一种具有抗氧化作用的食品添加剂叔丁基对苯二酚(TBHQ)的几种可能的抗氧化机制。作为核因子 E2 相关因子 2(Nrf2)激动剂,TBHQ 可能通过以下三种机制抑制氧化应激引起的神经毒性:烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶系统、星形胶质细胞激活和谷胱甘肽途径。甲基苯丙胺的毒性作用及其抗氧化治疗药物的机制将成为该领域的研究热点,具有非常重要的研究意义。