Chemical agents protective against rotenone-induced neurotoxicity

被引:5
|
作者
Najafi, Nahid [1 ,2 ]
Rahbardar, Mahboobeh Ghasemzadeh [3 ]
Hosseinzadeh, Hossein [2 ,3 ]
Hayes, A. Wallace [4 ]
Karimi, Gholamreza [2 ,3 ]
机构
[1] Mashhad Univ Med Sci, Student Res Comm, Mashhad, Razavi Khorasan, Iran
[2] Mashhad Univ Med Sci, Sch Pharm, Dept Pharmacodynam & Toxicol, Mashhad, Razavi Khorasan, Iran
[3] Mashhad Univ Med Sci, Pharmaceut Res Ctr, Pharmaceut Technol Inst, Mashhad, Razavi Khorasan, Iran
[4] Univ S Florida, Coll Publ Hlth, Dept Toxicol, Tampa, FL 33620 USA
来源
TOXICOLOGICAL AND ENVIRONMENTAL CHEMISTRY | 2022年 / 104卷 / 01期
关键词
Neuroprotective; mitochondrial complex I; oxidative stress; apoptosis; autophagy; INDUCED OXIDATIVE STRESS; INDUCED TOXICITY; DOPAMINERGIC-NEURONS; PARKINSONS-DISEASE; SH-SY5Y CELLS; INDUCED DEGENERATION; AUTOPHAGIC FLUX; BRAIN-INJURY; IN-VIVO; RIFAMPICIN;
D O I
10.1080/02772248.2022.2030341
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Rotenone is a broadly used organic pesticide with neurotoxicity as a serious side effect for non-target organisms. The inhibition of mitochondrial complex I is the principal mechanism of rotenone toxicity that leads to oxidative stress, apoptosis, and decreased autophagy. Several chemical compounds have been demonstrated to exhibit antioxidant, antiapoptotic, and autophagy enhancement in both in vitro and in vivo studies. Some chemical agents can ameliorate rotenone-induced neurotoxicity through their antioxidant, anti-inflammatory, and anti-apoptotic properties. They also inhibit the accumulation of alpha-synuclein, control dopamine release, affect ion channels, and induce autophagy. Clinical trials are essential to reinforce the effectiveness of any chemical in managing patients with rotenone neurotoxicity.
引用
收藏
页码:149 / 175
页数:27
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