有证据表明，巯基基团修饰和活性氧参与了硫化氢诱导的大鼠小脑粒体通透性转换孔的开放。
Evidence that thiol group modification and reactive oxygen species are involved in hydrogen sulfide-induced mitochondrial permeability transition pore opening in rat cerebellum.
机构信息
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600-Attached, CEP 90035-003 Porto Alegre, RS, Brazil.
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Universidade Federal do Rio Grande do Sul, Ramiro Barcelos Street, 2600-Attached, CEP 90035-003 Porto Alegre, RS, Brazil; Departamento de Ciências Biológicas, Universidade Regional Integrada do Alto Uruguai e das Missões, Sete de Setembro Avenue, 1621, CEP 99709-910 Erechim, RS, Brazil.
出版信息
Mitochondrion. 2019 Jul;47:141-150. doi: 10.1016/j.mito.2018.11.001. Epub 2018 Nov 3.
We report here the effects of hydrogen sulfide (sulfide), that accumulates in ETHE1 deficiency, in rat cerebellum. Sulfide impaired electron transfer and oxidative phosphorylation. Sulfide also induced mitochondrial swelling, and decreased ΔΨm and calcium retention capacity in cerebellum mitochondria, which were prevented by cyclosporine A (CsA) plus ADP, and ruthenium red, suggesting mitochondrial permeability transition (mPT) induction. Melatonin (MEL) and N-ethylmaleimide also prevented sulfide-induced alterations. Prevention of sulfide-induced decrease of ΔΨm and viability by CsA and MEL was further verified in cerebellum neurons. The data suggest that sulfide induces mPT pore opening via thiol modification and ROS generation.
我们在此报告在 ETHE1 缺乏时积累的硫化氢（硫化物）对大鼠小脑的影响。硫化物损害电子传递和氧化磷酸化。硫化物还诱导线粒体肿胀，并降低小脑线粒体的ΔΨm 和钙保留能力，这可被环孢菌素 A（CsA）加 ADP 和钌红所预防，提示诱导了线粒体通透性转换（mPT）。褪黑素（MEL）和 N-乙基马来酰亚胺也可预防硫化物诱导的改变。CsA 和 MEL 进一步证实了预防硫化物诱导的小脑神经元ΔΨm 和活力降低。这些数据表明，硫化物通过巯基修饰和 ROS 生成诱导 mPT 孔的打开。
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