School of Medicine, Biomedical Research Institute, University of Antioquia, Medellin, Colombia.
Neurochem Res. 2010 Sep;35(9):1323-32. doi: 10.1007/s11064-010-0188-1. Epub 2010 Jun 1.
The effects of cannabinoids in mitochondria after acute oxidative stress insult are not fully established. We investigated the ability of CP55,940 and JWH-015 to scavenge reactive oxygen species and their effect on mitochondria permeability transition (MPT) in either a mitochondria-free superoxide anion generation system, intact rat brain mitochondria or in sub-mitochondrial particles (SMP) treated with paraquat (PQ). Oxygen consumption, mitochondrial membrane potential (Deltapsi(m)) and MPT were determined as parameters of mitochondrial function. It is found that both cannabinoids effectively attenuate mitochondrial damage against PQ-induced oxidative stress by scavenging anion superoxide radical (O(2)(*-)) and hydrogen peroxide (H(2)O(2)), maintaining Deltapsi(m) and by avoiding Ca(2+)-induced mitochondrial swelling. Understanding the mechanistic action of cannabinoids on mitochondria might provide new insights into more effective therapeutic approaches for oxidative stress related disorders.
大麻素在急性氧化应激损伤后对线粒体的影响尚未完全确定。我们研究了 CP55,940 和 JWH-015 清除活性氧的能力及其对超氧阴离子生成系统无线粒体、完整大鼠脑线粒体或百草枯（PQ）处理的亚线粒体颗粒（SMP）中线粒体通透性转换（MPT）的影响。氧消耗、线粒体膜电位（Deltapsi(m)）和 MPT 被确定为线粒体功能的参数。结果发现，这两种大麻素都能通过清除阴离子超氧自由基（O(2)(*-)）和过氧化氢（H(2)O(2)）、维持 Deltapsi(m)和避免 Ca(2+)诱导的线粒体肿胀，有效地减轻 PQ 诱导的氧化应激对线粒体的损伤。了解大麻素对线粒体的作用机制可能为与氧化应激相关的疾病提供更有效的治疗方法。
