香烟水溶性提取物对大鼠心肌线粒体的毒性

观察香烟水溶性提取物(CSE)和尼古丁对大鼠心肌线粒体的损伤作用.大鼠心肌线粒体分别与CSE或尼古丁于37℃温孵60min,结果表明,CSE明显降低线粒体细胞色素C氧化酶(COX)活性,呈剂量依赖性.但是ATPase活性不受影响.在线粒体呼吸活性受到抑制的同时,过氧化指标无明显变化.CSE对6.5mmol/L钙离子引起的线粒体肿胀反应具有抑制作用,但可加剧250mmol/L钙离子诱导的线粒体肿胀反应.维生素C对CSE造成的线粒体损伤无保护作用.未见尼古丁对体外大鼠心肌线粒体有毒性.CSE对心肌线粒体的损伤可能是由于它对呼吸酶活性的直接抑制作用而与氧自由基机制无关.尼古丁可能不是CSE损伤大鼠心肌线粒体的毒性成分.

Toxicity of cigarette smoke extract on heart mitochondria

The injury action of cigarette smoke extract (CSE) and nicotine on rat heart mitochondria was observed. Rat heart mitochondria were incubated with CSE or nicotine respectively. CSE lowered markedly the mitochondrial cytochrome C oxidase (COX) activity in a dose-dependent manner. But the ATPase activity was unaffected. There was no obvious change of peroxidation index during the inhibition of mitochondrial respiratory activity. CSE inhibited swelling of mitochondria induced by 6.5mmol/L Ca2+ but the swelling induced by 250mmol/L Ca2+ was getting worse. Vitamin C could not protect mitochondria from CSE-induced injury. Nicotine showed no toxicity on rat heart mitochondria in vitro. The injury of CSE on heart mitochondria might be due to its direct inhibition on respiratory enzyme activity, but not related with oxygen free radicals mechanism. Nicotine might not be the toxic component of CSE to injure the rat heart mitochondria.