Effects of acetaldehyde and L-carnitine on morphology and enzyme activity of myocardial mitochondria in rats
Effects of acetaldehyde and L-carnitine on morphology and enzyme activity of myocardial mitochondria in rats
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DOI：
10.1007/s11033-014-3686-4
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发表时间：
2014-09
影响因子：
2.8
通讯作者：
Yuanzhe Jin;Guo-feng Wang;Qi Wang;Xue-ying Zhang;Bin Yan;Wei-Na Hu
中科院分区：
文献类型：
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作者：
Yuanzhe Jin;Guo-feng Wang;Qi Wang;Xue-ying Zhang;Bin Yan;Wei-Na Hu
本研究旨在观察乙醛(AA)和L肉碱(LC)对大鼠心肌线粒体形态和酶活性的影响。将65只Wistar大鼠随机分为4组：对照组(n=20)、AA低剂量组(n=15)、AA高剂量组(n=15)和AA+生理盐水组(n=15)。不同剂量(110 mg/kg和220 mg/kg)AA每日1次腹腔注射，连续4周。给药4周后，用透射电子显微镜观察大鼠心肌线粒体的形态。检测血清琥珀酸脱氢酶(SDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)和心肌肌钙蛋白I(CTnI)水平以评价线粒体酶活性。光镜下可见对照组大鼠心肌细胞构筑正常。低剂量和高剂量AA组的线粒体数密度和数目均低于对照组。给药后，AA+Lc组大鼠的线粒体数密度和数目明显增加。透射电子显微镜显示，低剂量和高剂量AA均可剂量依赖性地引起大鼠心肌线粒体损伤，如线粒体肿胀、线粒体脊和膜破坏、线粒体缺乏症等。AA+LC组给药后线粒体损伤程度明显减轻。结果表明，AA+LLC组和对照组的血清SDH和SOD水平也高于AA低剂量组和高剂量组，而AA+LLC组和对照组的MDA水平低于低剂量组和高剂量AA组。AA低剂量组、高剂量AA组和AA+LLC组的血清cTnI水平均高于对照组。而血清cTnI水平在AA低剂量组、高剂量AA组和AA+LC组之间无显著差异。提示AA可导致大鼠心肌线粒体损伤和酶活性的诱导，而LC可减轻AA引起的大鼠心肌线粒体损伤。
This study aimed to investigate the effects of acetaldehyde (AA) and L-carnitine (LC) on morphology and enzyme activity of myocardial mitochondria in rats. Sixty-five Wistar rats were randomly divided into 4 groups: the control group (n= 20), the AA low-dose group (n= 15), the AA high-dose group (n= 15) and the AA + LC group (n= 15). Different doses (110 mg/kg and 220 mg/kg) AA was injected intraperitoneally once a day for 4 weeks. After 4 weeks administration, transmission electron microscope (TEM) observation of morphology of rat myocardial mitochondria was performed. Serum levels of succinate dehydrogenase (SDH), superoxide dismutase (SOD), malondialdehyde (MDA) and cardiac troponin I (cTnI) were detected to evaluate mitochondrial enzymes activities. Light micrograph of rat myocardiocytes in the control group showing normal architecture of myocytes. The numerical density and number of mitochondria in both low-dose and high-dose AA groups were lower than that of the control group. After administration of LC, the rats in the AA + LC group showed an obvious increase in the numerical density and number of mitochondria. TEM showed that both low-dose and high-dose AA could induce myocardial mitochondrial damage in rats in a dose-dependent manner, such as mitochondrial swelling, disruptions of crest and membrane, mitochondrial deficiency. The degree of mitochondrial damage of the AA + LC group was significantly decreased after administration of LC. Our results showed that serum levels of SDH and SOD in the AA + LC and control groups were also higher than those of the low-dose and high-dose AA groups; while the MDA level in the AA + LC and control groups were lower than that of the low-dose and high-dose AA groups. The low-dose AA, high-dose AA and AA + LC groups exhibited a higher level of serum cTnI than that of the control group. However, there was no significant difference in serum cTnI level among the low-dose AA, high-dose AA and AA + LC groups. Our findings indicate that AA may lead to myocardial mitochondrial damage and the induction of enzyme activity in rats, while administration of LC could alleviate AA-related damage of rat myocardial mitochondria.