龙葵碱对小鼠睾丸生殖细胞线粒体损伤的研究

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目的:研究龙葵碱对小鼠睾丸的毒性作用。方法:30只雄性小鼠,体质量20~24g。随机分成5组,每组6只。采用ip龙葵碱对小鼠进行染毒,染毒剂量分别是1/8LD50(5.25mg/kg)、1/4LD50(10.5mg/kg)、1/2LD50(21mg/kg)。另设阴性对照组(生理盐水组),阳性对照组(环磷酰胺,CP,给药剂量40mg/kg),龙葵碱不同浓度组连续染毒14d。应用紫外分光光度法测定睾丸中SDH、MDA、SOD、GSH的活力。结果:龙葵碱染毒两周后,GSH的量仅1/2LD50染毒剂量组与空白组相比较呈非常显著性差异(P<0.01);随着染毒剂量的增加,MDA含量增加,1/2LD50、1/4LD50、1/8LD50染毒剂量组与空白组比较呈非常显著性差异(P<0.01);随着染毒剂量的增加SOD的活性降低明显,1/2LD50、1/4LD50染毒剂量时,SOD活性的降低与空白组比较呈非常显著性差异(P<0.01);随着染毒剂量的增加SDH的活性降低明显,1/2LD50、1/4LD50染毒剂量时,SDH活性的降低与空白组比较呈非常显著性差异(P<0.01)。结论:龙葵碱能够使SDH、MDA、SOD、GSH活力降低,从而导致自由基增多,呼吸链和氧化磷酸化脱偶联,三羧酸循环被阻断,线粒体基质渗透压升高,内膜肿胀,使线粒体的功能发生障碍,线粒体氧化损伤。 Objective: To study the toxic effects of Solanum nigrum on the testis of mice. Methods: Thirty male mice, weighing 20-24g. Randomly divided into 5 groups of 6 per group. The mice were treated with ip Solanum nigrum at a dose of 1/8 LD50 (5.25 mg/kg), 1/4 LD50 (10.5 mg/kg), and 1/2 LD50 (21 mg/kg). A negative control group (saline group), a positive control group (cyclophosphamide, CP, a dose of 40 mg/kg) were set up, and different concentrations of solanine were continuously exposed for 14 days. UV spectrophotometry was used to determine the activity of SDH, MDA, SOD, and GSH in testis. RESULTS: Two weeks after the exposure to Solanum nigrum, there was a significant difference in the amount of GSH only 1/2 LD50 between the dose group and the blank group (P<0.01). With the increase of the dose, the content of MDA increased. The 1/2 LD50, 1/4 LD50, and 1/8 LD50 exposure dose groups were significantly different from the blank group (P<0.01), and the SOD activity was significantly reduced with the increase of exposure dose, 1/2 LD50, 1/4 LD50. When the dose was increased, the activity of SOD decreased significantly compared with the blank group (P<0.01); the activity of SDH decreased significantly with the increased dose, and the SDH was 1/2LD50 and 1/4LD50. The decrease in activity was significantly different from the blank group (P<0.01). Conclusion: Solanine can reduce the activities of SDH, MDA, SOD, and GSH, leading to increased free radicals, decoupling of respiratory chain and oxidative phosphorylation, blockage of the tricarboxylic acid cycle, and increased osmotic pressure of the mitochondrial matrix. Swelling impairs mitochondrial function and oxidative damage to mitochondria.
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