Gautam Dinesh K, Misro M M, Chaki S P, Chandra Mahesh, Sehgal N
Department of Reproductive Biomedicine, National Institute of Health and Family Welfare, Baba Gang Nath Marg, Munirka, New Delhi, 110067, India.
Apoptosis. 2007 Jul;12(7):1173-82. doi: 10.1007/s10495-007-0060-1.
The clinical significance of exogenous hCG treatment is to stimulate steroidogenesis and spermatogenesis in the testis. However, the pathogenesis of detrimental effects on the testis arising out of chronic hCG treatment is yet to be clearly ascertained. In the present study we have shown that hCG treatment (100 IU/day) to rats for 30 days raises testicular oxidative stress leading to germ cell apoptosis and impairment of spermatogenesis. The treatment raises testicular H(2)O(2) levels along with increase in lipid peroxidation and concomitant decrease in the enzymatic antioxidant activities like superoxide dismutase, catalase and glutathione-s-transferase. The rise in the number of apoptotic germ cells was associated with up regulation of Fas protein expression and caspase-3 activity in the testis. However, serum testosterone which was elevated by 15 days of hCG treatment declined to pretreatment levels by 30 days. No significant alteration in serum gonadotropins was observed. The above findings indicate that the pathogenesis of deleterious effects following chronic hCG treatment is due to increase in testicular oxidative stress with high H(2)O(2) availability leading to apoptosis among germ cells.
外源性人绒毛膜促性腺激素（hCG）治疗的临床意义在于刺激睾丸中的类固醇生成和精子发生。然而，长期hCG治疗对睾丸产生有害影响的发病机制尚未明确。在本研究中，我们发现对大鼠进行30天的hCG治疗（100国际单位/天）会增加睾丸氧化应激，导致生殖细胞凋亡和精子发生受损。该治疗会提高睾丸中的过氧化氢（H₂O₂）水平，同时脂质过氧化增加，超氧化物歧化酶、过氧化氢酶和谷胱甘肽 - S - 转移酶等酶促抗氧化活性随之降低。凋亡生殖细胞数量的增加与睾丸中Fas蛋白表达上调和半胱天冬酶 - 3活性增加有关。然而，hCG治疗15天时升高的血清睾酮在30天时降至治疗前水平。血清促性腺激素未观察到显著变化。上述发现表明，长期hCG治疗后有害影响的发病机制是由于睾丸氧化应激增加，H₂O₂水平升高导致生殖细胞凋亡。
