Earlier, we have shown the occurrence of oxidative impairments and their progression in the testis of diabetic adult rats. This study investigated the vulnerability of immature testis to oxidative stress and mitochondrial dysfunctions in a prepubertal (PP) diabetic rat model. PP male rats (4/6-week-old) rendered diabetic by an acute dose of streptozotocin were monitored for induction of oxidative stress in testis cytosol/mitochondria. Diabetic rats of both age groups showed severe hyperglycemia, testicular atrophy and marked oxidative damage as evidenced by enhanced generation of reactive oxygen species, hydroperoxide and malondialdehyde levels (4 week > 6 week). Mitochondrial dysfunctions manifested as reduction in the activities of aldehyde dehydrogenase, tricarboxylic acid cycle enzymes, enhanced activities of oxidative phosphorylation enzymes, perturbations in calcium homeostasis and membrane potential. These evidences suggest that an immature testis is vulnerable to oxidative stress under diabetes, which may play a significant role in the development of testicular degeneration, leading to impaired fertility in adulthood.

中文翻译：

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青春期前糖尿病大鼠睾丸中氧化应激和线粒体功能障碍的证据。

之前，我们已经显示了糖尿病成年大鼠睾丸中氧化损伤的发生及其进展。这项研究调查了青春期前（PP）糖尿病大鼠模型中睾丸对氧化应激和线粒体功能障碍的脆弱性。监测通过急性剂量的链脲佐菌素致糖尿病的PP雄性大鼠（4/6周龄）在睾丸细胞质/线粒体中氧化应激的诱导。两个年龄段的糖尿病大鼠均表现出严重的高血糖症，睾丸萎缩和明显的氧化损伤，其表现为活性氧，氢过氧化物和丙二醛水平的产生增加（4周> 6周）。线粒体功能障碍表现为醛脱氢酶，三羧酸循环酶，增强了氧化磷酸化酶的活性，钙稳态的扰动和膜电位。这些证据表明，未成熟的睾丸在糖尿病下易受氧化应激的影响，这可能在睾丸变性的发展中起重要作用，导致成年后生育能力受损。