Department of Pharmacology, Shenyang Pharmaceutical University, No. 103 Wenhua Road, Shenhe District, Shenyang, Liaoning 110016, China.
Department of Nutrition and Food Hygiene, Liaoning Center for Disease Prevention and Control, Shenyang, Liaoning 110001, China.
Oxid Med Cell Longev. 2018 May 17;2018:1861984. doi: 10.1155/2018/1861984. eCollection 2018.
This study evaluated the effects of di-(2-ethylhexyl) phthalate (DEHP) and obesity on male reproductive organ function in male mice and the potential mechanism of male secondary hypogonadism (SH) in such mice.
140 mice were assigned to six groups for 12 weeks: normal, DEHP, DIO, DIO + DEHP low, DIO + DEHP middle, and DIO + DEHP high. The effects of DEHP and obesity upon the reproductive organs were determined by measuring sperm count and motility, relative testis and epididymis weight, hormone level, and pathological changes. Oxidative stress was evaluated by determining malondialdehyde, T-AOC, SOD, GSH, HO, CAT, and GSH-PX in testicular tissues. Nrf2 and Keap1 protein were measured by Western blotting.
DEHP and obesity reduced sperm count and motility, relative testis and epididymis weight, and testosterone level but increased the levels of MDA, HO, leptin, and estradiol. Pathological injury was observed in the testicular Leydig cells. Moreover, the activity of CAT, SOD, and GSH-Px enzymes was inhibited. Nrf2 protein expression was reduced but that of Keap1 was increased.
DEHP and obesity jointly caused damage to male productive function. Oxidative stress in testicular tissue, and a high level of leptin, may provide some evidence to clarify the mechanisms of male SH with DEHP and obesity.
本研究旨在评估邻苯二甲酸二（2-乙基己基）酯（DEHP）和肥胖对雄性小鼠生殖器官功能的影响，以及这种肥胖雄性小鼠发生男性继发性性腺功能减退症（SH）的潜在机制。
将 140 只小鼠分为 6 组，每组 21 只，共 12 周：正常组、DEHP 组、DIO 组、DIO+DEHP 低剂量组、DIO+DEHP 中剂量组和 DIO+DEHP 高剂量组。通过检测精子计数和活力、相对睾丸和附睾重量、激素水平以及组织病理学变化来确定 DEHP 和肥胖对生殖器官的影响。通过测定睾丸组织中的丙二醛（MDA）、总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、谷胱甘肽（GSH）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和活性氧（HO）来评估氧化应激。采用 Western blot 法测定 Nrf2 和 Keap1 蛋白。
DEHP 和肥胖降低了精子计数和活力、相对睾丸和附睾重量以及睾酮水平，但增加了 MDA、HO、瘦素和雌二醇的水平。睾丸间质 Leydig 细胞发生病理损伤。此外，CAT、SOD 和 GSH-Px 酶的活性受到抑制。Nrf2 蛋白表达减少，但 Keap1 蛋白表达增加。
DEHP 和肥胖共同导致雄性生殖功能受损。睾丸组织中的氧化应激以及瘦素水平升高，可能为阐明 DEHP 和肥胖导致男性 SH 的机制提供一些依据。
