Selenium ameliorates oxidized phospholipid-mediated testicular dysfunction and epididymal sperm abnormalities following Bisphenol A exposure in adult Wistar rats

IF 3.3 4区医学 Q2 REPRODUCTIVE BIOLOGY

Reproductive toxicology Pub Date : 2024-11-15 DOI:10.1016/j.reprotox.2024.108751

Meenu Maniradhan , Narmadhaa Sivagurunathan , Ajay Krishnan Unnikrishnan , Vigil S. Anbiah , Latchoumycandane Calivarathan

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Abstract

Bisphenol A (BPA) is an endocrine-disrupting compound extensively utilized in the production of polycarbonate polymers and epoxy resins that, upon exposure, pose a significant threat to male reproductive health because of its estrogenic properties. Accumulating evidence suggests that BPA exposure disrupts the normal process of spermatogenesis, alters testicular morphology and function, and interferes with testicular steroidogenesis and hormonal signaling. However, the precise mechanism by which BPA affects testicular function remains unclear. In this study, we explored the mechanism underlying BPA-induced testicular abnormalities and evaluated the protective effects of Selenium (Se). Thirty-two adult male albino Wistar rats were divided into four groups, and BPA was administered at 50 mg/kg body weight, with or without Se supplementation, for 30 days. Se supplementation (2.5 mg/kg body weight) was initiated 1 week before BPA administration. BPA administration resulted in alterations in testicular architecture, characterized by basement membrane disintegration in the seminiferous tubules, reduced spermatogenic cell counts, and increased interstitial tubule noncellular space. Furthermore, BPA exposure increased the levels of oxidized phospholipids, lipid peroxides, and hydroxyl radicals and decreased the activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase. In addition, BPA significantly reduced the activities of 3β- and 17β-hydroxysteroid dehydrogenases, interfering with testicular steroidogenesis. In rats, coadministration of Se and BPA reduced the levels of oxidized phospholipids and increased the activities of antioxidant enzymes, leading to improved testicular function and epididymal sperm parameters, suggesting that Se plays a critical role in alleviating endocrine disruptor-induced testicular dysfunctions in rats.

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硒能改善成年 Wistar 大鼠接触双酚 A 后氧化磷脂介导的睾丸功能障碍和附睾精子异常。

双酚 A（BPA）是一种干扰内分泌的化合物，广泛用于生产聚碳酸酯聚合物和环氧树脂。越来越多的证据表明，接触双酚 A 会破坏精子生成的正常过程，改变睾丸的形态和功能，干扰睾丸的类固醇生成和激素信号转导。然而，双酚 A 影响睾丸功能的确切机制仍不清楚。在这项研究中，我们探讨了双酚 A 诱导睾丸异常的机制，并评估了硒（Se）的保护作用。研究人员将 32 只成年雄性白化 Wistar 大鼠分为四组，按每公斤体重 50 毫克的剂量给它们注射双酚 A，并在注射或不注射 Se 的情况下持续 30 天。在服用双酚 A 前一周开始补充 Se（2.5 毫克/千克体重）。服用双酚 A 会导致睾丸结构改变，表现为曲细精管基底膜崩解、生精细胞数量减少以及间质小管非细胞间隙增加。此外，暴露于双酚 A 会增加氧化磷脂、脂质过氧化物和羟基自由基的水平，降低超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶等抗氧化酶的活性。此外，双酚 A 会明显降低 3β- 和 17β- 羟基类固醇脱氢酶的活性，从而干扰睾丸类固醇的生成。在大鼠体内，联合给药 Se 和双酚 A 可降低氧化磷脂的水平，提高抗氧化酶的活性，从而改善睾丸功能和附睾精子参数，这表明 Se 在缓解内分泌干扰物引起的大鼠睾丸功能障碍方面发挥着关键作用。

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来源期刊

Reproductive toxicology 生物-毒理学

CiteScore

6.50

自引率

3.00%

发文量

131

审稿时长

45 days

期刊介绍： Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine. All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.