Uygur Ramazan, Aktas Cevat, Caglar Veli, Uygur Emine, Erdogan Hasan, Ozen Oguz Aslan
Department of Anatomy, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey
Department of Histology and Embryology, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey.
Toxicol Ind Health. 2016 May;32(5):848-59. doi: 10.1177/0748233713512891. Epub 2013 Dec 6.
This study aimed to investigate the protective effects of melatonin against arsenic-induced apoptosis and oxidative stress in rat testes. A total of 27 male rats were divided into 3 groups: control (saline: 5 ml kg(-1) day(-1), intragastrically), arsenic (sodium arsenite (NaAsO2): 5 mg kg(-1) day(-1), intragastrically), and arsenic + melatonin (sodium arsenite (NaAsO2): 5 mg kg(-1) day(-1), intragastrically and melatonin: 25 mg kg(-1) day(-1), intraperitoneally) group. At the end of 30 days, the rats were killed under anesthesia. Histopathological examination showed that testicular injury mediated by arsenic was ameliorated by the administration of melatonin. The number of apoptotic germ cell was increased, and the number of proliferating cell nuclear antigen (PCNA)-positive germ cell was decreased in testis after arsenic administration. Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and there was a rise in the expression of PCNA in testis of arsenic + melatonin group. The decreased superoxide dismutase, catalase, and glutathione peroxidase activities as well as increased malondialdehyde levels in testis due to arsenic administration were also counteracted by melatonin. These data suggested that melatonin has beneficial effects against arsenic-induced testicular damage by decreasing morphological damage, germ cell apoptosis, lipid peroxidation, and oxidative stress. Our results suggest that melatonin plays a protective role against arsenic-induced testicular apoptosis and oxidative stress.
本研究旨在探讨褪黑素对砷诱导的大鼠睾丸细胞凋亡和氧化应激的保护作用。将27只雄性大鼠分为3组:对照组(生理盐水:5 ml·kg⁻¹·d⁻¹,灌胃)、砷组(亚砷酸钠(NaAsO₂):5 mg·kg⁻¹·d⁻¹,灌胃)和砷+褪黑素组(亚砷酸钠(NaAsO₂):5 mg·kg⁻¹·d⁻¹,灌胃;褪黑素:25 mg·kg⁻¹·d⁻¹,腹腔注射)。30天结束时,将大鼠麻醉处死。组织病理学检查显示,褪黑素给药可改善砷介导的睾丸损伤。砷给药后,睾丸中凋亡生殖细胞数量增加,增殖细胞核抗原(PCNA)阳性生殖细胞数量减少。我们的数据表明,末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记活性显著降低,而砷+褪黑素组睾丸中PCNA的表达有所升高。褪黑素还抵消了砷给药导致的睾丸中超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶活性降低以及丙二醛水平升高的现象。这些数据表明,褪黑素通过减少形态学损伤、生殖细胞凋亡、脂质过氧化和氧化应激,对砷诱导的睾丸损伤具有有益作用。我们的结果表明,褪黑素对砷诱导的睾丸细胞凋亡和氧化应激具有保护作用。