Mechanism of cadmium poisoning on testicular injury in mice

• Published in: Oncology letters Vol. 18; no. 2; pp. 1035 - 1042
• Main Authors: Ren, Yaping, Shao, Wenhua, Zuo, Lijun, Zhao, Wei, Qin, Haizhang, Hua, Yingjie, Lu, Dejie, Mi, Chao, Zeng, Sien, Zu, Liao
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.08.2019; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Androgens; Apoptosis; Blood pressure; Cadmium; Endothelium; Enzyme-linked immunosorbent assay; Enzymes; Gene expression; Glycoproteins; Gonadotropins; Hormones; House mouse; Infertility; Laboratory animals; Luteinizing hormone; Nitric oxide; Nitrogen oxides; Oncology; Pituitary hormones; Poisoning; Proteins; Sperm; Spermatogenesis; Studies; Testosterone; Toxicity; United States; spermatogenesis; endothelial nitric oxide synthase; luteinizing hormone receptor; androgen; 17α-hydroxylase
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2019.10418

Cadmium is a heavy metal that is toxic to humans and the reproductive system. The present study aimed to investigate the mechanisms of cadmium-induced reproductive toxicity in a male Institute of Cancer Research mouse model of cadmium poisoning. Changes in luteinizing hormone receptor (LHR), 17α-hydroxylase and endothelial nitric oxide (NO) synthase (eNOS) expression levels were examined. A total of 24 male mice (4-week-old) were randomly divided into four groups (normal control group and low, medium and high cadmium groups) and subjected to gavage treatment with normal saline or cadmium-containing saline solutions for 8 weeks prior to sacrifice. To assess testicular injury, serum androgen levels were determined by ELISA, testicular tissue pathological changes were evaluated using hematoxylin and eosin staining. In addition, LHR, 17α-hydroxylase and eNOS expressions levels were examined by western blotting, and apoptosis was examined with a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The results demonstrated that the severity of testes injury increased with cadmium concentration. In addition, LHR, 17α-hydroxylase and eNOS expression levels increased with low and medium concentrations of cadmium; however, they were decreased following treatment with high concentrations of cadmium. The results from the present study demonstrated that cadmium altered LHR, 17α-hydroxylase and eNOS expression levels in testicular stromal cells, which may impact testosterone synthesis. Furthermore, NO was suggested to be involved in cadmium-induced testicular injury by measurements of eNOS expression in testicular stromal cells.