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Oncol Lett. 2019 Aug;18(2):1035-1042. doi: 10.3892/ol.2019.10418. Epub 2019 May 30.

Mechanism of cadmium poisoning on testicular injury in mice.

Author information

1
Department of Histology and Embryology, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
2
Laboratory of Tumor Immunology and Microenvironmental Regulation, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
3
Department of Pathology and Physiopathology, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
4
Evidence Identification Center, The Seven Star Branch in The Guilin City Public Security Bureau, Guilin, Guangxi 541004, P.R. China.

Abstract

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.

KEYWORDS:

17α-hydroxylase; androgen; endothelial nitric oxide synthase; luteinizing hormone receptor; spermatogenesis

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