4.7 Article

Cyanidin-3-O-glucoside protects against cadmium-induced dysfunction of sex hormone secretion via the regulation of hypothalamus-pituitary-gonadal axis in male pubertal mice

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 129, Issue -, Pages 13-21

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2019.04.033

Keywords

Cyanidin-3-O-Glucoside; Cadmium; Sex hormone; Hypothalamus-pituitary- gonadal axis; Puberty

Funding

  1. Guangdong Key Area Research and Development Program [2019B020210003]
  2. National Natural Science Foundation of China (NSFC) [31871816, 81703211]
  3. Science and Technology Program of Guangzhou [201704020050]
  4. Key Laboratory of Male Reproductive and Genetics, National Health and Family Planning Commission [KF201805]

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Cadmium (Cd) has been generally recognized as an endocrine-disrupting chemical for its toxic effects on the hypothalamus pituitary gonadal (HPG) axis accompanied by dysfunction in sex hormone secretion. Particularly, exposure to Cd during puberty versus post puberty exhibits differing age-dependent effects that require further examination. This study sought to determine if cyanidin-3-O-glucoside (C3G), a typical anthocyanin with neuroprotective bioactivity, could protect against Cd-induced sex hormone-disorder in Pubertal male mice. C3G treatment reversed the disruption of hormone levels and increased Gnrhl gene expression in the hypothalamus. In addition, the levels of gonadotropins, including luteinizing hormone (LH) and follicle stimulating hormone (FSH), were reversed by C3G. Interestingly, C3G improved the expression of LH and FSH receptor in the testis in mice exposed to Cd. Furthermore, C3G activated the signaling pathway related to the synthesis of testosterone processing. In conclusion, C3G protected against Cd-induced dysfunction of sex hormone secretion through the regulation of the HPG axis in male mice during puberty. The results of this study suggest that consumption of anthocyanins can be protective against metal-induced male reproductive dysfunction.

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