Cyanidin-3-O-glucoside ameliorates cadmium induced uterine epithelium proliferation in mice

• Published in: Journal of hazardous materials 2022-03, Vol.425, p.127571-127571, Article 127571
• Main Authors: Yang, Dacheng, Ran, Yanhong, Li, Xusheng, Jiang, Xinwei, Chen, Jiali, Sun, Jianxia, Tian, Lingmin, Teerds, Katia, Bai, Weibin
• Format: Article
• Language: English
• Subjects: Animals; Anthocyanin; Anthocyanins; Cadmium; Cadmium - toxicity; Cell Proliferation; Cyanidin-3-O-glucoside; Epithelium; Female; Female infertility; Glucosides; Mice; Uterus; Uterus hypertrophy
• ISSN: 0304-3894; 1873-3336
• DOI: 10.1016/j.jhazmat.2021.127571

Cadmium (Cd) is an environmental pollutant and endocrine disrupter, abundantly present in water, food, and soil. Accumulation of Cd in the body can negatively affect female reproduction; especially the uterus is exceptionally sensitive to the toxic actions of Cd. The anthocyanin cyanidin-3-O-glucoside (C3G) is a naturally occurring phenolic compound in fruits and plants that can antagonize the toxic effects of Cd. This capacity makes C3G a possible candidate to prevent Cd-induced female infertility. The present study aimed to investigate: 1) whether C3G intake could prevent Cd-induced female reproductive toxicity, and 2) the underlying mechanisms responsible for this protective effect. The results of our study indicated that Cd exposure did not affect ovarian function, but induced hypertrophy of the uterine endometrium. Oral intake of C3G markedly reduced the effects of Cd exposure on the thickness of the uterine epithelium cells. Transcriptomic analysis of the endometrium revealed that C3G intake had anti-estrogenic effects, attenuating Cd-induced endometrial epithelial cell proliferation by inhibiting estrogen-responsive genes, enhancing epithelial progesterone receptor expression, and regulating Klf4 expression. The current findings implicate that C3G has the potential to be used as a dietary supplement based on its capacity to intervene in Cd-induced female reproductive toxicity. [Display omitted] •Cadmium mediates an estrogenic effect as a contributor to uterus hyperplasia.•C3G ameliorates the uterine hypertrophy caused by Cd.•C3G normalizes the balance of E2 and P4 responsive genes for uterine cell.•C3G restores the DNA replication process caused by Cd.