Chronic Exposure to Diquat Causes Reproductive Toxicity in Female Mice

• Published in: PloS one Vol. 11; no. 1; p. e0147075
• Main Authors: Zhang, Jia-Qing, Gao, Bin-Wen, Wang, Jing, Wang, Xian-Wei, Ren, Qiao-Ling, Chen, Jun-Feng, Ma, Qiang, Xing, Bao-Song
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 19.01.2016; Public Library of Science (PLoS)
• Subjects: Aging; Animals; Anions; Antioxidants; Apoptosis; Apoptosis - drug effects; Biochemistry; Biocompatibility; Biology; Breeding of animals; Causes of; Chronic exposure; Complications and side effects; Cytotoxicity; Diquat; Diquat - toxicity; Domestic animals; Embryos; Exposure; Extrusion; Female; Fetuses; Free radicals; Gangrene; Gene expression; Gene Expression Regulation - drug effects; Granulosa Cells - metabolism; Granulosa Cells - pathology; Herbicides; In vivo methods and tests; Infertility; Mice; Mice, Inbred ICR; Oxidative stress; Oxygen; Physiological aspects; Polar Bodies - metabolism; Polar Bodies - pathology; Reactive oxygen species; Reactive Oxygen Species - metabolism; Reproduction; Reproduction - drug effects; Reproductive status; Reproductive system; Risk factors; Rodents; Science; Superoxide; Superoxide anions; Toxicity; Urogenital diseases; China
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0147075

Diquat is a bipyridyl herbicide that has been widely used as a model chemical for in vivo studies of oxidative stress due to its generation of superoxide anions, and cytotoxic effects. There is little information regarding the toxic effects of diquat on the female reproductive system, particularly ovarian function. Thus, we investigated the reproductive toxic effects of diquat on female mice. Chronic exposure to diquat reduced ovary weights, induced ovarian oxidative stress, resulted in granulosa cell apoptosis, and disrupted oocyte developmental competence, as shown by reactive oxygen species (ROS) accumulation, decreased polar body extrusion rates and increased apoptosis-related genes expression. Additionally, after diquat treatment, the numbers of fetal mice and litter sizes were significantly reduced compared to those of control mice. Thus, our results indicated that chronic exposure to diquat induced reproductive toxicity in female mice by promoting the ROS production of gruanousa cells and ooctyes, impairing follicle development, inducing apoptosis, and reducing oocyte quality. In conclusion, our findings indicate that diquat can be used as a potent and efficient chemical for in vivo studies of female reproductive toxicity induced by oxidative stress. Moreover, the findings from this study will further enlarge imitative research investigating the effect of ovarian damage induced by oxidative stress on reproductive performance and possible mechanisms of action in large domestic animals.