Exposure to 2,5-hexanedione is accompanied by ovarian and uterine oxidative stress and disruption of endocrine balance in rats.

2,5-Hexanedione (2,5-HD) is an aliphatic diketone identified as the main neurotoxic metabolite of the industrial chemicals n-hexane and methyl-n-butyl ketone. Considering the dearth of information on the female reproductive toxicity effects of 2,5-HD in the literature, we assessed the potential oxidative stress mechanisms of 2,5-HD in the ovary and uterus of Wistar rats. A total of 32 female rats were randomly allotted to four groups, in which rats were exposed to 2,5-HD at doses of 0% (control), 0.25%, 0.5% and 1.0% respectively in their drinking water for 21 days. The results showed that 2,5-HD significantly increased ovarian and uterine malondialdehyde (MDA) and hydrogen peroxide (H2O2) levels (p < 0.05). Additionally, while significant decreases in ovarian catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) activities occurred in all the 2,5-HD-treated groups, uterine catalase, GST, and GPx activities increased. Further, 2,5-HD increased follicle stimulating hormone, but decreased estrogen levels in all the 2,5-HD-treated groups, while prolactin increased in the 0.5, and 1.0% 2,5-HD-treated rats compared with the control (p < 0.05). Thus, these data imply that 2,5-HD exposure disrupts hormonal homeostasis and induces oxidative stress in the ovary and uterus of rats. These findings may therefore have toxicological implications in women occupationally exposed to n-hexane and methyl-n-butyl ketone.