Maternal Exposure to T-2 Toxin Affects Puberty Genes and Delays Estrus Cycle in Mice Offspring

Among foodborne toxicities, the T-2 toxin is the most toxic member of trichothecenes mycotoxins, which has been shown to impair the development and reproductive efficiency of animals. Pups are particularly more quickly prone to programming the effects of the maternal diet during the gestational and lactation periods. Few studies have reported the maternal toxic effect on the next generation. Dams were served the T-2 toxin at a dose of 0.005 and 0.05 mg/kg body weight/day and control group 0 mg/kg from gestation day 14 to lactation day 21. Female mice offspring were selected at the weaning age. Our observations indicate that age during the vaginal opening and di-estrus stage increased and the length of the estrus cycle, first di-estrus, and regular estrus cycling were delayed with prolonged di-estrus in the 0.05 mg/kg group compared to the 0.005 mg/kg and control group. Transcription level analysis showed that mice at a dose of 0.05 mg/kg exhibited a decrease in hypothalamic mRNA expression of Gnrh and Gnrhr, Lhb, and Fshb in the pituitary gland, with a significant decrease of Fshr and Lhr in the ovaries. Present findings report that postnatal exposure to the T-2 toxin delayed puberty age in female mice and induced oxidative stress, ovarian damage, and reduced vaginal epithelium wall majorly in the 0.05 mg/kg group, and showed fewer effects in the 0.005 mg/kg group.