Maternal T-2 Mycotoxin Exposure Impairs Liver Function and Growth in Both Dams and Offspring in Mice.

T-2 mycotoxin is a highly toxic type A trichothecene mycotoxin that widely contaminates livestock feed, posing a serious threat to animal and human health. Long-term exposure can lead to immunosuppression, growth retardation, and liver damage, causing significant economic losses to the livestock industry. Offspring are particularly susceptible to maternal dietary influences during pregnancy and lactation. This research aimed to evaluate the impact of T-2 mycotoxin exposure on both dams and their pups. Thirty pregnant mice were randomly allocated into three groups (n = 10). From gestational day 14 to lactational day 21, the dams received gavage doses of T-2 mycotoxin at concentrations of 0, 0.005, and 0.05 mg/kg/day. Randomly selected one male pup and one female pup from each dam were sacrificed on LD 1, 7, and 21; dams were dosed until the day they were sacrificed. T-2 mycotoxin decreased the relative body/organ weights of the dams and offspring (p < 0.05). Moreover, T-2 mycotoxin-induced oxidative stress in dams and offspring increased the malondialdehyde content, which led to reduced activities of antioxidant enzymes, including catalase, superoxide dismutase, and glutathione peroxidase, and total antioxidant capacity in the serum and liver (p < 0.05). T-2 mycotoxin induced histomorphological changes in the liver and early involution of the mammary gland acini in dams. The concentrations of liver-metabolizing enzymes such as glutamic oxaloacetic transaminase and glutamic pyruvic transaminase increased in offspring (p < 0.05). The serum insulin-like growth factor-1 level in offspring was decreased, which may impair the development of vital organs such as the liver, kidneys, and spleen in offspring. Consequently, the body weight and length of the offspring of exposed dams decreased. This study revealed that T-2 mycotoxin exposure during late gestation and entire lactation harms dams, damages mammary gland acini, alters liver biochemistry, induces oxidative stress, and delays offspring growth while also impairing maternal weight gain during lactation.