Exposure of pregnant and lactating parental mice to aflatoxin B promotes hepatotoxicity in offspring mice.

Aflatoxin B1 (AFB) taints feeds stuffs, endangering livestock's health and resulting in the liver and breast damage. At the same time, while breastfeeding, AFB crosses the mammary glands and enters the milk, harming the offspring. This study investigated the liver damaging effects of maternal AFB exposure during pregnancy and lactation in offspring mice. The livers of 8-day-old offspring mice were obtained from female mice who were administered AFB (2 mg/kg) 1 week prior to and 1 week following birth. The results showed that AFB increased the levels of malondialdehyde (MDA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), pro-inflammatory-related proteins (iNOS, COX-2, IL-6), and apoptosis-related proteins (Caspase-3, Caspase-9, Bax) by AFB-induced in liver of offspring mice. Furthermore, the use of F40/80, HE, and TUNEL staining further demonstrated the existence of inflammation and apoptosis in the liver. Intriguingly, in the liver of offspring mice, AFB increased antioxidant protein and inhibit ferroptosis-related protein activity (FTH, GPX4), mitochondrial function-associated proteins (UQCRC2, COX IV, Cyt C), lipid metabolism-associated proteins (HMGCR, SPEBE1, FAS), and autophagy-related proteins (Atg7, Beclin-1, LC3I/II) in the liver of mice. In conclusion, AFB enters the liver of offspring mice through milk, which in turn causes liver injury. This outcome explains how AFB exposure affects female animals and their progeny and lays the strategy for livestock prevention.