Exposure of pregnant and lactating parental mice to aflatoxin B1 promotes hepatotoxicity in offspring mice

Abstract

Aflatoxin B1 (AFB₁) taints feeds stuffs, endangering livestock’s health and resulting in the liver and breast damage. At the same time, while breastfeeding, AFB₁ crosses the mammary glands and enters the milk, harming the offspring. This study investigated the liver damaging effects of maternal AFB₁ exposure during pregnancy and lactation in offspring mice. The livers of 8-day-old offspring mice were obtained from female mice who were administered AFB₁ (2 mg/kg) 1 week prior to and 1 week following birth. The results showed that AFB₁ 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 AFB₁-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, AFB₁ 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, AFB₁ enters the liver of offspring mice through milk, which in turn causes liver injury. This outcome explains how AFB₁ exposure affects female animals and their progeny and lays the strategy for livestock prevention.