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

Arch Toxicol. 2025 Apr;99(4):1517-1529. doi: 10.1007/s00204-024-03955-4. Epub 2025 Feb 2.

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.

Keywords: Aflatoxin B1; Lactation; Liver; Offspring mice.

MeSH terms

  • Aflatoxin B1* / toxicity
  • Animals
  • Apoptosis / drug effects
  • Chemical and Drug Induced Liver Injury* / etiology
  • Chemical and Drug Induced Liver Injury* / pathology
  • Female
  • Lactation
  • Liver* / drug effects
  • Liver* / metabolism
  • Liver* / pathology
  • Male
  • Maternal Exposure* / adverse effects
  • Mice
  • Oxidative Stress / drug effects
  • Pregnancy
  • Prenatal Exposure Delayed Effects* / chemically induced

Substances

  • Aflatoxin B1