Assessment of Rats Exposed to Aflatoxin B1 Early in Life and Impact on the Offspring

Aflatoxin-producing Aspergillus fungi produce hazardous compounds that often contaminate food in tropical regions. In some areas, the most harmful kind, aflatoxin B1 (AFB1), is a primary contributor to liver cancer, often known as hepatocellular carcinoma, or HCC. There is a significant frequency of aflatoxin contamination, and early onset of HCC has been linked to perinatal exposure to AFB1. The possible consequences of perinatal exposure to AFB1and possible epigenetic changes whichmightaffect the risk of cancer in the future are investigated in this study. Two dosages of AFB1 (high: 5 mg/kg, low: 0.5 mg/kg) were administered to pregnant rats before conception, during pregnancy, and during the weaning process to investigate this. Next, these groups were contrasted with a control group that had not been exposed. The babies were kept under observation until they were three weeks or three months old, at which time samples of their liver and blood were taken for examination. Hormones related to reproduction, gonadotropin, and thyroid were assessed after three months, whereas body weights and lipid profiles were determined at three weeks and three months. The children of high-dose prenatal AFB1 exposure had notable weight reductions: 16.3% at birth, 31.6% at three weeks, and 7.5% at three months, according to the results. The lipid and hormone profiles were likewise changed by both exposure levels. TP53gene and H19's DNA methylation levels in blood and liver samples were assessed using pyrosequencing. TP53 methylation was markedly elevated in blood samples from rats subjected to both low- and high-doses, but dramatically decreased in liver samples as compared to controls. In contrast, Rats exposed to the high-dose group had increased liver and decreased H19 methylation in their 3-month blood samples. These findings thus point toward an increased risk of early-onset HCC, whether perinatal AFB1 exposure can lead to overt alterations in hormone, lipid, and weight profiles with modulation of epigenetic regulation. Further studies are needed to completely understand the long-term implications of these modifications leading to cancer development.