Gestational and lactational transmission of Aflatoxin B1 (AFB1) can elicit several toxic effects emphasizing the severity of aflatoxicosis. The present study aimed to investigate the genotoxic effects of prenatal and postnatal exposure to AFB1 on the livers of exposed offspring. With this aim, 50 μg/kg/body weight per day AFB1 was administered intraperitoneally (i.p.) to pregnant and lactating dam rats. Pups grouped as newborns (GD21/PND0) exposed in utero and infants exposed through breast milk (PND21) were compared with body weight measurements. Liver tissues were weighed after removal and subjected to histochemical (HC), immunohistochemical (IHC) and biochemical analyzes. The body weight and liver weight of exposed newborns were significantly lower than control (P<0.05). The histomorphological changes were more pronounced in exposed newborns. A decrease (P<0.05) in the histological score (HSCORE) of cytokeratin 19 (CK19) IHC, fetal stem/progenitor cells marker, and an increase (P<0.05) in the HSCORE of alpha-fetoprotein (AFP) IHC, hepatocellular carcinoma (HCC) marker, were detected in both exposed groups. Exposed newborns showed higher CK19 and AFP HSCORE than exposed infants (P<0.05). Both groups exhibited a low proliferation index score of proliferating cell nuclear antigen (PCNA) IHC (P<0.05). The high apoptotic index score of immunofluorescence (IF) staining of the terminal deoxytransferase-mediated dUTP nick-end labeling (TUNEL) method was significant in exposed newborns (P<0.05). Evaluation of oxidative stress and antioxidant systems revealed that tissue malondialdehyde (MDA) levels decreased in exposed newborns and increased in exposed infants (P<0.05), and tissue catalase (CAT) levels increased in both groups (P<0.05). In conclusion, the effects of AFB1 exposure during the gestational period occurred more severely, and the importance of preventing AFB1 exposure was revealed.