Background: hypervitaminosis A causes hyperplasia and vacuolation of hepatocytes and hepatic stellate cells (HSCs). The temporal sequence of these changes and the sequalae of their spontaneous reversion, however, remain largely unquantified. Methods: ethical approval was obtained from the Biosafety, Animal Use and Ethics Committee of the School of Veterinary Medicine at the University of Nairobi. A total of 45 adult albino rats were randomly divided into 3 groups. In groups A and B, 300,000 IU/Kg of vitamin A were administered to the rats every other day via subcutaneous injection for 4 and 8 weeks respectively. The rats in group C formed the control group. In total, 5 rats from group A were euthanized weekly at weeks 2, 4, 6 and 8, while those from group B were euthanized at weeks 6, 8, 10 and 12. Multistage systematic uniform random sampling was used to select harvested liver segments that were processed for histological staining. A one-way analysis of variance (ANOVA) was used to compare cell density in the 3 groups and over time. The Tukey test was used to detect the differences between the groups. Values of p < 0.05 were considered statistically significant at 95%confidence interval (95%CI). Results: in both the acutely-and chronically-exposed groups, there was a significant increaseinhepatocyte(p < 0.001) and HSC (p − 0.066) density over time. Stopping the exposure resulted in a significant decline in both cell lines (p < 0.05). Compensatory hyperplasia and hypertrophy of these cells emanated from the periportal areas. Conclusion: hepatocytes are more adversely affected by hypervitaminosis A compared to HSC, which reflects their active role in the metabolism of vitamin A.