Abstract
Simple Summary
Aflatoxins can affect hepatocytes, which results in a series of histological and ultrastructural changes to the cells. We investigated the hepatocellular alterations induced by aflatoxin B1 in rats. Interestingly, we observed several histopathological and ultrastructural alterations in hepatocytes, including necrotic changes and massive vacuolar degeneration. Ultrastructural examinations of treated groups revealed damage to the sinusoidal endothelium, as well as aggregations of hyperactive Kupffer cells in the space of Disse and damaged telocytes. Our findings provide novel insights into the induction of a series of irreversible adverse effects on hepatocytes by aflatoxin B1. Based on our results, we suggest future investigations for the exploration of mechanistic pathways related to these induced hepatocellular alterations.
Liver sinusoids are lined by fenestrated endothelial cells surrounded by perisinusoidal cells, Kupffer cells, and pit cells, as well as large granular lymphocytes. The functional ability of the liver cells can be substantially modified by exposure to toxins. In the current work, we assessed the histopathological and ultrastructural effects of a time-course exposure to aflatoxin B1 (AFB1) on the hepatic structures of rats. A total of 30 adult female Wistar rats were randomly divided into three groups: a control group, a group orally administered 250 mu g/kg body weight/day of AFB1 for 5 days/week over 4 weeks, and a group that received the same AFB1 treatment but over 8 weeks. Histopathological and ultrastructural examinations of hepatocytes revealed massive vacuolar degeneration and signs of necrosis. Furthermore, the rat liver of the treated group exhibited damage to the sinusoidal endothelium, invasion of the space of Disse with hyperactive Kupffer cells, and some immune cells, as well as Ito cells overloaded with lipids. In addition, damaged telocytes were observed. Taken together, our results indicate that AFB1 induces irreversible adverse effects on the livers of rats.