Abstract

Acute hepatic alterations was induced in young male rats by a single intraperitoneal injection of aflatoxin B₁ dissolved within diaethylsulfoxide, and their histopathologic characteristics were correlated with mitotic activity and incooperation of 3H-thymidine uptake into hepatocytes and Kupffer cells using microautoradiography. 1. Major morphological changes in the earl phase included little periportal necrosis but accompanied features of much significant hepatocellular degeneration and unrest as well as kupffer cell reaction and minimal ductular cell proliferation; Evidences of hepatocellular injuries started to appear within 24 hours after exposure, but became regressed 72 hours later to restore normal hepatic architectures and cellular details after the 7th day. 2. Indices of both 3H-thymidine uptake and mitosis of the hepatocytes was lowest at the 24 hour-group, being followed by rather rapid increase up to the levels of 2∼3 times higher than those in the control group at the 5th day, and thereafter both returned to the normal status. 3. Those transient increases of both indices were assumed to be resulted by compersatory proliferation for hepatic injuries. 4. Hepatic megalocytosis during morphological architectural restore supported that abnormal increase of metabolism was involved against antimetabolic effect of aflatoxin. 5. Kupffer cells were also similarly but less severely affected by aflatoxin in terms of both 3H-thymidine uptake and mitotic indices. The above features during the early phase of hepatic alterations suggested that administration of aflatoxin B₁ results in impairment or blockage of DNA synthesis and antimetabolic effect within 24 hours on both hetpatocytes and kupffer cells, after which both of 3H-thymidine uptake and mitotic indices return to the normal as with morphologic restorement.