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KMID : 0357919740080010029
Korean Journal of Pathology
1974 Volume.8 No. 1 p.29 ~ p.41
Acute Hepatic Alterations Induced by Aflatoxin B1 -Correlation of Histopathologic Findings with 3H-thynidine Uptake by Autoradiography and Mitotic Index-
¾ç¹®È£(åÄÙþûÇ)/Moon Ho Yang
ÀÌÁ¦±¸(ì°ð­Îú)/Chae Koo Lee
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.
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