2-Acetylamiriofluorene (AAF) reacts in acidic conditions with nitrous fume yielding N-Nitros-2-acetylaminofluorene (N-NO-AAF),as previously shown, to exert more genotoxic and mutagenic effects than its parent compound. To predict the endogenous formation of N -NO-AAF, the effects of sodium nitrite on sister-chromatid exchange and tumorigenicity of AAF in rats administered AAF and
NaN02 were observed. For this stud, male Wistar rats were divided into five groups : group 1 served as the control group; group 2 treated with NaN02 (0.3%); group 3 was given 0.02% AAF alone; group 4 received both AAF and NaN02 (0.2%) and group 5 received both AAF and NaN02 (0.3%) in diet for 6 months.
At the end of the experiment, the SCE frequencies of group 3、group 4 and group 5 were significantly higher than the control group, but the frequencis were not significantly different among group 3 、group 4 and group 5. Additionally, nearly all rats in group 3(6/6 )group 4 (6/6)and group 5 (5/6) developed hepatocellular carcinoma in the histopathological examination. Those rats developed tumors were also shown combined with elevatin of relative liver weight, activities of hepatic function markers.
The rats received the combination of AAF and NaN02 in diet (group 4) with significant enhancement of tumor size and higher activities of GGT and AST in serum compared with AAF treated group , but the group 5 was not significant enhancement of tumorsize compared with AAF treated group.
We concluded that administration of sodium nitrite with AAF may increase the frequency of sister chromatid exchange and induce the formation of hepatocellular carcinoma , but the different effect between group 4 and group 5 was significant for hepatocarcinogenesis. We must makean effort to further study.
