Zalatnai A, Lapis K
1stInstitute of Pathology and Experimental Cancer Research, Semmelweis Medical University, Budapest, Hungary.
Acta Morphol Hung. 1987;35(3-4):211-8.
The aim of this study was to clarify how the CCl4-induced cirrhosis modifies the process of diethylin-nitrosamine hepatocarcinogenesis. Two strains of rats (CFY and F-344) were used. CFY rats proved to be resistant toward both the cirrhogenic effect of CCl4 and carcinogenic effect of DEN. In the F-344 rats, on the other hand, a large number of foci, neoplastic nodules and hepatocellular carcinomas occurred following DEN treatment only and fullblown liver cirrhosis did develop in the CCl4-treated group. In F-344 rats with cirrhotic liver, foci and neoplastic nodules appeared in the usual number and at the usual time following DEN treatment, but--opposite to the expectations--much less carcinomas developed than in the rats receiving DEN only. When, however the CCl4-treatment was applied following the DEN administration, a promoting effect was seen. The mechanism of the inhibitory effect of the CCl4-induced liver cirrhosis upon hepatocarcinogenesis is not clarified, similarly to the mechanism of of the promoting effect of the CCl4-treatment applied following the DEN administration.
本研究的目的是阐明四氯化碳诱导的肝硬化如何改变二乙基亚硝胺诱导肝癌发生的过程。使用了两种品系的大鼠(CFY和F-344)。结果证明CFY大鼠对四氯化碳的致肝硬化作用和二乙基亚硝胺的致癌作用均有抗性。另一方面,在F-344大鼠中,仅在给予二乙基亚硝胺后出现大量病灶、肿瘤结节和肝细胞癌,而在接受四氯化碳处理的组中确实发生了典型的肝硬化。在患有肝硬化的F-344大鼠中,给予二乙基亚硝胺后,病灶和肿瘤结节的出现数量和时间与通常情况相同,但与预期相反,发生的癌比仅接受二乙基亚硝胺的大鼠少得多。然而,当在给予二乙基亚硝胺后进行四氯化碳处理时,则会出现促进作用。四氯化碳诱导的肝硬化对肝癌发生的抑制作用机制尚不清楚,同样,在给予二乙基亚硝胺后进行四氯化碳处理的促进作用机制也不清楚。