Modification of Nitrosamine Carcinogenesis by Ascorbic Acid
The modifying action of ascorbic acid (AA) on endogenous formation of NNitroso compounds is well known. We have studied the action of AA on the mortality of rats due to hepatoma induced by N-nitrosodiethylamine (NDEA) and on the activity of some marker enzymes of hepatocarcinogenesis. AA (50 mg per animal intraperitoneally three times a week during three months) accelerated the NDEA induced hepatocarcinogenesis. In the NDEA group one rat died after 400 days, in the NDEA+AA group 11 rats (P<0.01). At later stages the mortality difference of both groups was less distinct. The macroscopic grading of hepatomas in necropsied rats of the NDEA+AA group was significantly higher (grade 4.41) than in the NDEA only group (grade 3.09, P<0.02). Administration of AA augmented the increase of activity of glucose-6-phosphate dehydrogenase and the decrease of the activity of glucose-6-phosphatase compared with activities in the NDEA group. The activity of hexokinase, pyruvate kinase and glucose-6-phosphate dehydrogenase in the liver increased in the NDEA+AA group much earlier than in the NDEA group. The accelerating action of high doses of AA on nitrosamine hepatocarcinogenesis has to be taken into account in cancer chemoprevention and treatment.
KeywordsAscorbic Acid Pyruvate Kinase Betel Quid Endogenous Formation Lung Adenoma
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