Co-Carcinogenic Effect of Vitamin A and C in Laboratory Studies

BrooklynDodger previously posted a mega chemoprevention study of Vitamin A in smokers and asbestos workers in which the vitamins were was stopped in mid stream as it became evident that there was increased cancer in the vitamin treated patients. [The non treatment arm of the study in asbestos workers provided useful information about the natural history of disease among those people. BrooklynDodger will return to that in another post.]

Now comes a laboratory study which duplicates this effect in guinea pigs. The abstract is paraphrased here and repeated in full below:

…guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. …Compared with a diet low in vitamin C …and vitamin E …, a diet high in vitamin C … and vitamin E … significantly increased the incidence of these lesions. … As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results … provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.

Probably this applies to all environmental risks for lung cancer, fine particles as well as asbestos. The “healthy” diet promoted by the blame the victim establishment increases risk. Nothing to be done but prevent the exposures.

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Carcinogenesis 2005 26(3):605-612; doi:10.1093/carcin/bgh341

Induction of preneoplastic lung lesions in guinea pigs by cigarette smoke inhalation and their exacerbation by high dietary levels of vitamins C and E

Emerich S. Fiala2, Ock Soon Sohn, Chung-Xiou Wang, Eleanore Seibert, Junji Tsurutani1, Phillip A. Dennis1, Karam El-Bayoumy, Rama S. Sodum, Dhimant Desai, Joel Reinhardt and Cesar Aliaga
Institute for Cancer Prevention, Valhalla, NY, USA and 1 Cancer Therapeutics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA

The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by the availability of suitable laboratory animal models. Here we report that male Hartley guinea pigs treated with cigarette smoke by inhalation twice a day for 28 days developed preneoplastic lung lesions, including bronchial hyperplasia, dysplasia and squamous metaplasia, analogous to those found in human smokers. The lesions were accompanied by increased expression of proliferating cell nuclear antigen and activation of the serine/threonine kinase Akt in the bronchial epithelium. In contrast, no lung lesions were found in guinea pigs (‘sham smoked’) that were submitted to identical procedures but without cigarettes. Compared with a diet low in vitamin C (50 p.p.m.) and vitamin E (15 p.p.m.), a diet high in vitamin C (4000 p.p.m.) and vitamin E (40 p.p.m.) significantly increased the incidence of these lesions. The inclusion of 1,4-phenylenebis(methylene)selenocyanate (p-XSC), a synthetic chemopreventive organoselenium compound, in the high vitamin C–high vitamin E diet at a level of 15 p.p.m. as selenium appeared to decrease the lesion incidence. Administration of (–)-epigallocatechin gallate, a powerful green tea polyphenolic antioxidant, at 560 p.p.m. in the drinking water had no effect. As in human smokers, levels of ascorbate in blood plasma, lung, liver and the adrenal glands were significantly decreased by cigarette smoke inhalation. These results identify a relevant in vivo laboratory model of cigarette smoke-induced lung cancer, suggest that p-XSC may have activity as a chemopreventive agent against cigarette smoke-induced lung lesions and provide additional evidence that very high dietary levels of certain antioxidants can have co-carcinogenic activity in cigarette smoke-induced lung cancer.