Gastric carcinogenesis: a model for the identification of risk factors.

In a series of extensive studies on gastric carcinogenesis, we have used Sprague-Dawley rats to examine the morphologic, histochemical, and biochemical effects of risk and protective factors on N-methyl-N'-nitro-N-nitroso guanidine (MNNG)-induced tumors in an attempt to link early observations with the end-point lesion, gastric cancer. We have observed that the putative risk factors sodium chloride (NaCl); a mixture of bile acids; aspirin; alcohol; and nitrite enhance MNNG-induced neoplasia of the gastric mucosa. On the other hand butylated hydroxyanisol (BHA), Se and difluromethylornithine (DFMO) were protective and inhibited the induction of gastric mucosal neoplasia.

The effect of pumpkin seeds on oxalcrystalluria and urinary compositions of children in hyperendemic area.

We investigated the effect of pumpkin-seed supplementation on oxalcrystalluria and urinary composition in 20 boys age 2-7 yr from a hyperendemic area of Ubol province in Thailand. The experiment had four periods: control (before treatment), oxalate supplementation 5mg X kg-1 body wt X day-1, pumpkin-seed or orthophosphate supplementation 60 mg X kg body wt-1 X day-1, and posttreatment. Causal morning and 24-h urines were collected analyzed for crystalluria, pH, calcium, phosphorous, oxalate, creatinine, sodium, potassium, citrate glycosaminoglycans, and pyrophosphate.

The role of necrosis in hepatocellular proliferation and liver tumors.

A sequence of events which appear to be common in the development of cancer in all mammalian species includes atrophy, hyperplasia, and neoplasia. Evidence to date suggests that cell death (necrosis) is an integral, perhaps essential, factor in the initiation and maintenance of the process but the extent to which necrosis is involved, and the nature of that participation is unclear. Choline deficient B6C3F1 mice have been used to accentuate and investigate necrosis and the development of liver neoplasia following exposure to aflatoxin B1.

Vitamin A and aflatoxin: effect on liver and colon cancer.

A vitamin A (retinyl acetate)-deficient diet enhanced liver cancer in rats exposed to aflatoxin B1 (AFB1) and also caused a 29% incidence of colon cancer. The following factors were considered in attempts to define conditions under which vitamin-A-deprived rats were more susceptible to colon cancer induced by AFB1: liver morphology, enterohepatic recirculation, level of reduced glutathione (GSH) in liver, and differing capacities for conjugation of aflatoxin to GSH. Enzyme concentrations in liver, in intestinal and colon mucosa, and in intestinal and colon contents suggested that AFB1 may have different metabolites and that there may be differing susceptibilities of colon mucosa to carcinogenesis.

Nutrition and cancer: a review, with emphasis on the role of vitamins C and E and selenium.

The evidence provided by epidemiologic studies and observations in human populations as well as the more controlled studies in animals point to some effects of vitamins C and E, and of selenium, on cancer. The nature of this relationship is not clear at present, but ongoing epidemiologic and experimental work should help to clarify these interrelationships.