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The role of nicotinamide and of certain other modifying factors in diethylnitrosamine carcinogenesis: fusaria mycotoxins and "spontaneous" tumors in animals and man.

Authors
Type
Published Article
Journal
Cancer
0008-543X
Publisher
Wiley Blackwell (John Wiley & Sons)
Publication Date
Volume
40
Issue
4 Suppl
Pages
1833–1840
Identifiers
PMID: 143341
Source
Medline

Abstract

Pretreatment of rats with large doses of nicotinamide, which has been shown to increase the incidence of pancreatic islet-cell tumors after streptozotocin and after heliotrine, appears to promote the development of kidney neoplasias in rats given several doses of diethylnitrosamine. Nicotinamide, one of the B vitamins, and a constituent of NAD coenzymes, will prevent the depletion of NAD coenzymes by alkylating agents. It may protect the animal to some extent from the acute effects of hepatocarcinogens but not from the induction of tumors, although it may change the localization of the latter. The possible mechanisms involved in the action of nicotinamide and of certain other modifying agents are discussed. Attention is drawn to the possibility that pituitary, mammary and certain other tumors that sometimes occur among the controls, as well as among experimental animals, may be due to the occasional presence in laboratory animal diets of estrogenic and/or toxic secondary metabolites of the field fungi, Fusaria. Mycotoxins, such as zearalenone and the trichothecenes, are also likely to contaminate human foods; this could explain why multiple tumors in man occur mainly in the sex organs and in the digestive tract.

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