Book contents
- Frontmatter
- Contents
- Preface
- List of abbreviations
- 1 Introduction: the problem, incidence, etiology. A working hypothesis
- 2 Biology of the esophagus
- 3 Esophageal carcinogenesis
- 4 Epidemiology
- 5 Chemicals carcinogenic for the esophagus: the nitrosamines
- 6 Alcoholic beverages and tobacco
- 7 Plant products: phenolics, tannins, tea
- 8 Plant products: opium, silica, bracken, dihydrosafrole
- 9 Molds and mycotoxins
- 10 Dietary deficiencies: micronutrients, fresh plant food and protective factors
- 11 Possible mechanisms involved in carcinogenesis
- Index
5 - Chemicals carcinogenic for the esophagus: the nitrosamines
Published online by Cambridge University Press: 07 September 2010
- Frontmatter
- Contents
- Preface
- List of abbreviations
- 1 Introduction: the problem, incidence, etiology. A working hypothesis
- 2 Biology of the esophagus
- 3 Esophageal carcinogenesis
- 4 Epidemiology
- 5 Chemicals carcinogenic for the esophagus: the nitrosamines
- 6 Alcoholic beverages and tobacco
- 7 Plant products: phenolics, tannins, tea
- 8 Plant products: opium, silica, bracken, dihydrosafrole
- 9 Molds and mycotoxins
- 10 Dietary deficiencies: micronutrients, fresh plant food and protective factors
- 11 Possible mechanisms involved in carcinogenesis
- Index
Summary
Experimental studies: N-nitroso compounds
Introduction
The esophagus is an organ which might not be expected to be especially sensitive to chemical carcinogens. After ingestion, food and drink remain for a short period in the mouth, for a much longer time in the stomach, but pass rapidly through the lumen of the esophagus. Exposure of the oral and gastric mucosa is of very much longer duration than that of the esophageal epithelium, so that direct-acting chemicals, i.e. those which do not require metabolic activation to be effective carcinogens, are more likely to cause oral or gastric cancer. Chemicals which remain inert until activated by metabolism can be absorbed into the circulation and reach the esophagus by this route. However, the chemicals which do require metabolic activation before they become effective are more likely to be carcinogenic for the more metabolically active organs, i.e. liver and kidney, than for organs with lower metabolic activity, and lower cytochrome P450 levels, such as muscle, nerve and esophagus.
In general, this concept appears to be justified, as of all the huge number of chemicals which have been tested for carcinogenicity, very few are carcinogenic for the esophagus. The outstanding exception is a large group of compounds which are very potent esophageal carcinogens: the Nnitrosamines. The outstanding exception is a large group of compounds which are very potent esophageal carcinogens: the N-nitrosamines.
- Type
- Chapter
- Information
- Cancer of the EsophagusApproaches to the Etiology, pp. 69 - 116Publisher: Cambridge University PressPrint publication year: 1993