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In vivo ethane production in vitamin E‐deficient rats with DMH‐induced colon cancer
Author(s) -
Slater Gary,
Kang Jae,
Cohen Gerald,
Szporn Arnold,
Aufses Arthur H.
Publication year - 1987
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.2930360215
Subject(s) - polyunsaturated fatty acid , vitamin e , lipid peroxidation , exhalation , medicine , in vivo , colorectal cancer , vitamin , endocrinology , polyunsaturated fat , carcinogen , 1,2 dimethylhydrazine , chemistry , antioxidant , biochemistry , cancer , dimethylhydrazine , biology , oxidative stress , fatty acid , anesthesia , microbiology and biotechnology
The effect of both a vitamin E‐deficient and a high polyunsaturated fat (PUFA) diet was tested on rats injected with the colon carcinogen 1,2‐dimethylhydrazine (DMH). In vivo lipid peroxidation was monitored by measuring exhaled ethane from the animals. Higher mean weights were found in animals fed high PUFA and vitamin E‐sufficient diets. There was no difference in ethane exhalation between DMH‐treated and control animals regardless of diet. Mean ethane exhalation was highest in animals fed either vitamin E‐deficient or high PUFA diets. There was no difference in tumor formation between the vitamin E‐deficient and the vitamin E‐sufficient groups. The high PUFA groups had more tumors than the low PUFA groups. Diet was shown to be the major factor affecting ethane exhalation. There was no evidence that vitamin E‐deficiency promoted DMH‐induced tumors or that DMH caused increased lipid peroxidation.