Alcohol stimulation of lipid peroxidation and esophageal tumor growth in mice immunocompromised by retrovirus infection.
Tumor appearance can be accelerated in the immunodeficient and immunosuppressed animal. The role of lipid peroxidation and immune dysfunction induced by retrovirus and ethanol treatments on cancer promotion were investigated. Following the initiation of esophageal cancer by methylbenzylnitrosamine, ethanol consumption and retrovirus infection individually and concomitantly increased growth of esophageal tumors. Dietary supplementation with vitamin E reduced the size and frequency of the developed tumors. Tumor growth modifications in the vitamin E supplemented animals may be due to changes in T-cell numbers and functions stimulated by vitamin E. In addition, increased production of free radicals following ethanol treatment and retrovirus infection, and the suppression of these formations lipid peroxide by vitamin E is accompanied by lower incidence and size of tumors. Thus, the mechanisms of tumor enhancement observed in immunocompromised animals may include a combination of immunomodulation and modification of oxidant production by ethanol consumption and retrovirus infection.
Watson
R R
RR
Department of Family and Community Medicine, University of Arizona, Tucson 85724.
Odeleye
O E
OE
Eskelson
C D
CD
Mufti
S I
SI
D000163:Acquired Immunodeficiency Syndrome / Q000378:metabolism; D000818:Animals; D004938:Esophageal Neoplasms / Q000473:pathology*; D000431:Ethanol / Q000633:toxicity*; D005260:Female; D005609:Free Radicals; D016867:Immunocompromised Host; D015227:Lipid Peroxidation / Q000187:drug effects*; D051379:Mice; D008810:Mice, Inbred C57BL; D012192:Retroviridae Infections / Q000276:immunology*; D014810:Vitamin E / Q000494:pharmacology
D005609:Free Radicals; D014810:Vitamin E; D000431:Ethanol