TY - JOUR

T1 - Alkohol und krebs

AU - Bode, Christiane

AU - Parlesak, Alexandr

N1 - (Ekstern)

PY - 2001

Y1 - 2001

N2 - Neoplasias of the aero-digestive tract are the most common types of cancer occurring after excess alcohol consumption. The mammary gland and the liver are further organs in which the effect of alcohol abuse on cancer development has been verified. Chronic alcohol intake seems to contribute to formation of colorectal neoplasms, but the induction of malignant processes in other organs by alcohol seems unlikely. Ethanol itself is generally accepted not to possess any direct carcinogenic properties. Increased migration of (pro-)carcinogens into the cell due to the solvent-mediated effects of ethanol and an impairment of leukocyte function being involved in killing of malignant cells are mechanisms discussed as causes for carcinogenesis. Further effects of chronic alcohol consumption are induction of enzymes (cytochrome P450) being involved in toxification of procarcinogens and formation of acetaldehyde, the first metabolite of ethanol. A current theory deals with the interaction between alcohol and retinoid metabolism as a possible reason for development of colorectal cancer. In alcoholics, decreased plasma levels of folic acid, vitamins B1, B6 and zinc can lead to a limited DNA methylation, which in turn may result in a loss of controlled cell growth. The reason for this is rather a limited absorption than supplementation with these micronutrients. Just as for zinc, the same holds true for tocopherol, vitamin C and selenium, which are also deficient in the plasma of alcoholics, which may lead to an impairment of antioxidative mechanisms protecting cells against DNA damage.

AB - Neoplasias of the aero-digestive tract are the most common types of cancer occurring after excess alcohol consumption. The mammary gland and the liver are further organs in which the effect of alcohol abuse on cancer development has been verified. Chronic alcohol intake seems to contribute to formation of colorectal neoplasms, but the induction of malignant processes in other organs by alcohol seems unlikely. Ethanol itself is generally accepted not to possess any direct carcinogenic properties. Increased migration of (pro-)carcinogens into the cell due to the solvent-mediated effects of ethanol and an impairment of leukocyte function being involved in killing of malignant cells are mechanisms discussed as causes for carcinogenesis. Further effects of chronic alcohol consumption are induction of enzymes (cytochrome P450) being involved in toxification of procarcinogens and formation of acetaldehyde, the first metabolite of ethanol. A current theory deals with the interaction between alcohol and retinoid metabolism as a possible reason for development of colorectal cancer. In alcoholics, decreased plasma levels of folic acid, vitamins B1, B6 and zinc can lead to a limited DNA methylation, which in turn may result in a loss of controlled cell growth. The reason for this is rather a limited absorption than supplementation with these micronutrients. Just as for zinc, the same holds true for tocopherol, vitamin C and selenium, which are also deficient in the plasma of alcoholics, which may lead to an impairment of antioxidative mechanisms protecting cells against DNA damage.

U2 - 10.1055/s-2001-11912

DO - 10.1055/s-2001-11912

M3 - Tidsskriftartikel

AN - SCOPUS:0034792510

VL - 26

SP - 47

EP - 55

JO - Aktuelle Ernahrungsmedizin Klinik und Praxis

JF - Aktuelle Ernahrungsmedizin Klinik und Praxis

SN - 0341-0501

IS - 2

ER -