Zusammenfassung
Der Zusammenhang zwischen übermäßigem Alkoholkonsum und dem Auftreten von Krebserkrankungen
wird bei den malignen Erkrankungen der Speiseröhre und des Mund-Rachen-Raumes besonders
deutlich. Weitere Organe, die eine signifikant erhöhte Inzidenz für Krebserkrankungen
bei Alkoholabusus aufweisen, sind die Leber und die weibliche Brust. Für den Zusammenhang
zwischen Alkoholmissbrauch und Dickdarmkrebs gibt es Hinweise, während der Einfluss
von Alkoholabusus auf maligne Entartungen anderer Organe als unwahrscheinlich gilt.
Ethanol selbst kann keine direkte krebserzeugende Wirkung zugeschrieben werden. Als
mögliche Mechanismen, die bei übermäßigem Alkoholkonsum zur Zellentartung führen,
werden eine erhöhte, durch die Löseeigenschaften von Alkohol hervorgerufene Migration
von (Pro-)Kanzerogenen in die Zelle und eine Störung der Funktion von Leukozyten diskutiert,
die an der Bekämpfung entarteter Zellen beteiligt sind. Des Weiteren werden die Induktion
von Enzymen (Zytochrom P450), deren Aktivierung eine Giftung von Prokarzinogenen zur
Folge hat und die Bildung von Azetaldehyd, dem ersten Stoffwechselprodukt von Ethanol,
als wichtige Ursachen der Krebsentstehung angesehen. Eine aktuelle Hypothese berücksichtigt
die Interferenzen zwischen dem Ethanol- und Retinoidstoffwechsel als mögliche Ursache
der Zellentartung. Der bei Alkoholikern beobachtbare signifikant niedrigere Plasmaspiegel
an Vitaminen und Spurenelementen (vor allem die Vitamine Folsäure, B1, B6 und Zink) kann zu einer Einschränkung bei der Methylierung von DNA führen, die gleichfalls
mit einer Risikoerhöhung für maligne Erkrankungen in Verbindung gebracht wird. Dies
kann auf eine Störung der intestinalen Absorption zurückgeführt werden, die auch einen
Mangel an antioxidativ wirksamen Vitaminen und Spurenelementen (Tocopherol, Vitamin
C, Zink, Selen) zur Folge haben kann.
Alcohol and Cancer
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.
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Prof. Dr. Christiane Bode
Universität Hohenheim (140)
Abt. für Ernährungsphysiologie
Garbenstraße 28
70593 Stuttgart
