Dietary ethanol induces intestinal tumorigenesis in MIN mice

Roy, Hemant K.; Gulizia, James M.; Karolski, William J.; Ratashak, Anne

doi:10.1016/s0016-5085(08)83686-4

Cited by 2 publications

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“…Hepatic ethanol‐induced hyperproliferation has been linked with increased activator protein‐1 levels and retinoic acid depletion related to the induction of Cyp2e1 . Stimulation of proliferation by ethanol has also been reported in the oesophagus , small intestines , and large intestines of ethanol‐treated rats as well as in human alcoholics , but has not been detected in the distal small intestine of ethanol‐treated Apc Min mice . Increased acetaldehyde levels after ethanol consumption have been suggested to play a role in ethanol‐induced hyperproliferation , as acetaldehyde treatment of rats induced proliferation of the upper gastrointestinal tract mucosa and large intestinal proliferation in ethanol‐treated rats was found to correlate with mucosal acetaldehyde levels .…”

Section: Discussionmentioning

confidence: 99%

“…Most data are derived from rodent studies where ethanol led to increased tumour formation when co‐administered with a chemical carcinogen (reviewed in refs 1 and 7). Furthermore, two studies reported an increased polyp number and size after ethanol treatment of Apc Min mice, which are predisposed to intestinal tumour development due to a germline mutation in the Apc gene . However, there are presently no long‐term ethanol consumption studies demonstrating intestinal tumour induction in rodents by ethanol treatment alone.…”

Section: Introductionmentioning

confidence: 99%

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Effects of long‐term ethanol consumption and Aldh1b1 depletion on intestinal tumourigenesis in mice

Müller

Zhou

Adams

et al. 2017

The Journal of Pathology

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Ethanol and its metabolite acetaldehyde have been classified as carcinogens for the upper aerodigestive tract, liver, breast, and colorectum. Whereas mechanisms related to oxidative stress and Cyp2e1 induction seem to prevail in the liver, and acetaldehyde has been proposed to play a crucial role in the upper aerodigestive tract, pathological mechanisms in the colorectum have not yet been clarified. Moreover, all evidence for a pro-carcinogenic role of ethanol in colorectal cancer is derived from correlations observed in epidemiological studies or from rodent studies with additional carcinogen application or tumour suppressor gene inactivation. In the current study, wild-type mice and mice with depletion of aldehyde dehydrogenase 1b1 (Aldh1b1), an enzyme which has been proposed to play an important role in acetaldehyde detoxification in the intestines, received ethanol in drinking water for 1 year. Long-term ethanol consumption led to intestinal tumour development in wild-type and Aldh1b1-depleted mice, but no intestinal tumours were observed in water-treated controls. Moreover, a significant increase in DNA damage was detected in the large intestinal epithelium of ethanol-treated mice of both genotypes compared with the respective water-treated groups, along with increased proliferation of the small and large intestinal epithelium. Aldh1b1 depletion led to increased plasma acetaldehyde levels in ethanol-treated mice, to a significant aggravation of ethanol-induced intestinal hyperproliferation, and to more advanced features of intestinal tumours, but it did not affect intestinal tumour incidence. These data indicate that ethanol consumption can initiate intestinal tumourigenesis without any additional carcinogen treatment or tumour suppressor gene inactivation, and we provide evidence for a role of Aldh1b1 in protection of the intestines from ethanol-induced damage, as well as for both carcinogenic and tumour-promoting functions of acetaldehyde, including increased progression of ethanol-induced tumours.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of long‐term ethanol consumption and Aldh1b1 depletion on intestinal tumourigenesis in mice

Müller

Zhou

Adams

et al. 2017

The Journal of Pathology

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“…No entanto, a literatura é bastante controversa em relação a qual dos dois têm maior potencial anti-carcinogênico.Os autores DIAS e MENEGON analisaram amostras de vinho e suco de uva e observaram que, embora os teores de compostos fenólicos totais não alcohol consumption remains unacceptably high". Alcohol consumption is associated with increased risk for various types of cancer, including colon cancer, as observed both in epidemiological(Roswall & Weiderpass, 2015; Vanella et al, 2019) and experimental studies(Hayashi et al, 2007;Roy et al, 2002). eventual chemopreventive of wine against colonic carcinogenesis remains controversial, with a number of studies showing opposite results(Xu et al, 2019).pág 135.…”

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confidence: 99%

Estudo comparativo dos efeitos do álcool, vinho tinto e suco de uva na carcinogênese colônica experimental

Cesar

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Dietary ethanol induces intestinal tumorigenesis in MIN mice

Cited by 2 publications

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Effects of long‐term ethanol consumption and Aldh1b1 depletion on intestinal tumourigenesis in mice

Effects of long‐term ethanol consumption and Aldh1b1 depletion on intestinal tumourigenesis in mice

Estudo comparativo dos efeitos do álcool, vinho tinto e suco de uva na carcinogênese colônica experimental

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