Inhibition of Alcohol‐Associated Colonic Hyperregeneration by α‐Tocopherol in the Rat

Vincon, P.; Wunderer, J.; Simanowski, Ulrich A.; Koll, Michael; Preedy, Victor R.; Werner, Jens; Waldherr, Rüdiger; Seitz, Helmut K.

doi:10.1111/j.1530-0277.2003.tb02728.x

Cited by 14 publications

(12 citation statements)

References 48 publications

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“…Our results are in contrast to several reports regarding the protective effect of VE in other tissues of ethanol-treated animals, including prevention of ethanol-induced hyperregeneration of colon crypt cells in rats [37] and inhibition of a promotional effect of ethanol on chemically induced esophageal cancers with dietary VE supplementation [38]. This suggests that the effect of VE on cell proliferation may vary depending on the organ or cell type.…”

Section: Discussioncontrasting

confidence: 99%

Vitamin E supplementation does not prevent ethanol-reduced hepatic retinoic acid levels in rats

et al. 2009

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Chronic, excessive ethanol intake can increase retinoic acid (RA) catabolism by inducing cytochrome P450 2E1 (CYP2E1). Vitamin E (VE) is an antioxidant implicated in CYP2E1 inhibition. In the current study, we hypothesized that VE supplementation inhibits CYP2E1 and decreases RA catabolism, thereby preventing ethanol-induced hepatocyte hyperproliferation. For 1 month, four groups of Sprague-Dawley rats were fed a Lieber-DeCarli liquid ethanol (36% of the total calories) diet as follows: either ethanol alone (Alc group) or ethanol in combination with 0.1 mg/kg body wt of all-trans RA (Alc+RA group), 2 mg/kg body wt of VE (Alc+VE group), or both together (Alc+RA+VE group). Control rats were pair-fed a liquid diet with an isocaloric amount of maltodextrin instead of ethanol. The ethanol-fed groups had three-fold higher hepatic CYP2E1 levels, 50% lower hepatic RA levels, and significantly increased hepatocyte proliferation when compared with the controls. The ethanol-fed rats given VE had more than four-fold higher hepatic VE concentrations than did ethanol-fed rats without VE, but this did not prevent ethanol induction of CYP2E1, lower hepatic retinoid levels, or hepatocellular hyperproliferation. Further, VE supplementation could not prevent RA catabolism in liver microsomal fractions of the ethanol-fed rats in vitro. These results show that VE supplementation can neither inhibit ethanol-induced changes in RA catabolism nor prevent ethanol-induced hepatocyte hyperproliferation in the rat liver.

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Section: Discussioncontrasting

confidence: 99%

Vitamin E supplementation does not prevent ethanol-reduced hepatic retinoic acid levels in rats

et al. 2009

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“…This induction may lead to the production of reactive oxygen species (ROS). In a series of experiments in rodents, alcohol-induced hyperproliferation of the colorectal mucosa could be inhibited partly by the concomitant administration of vitamin E, which demonstrated that this inhibition is possibly due to a reduction of ROS by vitamin E application (Vincon et al, 2000). In conclusion, chronic alcohol consumption is associated with an increased risk for colorectal cancer.…”

Section: Alcohol and Colorectal Cancermentioning

confidence: 86%

Alcohol and Cancer

Seitz

Matsuzaki

Yokoyama

et al. 2001

Alcoholism Clin & Exp Res

108

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This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Helmut K. Seitz and Shohei Matsuzaki. The presentations were (1) Alcohol dehydrogenase-2 and aldehyde dehydrogenase-2 genotype and cancer risk for upper aerodigestive tract in Japanese alcoholics, by Akira Yokoyama; (2) The role of acetaldehyde in alcohol-associated carcinogenesis, by Nils Homann; (3) High salivary acetaldehyde levels after a moderate dose of alcohol in ALDH2deficient subjects, by Satu Väkeväinen; (4) Alcohol and vitamin A interactions, by Xian Dong Wang; and (5) Alcohol and colorectal cancer, by Helmut K. Seitz.

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“…Indeed, the coadministration of vitamin E, a radical scavenger, diminished esophageal carcinogenesis in the rat model induced by nitrosamines (Eskelson et al, 1993). Most recently it was shown that the alcohol-associated colorectal hyperproliferation can be diminished by the coadministration of vitamin E (Vincon et al, 2000), underlining that besides AA, also reactive oxygen species may be involved in changes of cell turnover in the colorectal mucosa.…”

Section: Helmut K Seitzmentioning

confidence: 99%

Alcohol Metabolism: Role in Toxicity and Carcinogenesis

Badger

Ronis

Seitz

et al. 2003

Alcoholism Clin & Exp Res

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This article contains the proceedings of a symposium at the 2002 RSA Meeting in San Francisco, organized and co-chaired by Thomas M. Badger, Paul Shih-Jiun Yin, and Helmut Seitz. The presentations were (1) First-pass metabolism of ethanol: Basic and clinical aspects, by Charles Lieber; (2) Intracellular CYP2E1 transport, oxidative stress, cytokine release, and ALD, by Magnus Ingelman-Sundberg; (3) Pulsatile ethanol metabolism in intragastric infusion models: Potential role in toxic outcomes, by Thomas M. Badger and Martin J.J. Ronis; (4) Free radicals, adducts, and autoantibodies resulting from ethanol metabolism: Role in ethanol-associated toxicity, by Emanuele Albano; and (5) Gastrointestinal metabolism of ethanol and its possible role in carcinogenesis, by Helmut Seitz.

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Inhibition of Alcohol‐Associated Colonic Hyperregeneration by α‐Tocopherol in the Rat

Abstract: Alcohol-associated hyperproliferation could be prevented, at least in part, by supplementation with alpha-tocopherol. This may support the hypothesis that free radicals are involved in the pathogenesis of alcohol-associated colorectal hyperproliferation.

Cited by 14 publications

References 48 publications

Vitamin E supplementation does not prevent ethanol-reduced hepatic retinoic acid levels in rats

Vitamin E supplementation does not prevent ethanol-reduced hepatic retinoic acid levels in rats

Alcohol and Cancer

Alcohol Metabolism: Role in Toxicity and Carcinogenesis

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