Abstract
Alcohol has been a widely used and abused substance throughout human civilization, with use reported as early as the Neolithic period circa 10,000 B.C.[1]. Alcohol remains a highly popular substance today with approximately 51 % of Americans over the age of 21 reporting alcohol use. Of these individuals, 11 % meet the criteria for alcohol abuse with approximately 18 million alcoholics in the United States. The consequences of alcohol abuse are numerous including liver cirrhosis, liver transplantation [2], and death occurring secondary to traffic accidents [3]. Thus, it is clear that chronic alcohol use/abuse is a significant public health problem.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
O’Shea RS, Dasarathy S, McCullough AJ. Alcoholic liver disease. Hepatology. 2010;51(1):307–28.
Blazer DG, Wu LT. The epidemiology of alcohol use disorders and subthreshold dependence in a middle-aged and elderly community sample. Am J Geriatr Psychiatry. 2011;19(8):685–94.
World Health Organization (W.H.O.). Global Status Report on Alcohol and Health. Geneva: World Health Organization; 2011.
Comporti M, et al. Ethanol-induced oxidative stress: basic knowledge. Genes Nutr. 2010;5(2):101–9.
Wang HJ, Zakhari S, Jung MK. Alcohol, inflammation, and gut-liver-brain interactions in tissue damage and disease development. World J Gastroenterol. 2010;16(11):1304–13.
Wu D, Cederbaum AI. Alcohol, oxidative stress, and free radical damage. Alcohol Res Health. 2003;27(4):277–84.
Wu D, Zhai Q, Shi X. Alcohol-induced oxidative stress and cell responses. J Gastroenterol Hepatol. 2006;21(Suppl 3):S26–9.
Cederbaum AI. Role of CYP2E1 in ethanol-induced oxidant stress, fatty liver and hepatotoxicity. Dig Dis. 2010;28(6):802–11.
Albano E. Alcohol, oxidative stress and free radical damage. Proc Nutr Soc. 2006;65(3):278–90.
Roberts BJ, et al. Ethanol induces CYP2E1 by protein stabilization. Role of ubiquitin conjugation in the rapid degradation of CYP2E1. J Biol Chem. 1995;270(50):29632–5.
Halliwell B. Free radicals and antioxidants – quo vadis? Trends Pharmacol Sci. 2011;32(3):125–30.
Lieber CS. Alcoholic fatty liver: its pathogenesis and mechanism of progression to inflammation and fibrosis. Alcohol. 2004;34(1):9–19.
McClain CJ, et al. Cytokines in alcoholic liver disease. Semin Liver Dis. 1999;19(2):205–19.
Jampana SC, Khan R. Pathogenesis of alcoholic hepatitis: role of inflammatory signaling and oxidative stress. World J Hepatol. 2011;3(5):114–7.
Ishak KG, Zimmerman HJ, Ray MB. Alcoholic liver disease: pathologic, pathogenetic and clinical aspects. Alcohol Clin Exp Res. 1991;15(1):45–66.
Tsukamoto H, et al. Severe and progressive steatosis and focal necrosis in rat liver induced by continuous intragastric infusion of ethanol and low fat diet. Hepatology. 1985;5(2):224–32.
Nanji AA, French SW. Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res. 1986;10(3):271–3.
Nanji AA, et al. Effect of type of dietary fat and ethanol on antioxidant enzyme mRNA induction in rat liver. J Lipid Res. 1995;36(4):736–44.
Lieber CS. Biochemical and molecular basis of alcohol-induced injury to liver and other tissues. N Engl J Med. 1988;319(25):1639–50.
Grant BF, Dufour MC, Harford TC. Epidemiology of alcoholic liver disease. Semin Liver Dis. 1988;8(1):12–25.
Rao RK, Seth A, Sheth P. Recent advances in alcoholic liver disease I. Role of intestinal permeability and endotoxemia in alcoholic liver disease. Am J Physiol Gastrointest Liver Physiol. 2004;286(6):G881–4.
Purohit V, et al. Alcohol, intestinal bacterial growth, intestinal permeability to endotoxin, and medical consequences: summary of a symposium. Alcohol. 2008;42(5):349–61.
Bigatello LM, et al. Endotoxemia, encephalopathy, and mortality in cirrhotic patients. Am J Gastroenterol. 1987;82(1):11–5.
Bode C, Kugler V, Bode JC. Endotoxemia in patients with alcoholic and non-alcoholic cirrhosis and in subjects with no evidence of chronic liver disease following acute alcohol excess. J Hepatol. 1987;4(1):8–14.
Enomoto N, et al. Alcohol causes both tolerance and sensitization of rat Kupffer cells via mechanisms dependent on endotoxin. Gastroenterology. 1998;115(2):443–51.
Mathurin P, et al. Exacerbation of alcoholic liver injury by enteral endotoxin in rats. Hepatology. 2000;32(5):1008–17.
Yamashina S, et al. Ethanol-induced sensitization to endotoxin in Kupffer cells is dependent upon oxidative stress. Alcohol Clin Exp Res. 2005;29(12 Suppl):246S–50.
Keshavarzian A, et al. Evidence that chronic alcohol exposure promotes intestinal oxidative stress, intestinal hyperpermeability and endotoxemia prior to development of alcoholic steatohepatitis in rats. J Hepatol. 2009;50(3):538–47.
Ferrier L, et al. Impairment of the intestinal barrier by ethanol involves enteric microflora and mast cell activation in rodents. Am J Pathol. 2006;168(4):1148–54.
Tang Y, et al. Nitric oxide-mediated intestinal injury is required for alcohol-induced gut leakiness and liver damage. Alcohol Clin Exp Res. 2009;33(7):1220–30.
Keshavarzian A, et al. Leaky gut in alcoholic cirrhosis: a possible mechanism for alcohol-induced liver damage. Am J Gastroenterol. 1999;94(1):200–7.
Adachi Y, et al. Antibiotics prevent liver injury in rats following long-term exposure to ethanol. Gastroenterology. 1995;108(1):218–24.
Crews FT, Nixon K. Mechanisms of neurodegeneration and regeneration in alcoholism. Alcohol Alcohol. 2009;44(2):115–27.
Crews FT, Zou J, Qin L. Induction of innate immune genes in brain create the neurobiology of addiction. Brain Behav Immun. 2011;25(Suppl 1):S4–12.
Enomoto N, et al. Role of Kupffer cells and gut-derived endotoxins in alcoholic liver injury. J Gastroenterol Hepatol. 2000;15(Suppl):D20–5.
Szabo G, Bala S. Alcoholic liver disease and the gut-liver axis. World J Gastroenterol. 2010;16(11):1321–9.
Gao B, et al. Innate immunity in alcoholic liver disease. Am J Physiol Gastrointest Liver Physiol. 2011;300(4):G516–25.
Thurman RG. II. Alcoholic liver injury involves activation of Kupffer cells by endotoxin. Am J Physiol. 1998;275(4 Pt 1):G605–11.
McClain CJ, Cohen DA. Increased tumor necrosis factor production by monocytes in alcoholic hepatitis. Hepatology. 1989;9(3):349–51.
Thurman RG, et al. The role of gut-derived bacterial toxins and free radicals in alcohol-induced liver injury. J Gastroenterol Hepatol. 1998;13(Suppl):S39–50.
Yin M, et al. Essential role of tumor necrosis factor alpha in alcohol-induced liver injury in mice. Gastroenterology. 1999;117(4):942–52.
Naqvi A, et al. Network-based modeling of the human gut microbiome. Chem Biodivers. 2010;7(5):1040–50.
Bjarnason I, Peters TJ, Wise RJ. The leaky gut of alcoholism: possible route of entry for toxic compounds. Lancet. 1984;1(8370):179–82.
Bode C, Bode JC. Effect of alcohol consumption on the gut. Best Pract Res Clin Gastroenterol. 2003;17(4):575–92.
Mutlu E, et al. Intestinal dysbiosis: a possible mechanism of alcohol-induced endotoxemia and alcoholic steatohepatitis in rats. Alcohol Clin Exp Res. 2009;33(10):1836–46.
Kirpich IA, et al. Probiotics restore bowel flora and improve liver enzymes in human alcohol-induced liver injury: a pilot study. Alcohol. 2008;42(8):675–82.
Forsyth CB, et al. Lactobacillus GG treatment ameliorates alcohol-induced intestinal oxidative stress, gut leakiness, and liver injury in a rat model of alcoholic steatohepatitis. Alcohol. 2009;43(2):163–72.
Frazier TH, Dibaise JK, McClain CJ. Gut microbiota, intestinal permeability, obesity-induced inflammation, and liver injury. JPEN J Parenter Enteral Nutr. 2011. doi:10.1177/0148607111413772.
Mennigen R, et al. Probiotic mixture VSL#3 protects the epithelial barrier by maintaining tight junction protein expression and preventing apoptosis in a murine model of colitis. Am J Physiol Gastrointest Liver Physiol. 2009;296(5):G1140–9.
Ulluwishewa D, et al. Regulation of tight junction permeability by intestinal bacteria and dietary components. J Nutr. 2011;141(5):769–76.
Resta-Lenert S, Barrett KE. Live probiotics protect intestinal epithelial cells from the effects of infection with enteroinvasive Escherichia coli (EIEC). Gut. 2003;52(7):988–97.
Resta-Lenert S, Barrett KE. Probiotics and commensals reverse TNF-alpha- and IFN-gamma-induced dysfunction in human intestinal epithelial cells. Gastroenterology. 2006;130(3):731–46.
Keshavarzian A, Fields J. Alcohol: “ice-breaker” yes, “gut barrier-breaker,” maybe. Am J Gastroenterol. 2000;95(5):1124–5.
Farhadi A, et al. Intestinal barrier: an interface between health and disease. J Gastroenterol Hepatol. 2003;18(5):479–97.
Laukoetter MG, Nava P, Nusrat A. Role of the intestinal barrier in inflammatory bowel disease. World J Gastroenterol. 2008;14(3):401–7.
Menard S, Cerf-Bensussan N, Heyman M. Multiple facets of intestinal permeability and epithelial handling of dietary antigens. Mucosal Immunol. 2010;3(3):247–59.
Lambert JC, et al. Prevention of alterations in intestinal permeability is involved in zinc inhibition of acute ethanol-induced liver damage in mice. J Pharmacol Exp Ther. 2003;305(3):880–6.
Ma TY, et al. Ethanol modulation of intestinal epithelial tight junction barrier. Am J Physiol. 1999;276(4 Pt 1):G965–74.
Zhong W, et al. The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction. Am J Physiol Gastrointest Liver Physiol. 2010;298(5):G625–33.
Banan A, et al. NF-kappaB activation as a key mechanism in ethanol-induced disruption of the F-actin cytoskeleton and monolayer barrier integrity in intestinal epithelium. Alcohol. 2007;41(6):447–60.
Banan A, et al. Ethanol-induced barrier dysfunction and its prevention by growth factors in human intestinal monolayers: evidence for oxidative and cytoskeletal mechanisms. J Pharmacol Exp Ther. 1999;291(3):1075–85.
Banan A, et al. Nitric oxide and its metabolites mediate ethanol-induced microtubule disruption and intestinal barrier dysfunction. J Pharmacol Exp Ther. 2000;294(3):997–1008.
Rao RK. Acetaldehyde-induced barrier disruption and paracellular permeability in caco-2 cell monolayer. Methods Mol Biol. 2008;447:171–83.
Forsyth CB, et al. Role of snail activation in alcohol-induced iNOS-mediated disruption of intestinal epithelial cell permeability. Alcohol Clin Exp Res. 2011. doi:10.1111/j.1530-0277.2011.01510.x.
Tang Y, et al. Oats supplementation prevents alcohol-induced gut leakiness in rats by preventing alcohol-induced oxidative tissue damage. J Pharmacol Exp Ther. 2009;329(3):952–8.
Keshavarzian A, et al. Preventing gut leakiness by oats supplementation ameliorates alcohol-induced liver damage in rats. J Pharmacol Exp Ther. 2001;299(2):442–8.
Chen CY, et al. Avenanthramides are bioavailable and have antioxidant activity in humans after acute consumption of an enriched mixture from oats. J Nutr. 2007;137(6):1375–82.
Chen CY, et al. Avenanthramides and phenolic acids from oats are bioavailable and act synergistically with vitamin C to enhance hamster and human LDL resistance to oxidation. J Nutr. 2004;134(6):1459–66.
Meydani M. Potential health benefits of avenanthramides of oats. Nutr Rev. 2009;67(12):731–5.
Bratt K, et al. Avenanthramides in oats (Avena sativa L.) and structure-antioxidant activity relationships. J Agric Food Chem. 2003;51(3):594–600.
Emmons CL, Peterson DM, Paul GL. Antioxidant capacity of oat (Avena sativa L.) extracts. 2. In vitro antioxidant activity and contents of phenolic and tocol antioxidants. J Agric Food Chem. 1999;47(12):4894–8.
Ren Y, et al. Chemical characterization of the avenanthramide-rich extract from oat and its effect on D-galactose-induced oxidative stress in mice. J Agric Food Chem. 2011;59(1):206–11.
Koenig RT, et al. Avenanthramides are bioavailable and accumulate in hepatic, cardiac, and skeletal muscle tissue following oral gavage in rats. J Agric Food Chem. 2011;59(12):6438–43.
Wang C, et al. Ethanol upregulates iNOS expression in colon through activation of nuclear factor-kappa B in rats. Alcohol Clin Exp Res. 2011;34(1):57–63.
Tiwari V, Chopra K. Resveratrol prevents alcohol-induced cognitive deficits and brain damage by blocking inflammatory signaling and cell death cascade in neonatal rat brain. J Neurochem. 2011;117(4):678–90.
Gloire G, Legrand-Poels S, Piette J. NF-kappaB activation by reactive oxygen species: fifteen years later. Biochem Pharmacol. 2006;72(11):1493–505.
Bubici C, et al. Mutual cross-talk between reactive oxygen species and nuclear factor-kappa B: molecular basis and biological significance. Oncogene. 2006;25(51):6731–48.
Liu L, et al. The antiatherogenic potential of oat phenolic compounds. Atherosclerosis. 2004;175(1):39–49.
Guo W, et al. Avenanthramides, polyphenols from oats, inhibit IL-1beta-induced NF-kappaB activation in endothelial cells. Free Radic Biol Med. 2008;44(3):415–29.
Guo W, et al. Avenanthramides inhibit proliferation of human colon cancer cell lines in vitro. Nutr Cancer. 2010;62(8):1007–16.
Wan XY, et al. Inhibitory effects of taurine and oat fiber on intestinal endotoxin release in rats. Chem Biol Interact. 2011;184(3):502–4.
Preidis GA, Versalovic J. Targeting the human microbiome with antibiotics, probiotics, and prebiotics: gastroenterology enters the metagenomics era. Gastroenterology. 2009;136(6):2015–31.
Roberfroid M, et al. Prebiotic effects: metabolic and health benefits. Br J Nutr. 2010;104(Suppl 2):S1–63.
Broekaert WF, et al. Prebiotic and other health-related effects of cereal-derived arabinoxylans, arabinoxylan-oligosaccharides, and xylooligosaccharides. Crit Rev Food Sci Nutr. 2011;51(2):178–94.
Acknowledgements
The authors wish to especially thank Maliha Shaikh, M.S.; Lijuan Zhang, M.D.; and Phillip Engen for their contributions to the research that made this chapter possible. In addition, we wish to acknowledge that this research was made possible with support through NIH/NIAAA grants AA013645, AA020216, and RC2AA01940 (A.K) and AA018729 (Y.T.).
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2013 Springer Science+Business Media New York
About this chapter
Cite this chapter
Forsyth, C.B., Tang, Y., Voigt, R.M., Rai, T., Keshavarzian, A. (2013). Oats Supplementation and Alcohol-Induced Oxidative Tissue Damage. In: Watson, R., Preedy, V., Zibadi, S. (eds) Alcohol, Nutrition, and Health Consequences. Nutrition and Health. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-62703-047-2_16
Download citation
DOI: https://doi.org/10.1007/978-1-62703-047-2_16
Published:
Publisher Name: Humana Press, Totowa, NJ
Print ISBN: 978-1-62703-046-5
Online ISBN: 978-1-62703-047-2
eBook Packages: MedicineMedicine (R0)