|Year : 2015 | Volume
| Issue : 1 | Page : 1-5
Alcohol, glycine, and gastritis
Shubham Singh, Supraj Raja Sangam, Venkateshwara Rao Joginapally, Senthilkumar Rajagopal
Department of Zoology, Nizam College, Hyderabad, Telangana, India
|Date of Submission||19-Nov-2014|
|Date of Acceptance||11-Dec-2014|
|Date of Web Publication||27-Jan-2015|
Department of Zoology, Nizam College, Hyderabad, Telangana
Source of Support: This work was supported by Department of
Biotechnology, Ministry of Science and Technology, Govt. of India to
R.S (BT/RLF/Re-entry/42/2012)., Conflict of Interest: None
| Abstract|| |
Alcohol, or ethanol, is an aggressive factor for the gastrointestinal tract (GI). Alcohol may regulate the function and structure of gastrointestinal segments. In the stomach, alcohol modulates the gastric acid secretion and the activity of muscles surrounding the stomach. The inflammation in the lining of the stomach is termed gastritis. It may be due to excessive alcohol consumption, long-term use of the nonsteroidal anti-inflammatory drugs (NSAIDS), and other factors. Glycine is the smallest of the 20 amino acids commonly found in proteins, and indeed is the smallest possible. Moreover, elevation of blood glycine has shown a remarkable improvement in shock, alcoholic liver injury, gastric inflammation, some forms of cancer, nephrotoxicity, and it can also act as an anti-inflammatory immunonutrient. This article will discuss the responsible mechanisms of protection against gastric and hepatic toxicity, and review the beneficial effects of glycine in alcohol-induced inflammation.
Keywords: Ethanol, gastritis, hepatotoxicity, inflammation, nonessential amino acids
|How to cite this article:|
Singh S, Sangam SR, Joginapally VR, Rajagopal S. Alcohol, glycine, and gastritis. Int J Nutr Pharmacol Neurol Dis 2015;5:1-5
|How to cite this URL:|
Singh S, Sangam SR, Joginapally VR, Rajagopal S. Alcohol, glycine, and gastritis. Int J Nutr Pharmacol Neurol Dis [serial online] 2015 [cited 2020 Jan 24];5:1-5. Available from: http://www.ijnpnd.com/text.asp?2015/5/1/1/150065
| Introduction|| |
Alcohol disturbs the function of several organs, including the stomach, liver,  and heart,  in both laboratory animals and humans.  Alcohol is a lipophilic and nonelectrolyte substance, hence it easily penetrates the mucosal epithelial and endothelial cells. High concentration of alcohol erodes the gastric mucosa, thus excessive alcohol consumption may induce gastrointestinal dysfunction, chronic/atrophic gastritis, and gastric carcinoma in rare cases. Alcohol affects the total biochemistry of the cells including protein, carbohydrate, and fat metabolism; ,, and reduces the responsibility of immune system infections, , impairs the ability of the host to counteract hemorrhagic shock,  augments corticosteroid release,  and delays wound healing, thus leading to higher morbidity and mortality, and prolonged recovery from trauma. 
| Alcohol metabolism|| |
Ethanol is readily absorbed by the gastrointestinal tract by passive diffusion through the stomach wall (about 20%), with the remaining 80% absorbed through the duodenum and small intestine wall. , Normally in adults, alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), cytochrome P450 2E1 (CYP2E1), and catalase are present in the liver and metabolizes (oxidizes) ethanol;  but in chronic alcohol consumers, a second pathway, the microsomal ethanol-oxidizing system (MEOS) present in the smooth endoplasmic reticulum of hepatocytes, helps the body to get rid of toxic compounds via CYP2E1, which, like ADH, converts alcohol to acetaldehyde. , This reaction also requires oxygen and reduced nicotinamide adenine dinucleotide phosphate (NADPH) to form NADP and water.  In a few cases, catalase located in the peroxisomes oxidizes a small amount (2%) of ethanol to acetaldehyde in the presence of a hydrogen peroxide (H 2 O 2 )-generating system [Figure 1].  Catalase does not require nicotinamide adenine dinucleotide (NAD) as a cofactor. 
|Figure 1: Ethanol metabolism ADH = Alcohol dehydrogenase, ALDH = Aldehyde hydrogenase. Adapted from Liu, 2014|
Click here to view
Effects of alcohol and its metabolites
Acetaldehyde, an oxidized product of ethanol, can bind to a wide range of proteins including enzymes, microsomal proteins, and microtubules to form adducts which affect the protein/enzyme function, e.g. protein adducts formation in hepatocytes impairs protein secretion, which has been proposed to play a role in hepatomegaly.  It also forms adducts with the brain signaling chemical dopamine to form salsolinol, which may contribute to alcohol dependence, and with DNA to form carcinogenic DNA adducts such as 1, N2-propanodeoxyguanosine.  Alcohol-induced impairment of hepatic glycoprotein secretion is known to be mediated by acetaldehyde. In experimental rats with induced hepatic inflammation, acetaldehyde has been reported to mediate alcohol-induced impairment of hepatic glycoprotein secretion.  Acetaldehyde may injure the electron transport chain (ETC) function, leading to production of reactive oxygen species (ROS), which can oxidize the subunits of ETC complexes, leading to injury over electron transport and oxidative phosphorylation, , therefore, decreasing the ATP levels.
Alcohol effects on the stomach
Alcohol is rich in calories and devoid of nutrients, thus contributing to accumulation of fat on the liver.  On the other hand, alcohol is known to reduce the absorption of other food components and nutrients from the intestine. Since alcohol is a lipophilic, it is absorbed rapidly through the bloodstream from the stomach and intestinal tract. High concentrations of ethanol induce vascular endothelium injury of the gastric mucosa, which becomes edematous and congestive; present point and scattered bleeding lesions, focal haemorrhage, necrosis, and giant and deep ulcers.  Principal and parietal cells become swollen and diminished due to alcohol exposure.  Principal and parietal cells are rich in mitochondria,  which is easily injured as mtDNA is the major target of ethanol-associated intracellular oxidative stress.  This disturbs the morphology (becomes swollen, disaggregated, and cristae are dissolved/disappeared)  and function of the gastric mucosa. Mitochondrial dysfunction disturbs ATP synthesis and the lack of ATP may lead to metabolic acidosis, cellular edema, intracellular calcium overload, and further damage to the gastric mucosa cells.  Gastric mucosa is rich in protein sulfhydryl groups, which may be the target of ROS. Oxidized protein sulfhydryl groups lead to protein denaturation or enzyme inactivation and receptor damage or modification of the cell membrane, thus contributing to mucosal injury. 
Gastritis is the inflammation in the lining of the stomach due to intake of alcohol; spicy and acidic food; long-term consumption of nonsteroidal anti-inflammatory drugs (NSAID), e.g. ibuprofen and aspirin; severe infections with bacteria, e.g. helicobacter pylori (H. pylori); chronic bile reflux; stress; certain autoimmune disorders; or the toxic substances such as carbon disulphide, asbestos, and iodoacetate. Blood disorders such as pernicious anemia can also cause gastritis. Chronic gastritis is related to ulcer and gastric cancer.  Gastric mucosal erosion (disruption in mucosal defenses) is termed erosive gastritis. Gastritis reduces the gastric acid secretion. Gastritis in the corpus (corpus predominant and type A gastritis) and the antrum (antrum predominant or type B gastritis) behave differently, i.e. type A gastritis is more related to gastric carcinoma and type B gastritis is more related to ulcer disease. Pangastritis results from antrum-predominant chronic gastritis and it may also play a  pivotal role in alcohol-induced gastritis. The metabolic product of alcohol-aldehyde is a well-known carcinogen and plays a major role in alcohol-induced gastritis. ,
Symptoms of gastritis
The symptoms of gastritis include indigestion, abdominal bloating, nausea, vomiting, pernicious anemia, burning, hiccups, loss of appetite, and black and starry stools. Anti-inflammatory drugs, proton pump inhibitors (PPI), antacids, and antibiotics are used to treat gastritis. Gastritis management is done by avoiding acidic foods, antacids supplements, and elimination of irritating foods like lactose, gluten, etc. ,,,
Medications for gastritis
In case of H. pylori infection, "triple therapy," including PPI to reduce acid production and two antibiotics is given, otherwise Bismuth salicylate (Pepto-Bismol) is replaced by the second antibiotic.
PPI decrease gastric acid production. PPI includes the following drugs: Esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec), pantoprazole (Protonix), and rabeprazole (Aciphex).
Antacids may affect the absorption of the mediations; thereby decreasing the medicine's effectiveness. Antacids include aluminum hydroxide (Amphojel, AlternaGEL) magnesium hydroxide (Phillips' Milk of Magnesia), aluminum hydroxide and magnesium hydroxide (Maalox, Mylanta) calcium carbonate (Rolaids, Titralac, and Tums), and sodium bicarbonate (Alka-Seltzer).
H 2 blockers reduce gastric acid secretion. They include cimetidine (Tagamet), ranitidine (Zantac), nizatidine (Axid), and famotidine (Pepcid). ,,,,
| GLYCINE AGAINST ALCOHOL-INDUCED TOXICITY|| |
Prophylactic activity of glycine
Glycine is a nonessential amino acid, having multiple roles in many reactions (such as gluconeogenesis, purine, haem), chlorophyll synthesis, and bile acid conjugation.  Glycine and alanine reveal a special ability to enhance alcohol metabolism.  Glycine is said to activate chloride channels in Kupffer cells that hyperpolarizes the cell membrane and blunts intracellular Ca 2+ concentrations similar to its action in neurons, and also decreases the levels of superoxide ions from neutrophils via glycine gated chloride channel.  Glycine inhibits the activation of macrophages and tumor necrosis factor (TNF)-α release and some of the herbal formulations also reduce the inflammation. , Glycine reduces reperfusion injury,  prevents liver alcohol-induced liver damage,  attenuates lipid peroxidation, and glutathione depletion induced by the different hepatotoxins. 
Recently it has been reported that, when injected intravenously prior to resuscitation, glycine reduces organ injury and mortality in rats with hemorrhagic shock.  A diet supplemented with glycine minimizes injury by endotoxic shock induced by things such as D-galactosamine  or cyclosporine A.  Glycine inhibits angiogenesis and endothelial cell proliferation, hence prevents hepatic cancer and certain melanomas like B16 in in vivo studies.  Glycine is known to have a cytoprotective effect during lethal cell injury, such as anoxia, by inhibiting Ca 2+ -dependant degradation by nonlysosomal proteases including calpains.  Glycine is a nonessential amino acid because the body can make it from other chemicals. The normal human diet contains about 2 g of glycine per day. Protein-rich foods including meat, fish, dairy, and legumes are good sources of glycine. Glycine is used for treating schizophrenia, stroke, benign prostatic hyperplasia (BPH), and some rare inherited metabolic disorders. It is also used to protect kidneys from the harmful side effects of certain drugs used after organ transplantation as well as the liver from harmful effects of alcohol.  Glycine may be applied directly to the skin to treat leg ulcers and heal other wounds and for treating the most common form of stroke (ischemic stroke). Glycine has been shown to have prophylactic property against alcohol-induced hepatotoxicity. ,,
The glycine is toxic to human body when supplemented in excess. The major drawback in oral supplementation is its rapid metabolism in the digestive system. Ethanol induces toxicity by activating macrophages and induces the release of pro-inflammatory cytokines such as TNF-α.  In rat models, the protective nature of dietary glycine against endotoxemia, liver ischemia-reperfusion, liver transplantation, and cyclosporine-toxicity has been reported. Therefore, glycine may be effective treatment for alcohol-induced gastritis - an inflammatory disease.
We demonstrated that oral administration of glycine confers a significant protective effect against alcohol-induced hepatotoxicity by virtue of its ability to optimize the activities of serum aspartate transaminase (AST), alanine transaminase (ALT), ALP (alkaline phosphatases) and g-glutamyltranspeptidase (GGT), as well as the tissue fatty acid composition,  and glycine maintain the integrity of membranes by optimizing the altered lipid levels on chronic alcohol feeding.  We have also observed lowered blood alcohol levels in rats supplemented with glycine, which was in correlation with those of Iimuro et al.  Glycine lowers the toxicity of ethanol, prevents the accumulation of free fatty acids and optimizes the composition of individual free fatty acids in the liver and brain of rats on chronic alcohol supplementation. On the basis of these observations, it can be concluded that glycine supplementation has a significant protective effect against ethanol-induced toxicity. Glycine administration has a hypolipidemic effect in an animal model of alcohol-induced hyperlipidemia. , Glycine is known to lower the rate of gastric emptying of ethanol, thereby minimizing damage.  Moreover, glycine may directly prevent acetaldehyde, the metabolic product of alcohol, from inducing changes in the carbohydrate moieties of glycoproteins, thereby protecting the structural and functional integrity of liver from the adverse consequences of alcohol.  The supplementation with glycine offers protection against free radical-mediated oxidative stress in the erythrocyte membrane, plasma and hepatocytes of animals with alcohol-induced liver injury. 
Problems associated with glycine supplementation
Glycine, being an amino acid, is easily metabolized in the digestive system. High doses of glycine are nontoxic to the body; however, few studies have stated that the higher concentration of glycine might be toxic to the body. The target specificity is required in order to reduce its toxicity and prophylactic activity against alcohol-induced gastritis.
| Conclusion|| |
The prophylactic effects of glycine are probably due to its direct effect on target cells or mediated by inhibition of inflammatory cell activation. More investigations are needed to study the effects of the amino acid in humans on diseases in which free radicals, pro-inflammatory cytokines, inflammation, and digestive disorders are involved. The underlying mechanisms are not totally clear. Several mechanisms have been proposed and caution should be paid to the safe dose and method of administration.
| References|| |
Klein H, Harmjanz D. Effect of ethanol infusion on the ultrastructure of human myocardium. Postgrad Med J 1975;51:325-9.
Regan TJ. Alcohol and the cardiovascular system. JAMA 1990;264:377-81.
Pachinger O, Mao J, Fauvel JM, Bing RJ. Mitochondrial function and excitation-contraction coupling in the development of alcohol cardiomyopathy. Recent Adv Stud Cardiac Struct Metab 1975;5:423-9.
Ting JW, Lautt WW. The effect of acute, chronic, and prenatal ethanol exposure on insulin sensitivity. Pharmacol Ther 2006;111:346-73.
Samundeeswari N, Rajadurai M, Ganapathy P, Shairibha SR. Effect of vimliv on lipid profile and histopathology in ethanol-induced hepatotoxicity in albino Wistar rats. Int J Nutr Pharmacol Neurol Dis 2013;3:114-20.
Persson I. Red wine, white wine, rosé wine, and grape juice inhibit angiotensin-converting enzyme in human endothelial cells. Int J Nutr Pharmacol Neurol Dis 2013;3:17-23.
Happel KI, Rudner X, Quinton LJ, Movassaghi JL, Clark C, Odden AR, et al
. Acute alcohol intoxication suppresses the pulmonary ELR-negative CXC chemokine response to lipopolysaccharide. Alcohol 2007;41:325-33.
Sagar R, Bhaiji A, Toppo FA, Rath B, Sahoo HB. A comprehensive review on herbal drugs for hepatoprotection of 21 st
Century. Int J Nutr Pharmacol Neurol Dis 2014;4:191-7.
Greiffensstein P, Mathis KW, Stouwe CV, Molina PE. Alcohol binge before trauma/hemorrhage impairs integrity of host defense mechanisms during recovery. Alcohol Clin Exp Res 2007;31:704-15.
Radek KA, Kovacs EJ, DiPierto LA. Matrix proteolytic activity during wound healing: Modulation by acute ethanol exposure. Alcohol Clin Exp Res 2007;31:1045-52.
Dolganiuc A, Szabo G. In vitro
and in vivo
models of acute alcohol exposure. World J Gastroenterol 2009;15:1168-77.
Norberg A, Jones AW, Hahn RG, Gabrielsson JL. Role of variability in explaining ethanol pharmacokinetics: Research and forensic applications. Clin Pharmacokinet 2003;42:1-31.
Hariharasubramony A, Chankramath S, Prathyusha D. A case of alcohol-dependent syndrome and pellagra. Int J Nutr Pharmacol Neurol Dis 2013;3:61-3.
Zakhari S. Overview: How is alcohol metabolized by the body? Alcohol Res Health 2006;29:245-54.
Marinho V, Laks J, Engelhardt E, Conn D. Alcohol abuse in an elderly woman taking donepezil for Alzheimer disease. J Clin Pyschopharmacol 2006;26:683-5.
Ohkubo T, Metoki H, Imai Y. Alcohol intake, circadian blood pressure variation, and stroke. Hypertension 2009;53:4-5.
Gemma S, Vichi S, Testai E. Individual susceptibility and alcohol effects: Biochemical and genetic aspects. Annu I st
Super Sanita 2006;42:8-16.
Agarwal DP. Genetic polymorphisms of alcohol metabolizing enzymes. Pathol Biol (Paris) 2001;49:703-9.
Njuma OJ, Ndontsa EN, Goodwin DC. Catalase in peroxidase clothing: Interdependent cooperation of two cofactors in the catalytic versatility of KatG. Arch Biochem Biophys 2014;544:27-39.
Volentine GD, Ogden KA, Kortje DK, Tuma DJ, Sorrell MF. Role of acetaldehyde in the ethanol-induced impairment of hepatic glycoprotein secretion in the rat in vivo
. Hepatology 1987;7:490-5.
Kowaltowski AJ, Castilho RF, Vercesi AE. Mitochondrial permeability transition and oxidative stress. FEBS Lett 2001;495:12-5.
Cortés-Rojo C, Clemente-Guerrero M, Saavedra-Molina A. Effects of D-amino acids on lipoperoxidation in rat liver and kidney mitochondria. Amino Acids 2007;32:31-7.
Tilg H, Moschen AR. Evoluation of inflammation in nonalcoholic fatty liver diseases: The multiple parallel hits hypothesis. Hepatology 2010;52:1836-46.
Pan JS, He SZ, Xu HZ, Zhan XJ, Yang XN, Xiao HM, et al
. Oxidative stress disturbs energy metabolism of mitochondria in ethanol-induced gastric mucosa injury. World J Gastroenterol 2008;14:5857-67.
Yin GY, Zhang WN, Shen XJ, Chen Y, He XF. Ultrastructural and molecular biological changes of chronic gastritis, gastric cancer and gastric precancerous lesions: A comparative study. World J Gastroenterol 2003;9:851-7.
Hoek JB, Cahill A, Pastorino JG. Alcohol and mitochondria: A dysfunctional relationship. Gastroenterology 2002;122:2049-63.
Giannessi F, Giambelluca MA, Grasso L, Scavuzzo MC, Ruffoli R. Curcumin protects Leydig cells of mice from damage induced by chronic alcohol administration. Med Sci Monit 2008;14:BR237-42.
Rong Q, Utevskaya O, Ramilo M, Chow DC, Forte JG. Nucleotide metabolism by gastric glands and H(+)-K(+) ATPase-enriched membranes. Am J Physiol 1998;274:G103-10.
Dey A, Cederbaum AI. Alcohol and oxidative liver injury. Hepatology 2006;43(Suppl 1):S63-74.
Peek RM Jr, Blaser MJ. Pathophysiology of Helicobacter pylori-induced gastritis and peptic ulcer disease. Am J Med 1997;102:200-7.
Borch K, Jönsson KA, Petersson F, Redéen S, Mårdh S, Franzén LE. Prevalence of gastroduodenitis and Helicobacter pylori
infection in a general population sample: Relations to symptomatology and life-style. Dig Dis Sci 2000;45:1322-9.
Salaspuro V, Salaspuro M. Synergistic effect of alcohol drinking and smoking on in vivo
acetaldehyde concentration in saliva. Int J Cancer 2004;111:480-3.
Tahara T, Shibata T, Nakamura M, Yoshioka D, Okubo M, Arisawa T, et al
. Gastric mucosal pattern by using magnifying narrow-band imaging endoscopy clearly distinguishes histological and serological severity of chronic gastritis. Gastrointest Endosc 2009;70:246-53.
Gao L, Weck MN, Stegmaier C, Rothenbacher D, Brenner H. Alcohol consumption and chronic atrophic gastritis: Population-based study among 9,444 older adults from Germany. Int J Cancer 2009;125:2918-22.
Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. Am J Surg Pathol 1996;20:1161-81.
Anderson DL, Boyce HW Jr. Use of parenteral hyperalimentation in treatment of alkaline reflux gastritis. Gastrointest Endosc 1973;20:15-8.
Blaser MJ. Who are we? Indigenous microbes and the ecology of human diseases. EMBO Rep 2006;7:956-60.
Zajac P, Holbrook A, Super ME, Voqt M. An overview: Current clinical guidelines for the evaluation, diagnosis, treatment, and management of dyspepsia. Ost Fam Phys 2013;5:79-85.
Boparai V, Rajagopalan J, Triadafilopoulos G. Guide to the use of proton pump inhibitors in adult patients. Drugs 2008;68:925-47.
Simonian SJ, Curtis LE. Treatment of hemorrhagic gastritis by antacid. Ann Surg 1976;184:429-34.
Kandulski A, Selgrad M, Malfertheiner P. Helicobacter pylori
infection: A clinical overview. Dig Liv Dis 2008;40:619-26.
Robert H. Carbohydrate Metabolism I: Major Metabolic Pathways and their Control. New Delhi: John Wiley and Sons; 1986. p. 432-40.
Wheeler M, Stachlewitz RF, Yamashina S, Ikejima K, Morrow AL, Thurman RG. Glycine-gated chloride channels in neutrophils attenuate calcium influx and superoxide production. FASEB J 2000;14:476-84.
Ikejima K, Iimuro Y, Forman DT, Thurman RG. A diet containing glycine improves survival in endotoxin shock in the rat. Am J Physiol 1996;271:G97-103.
Ruknuddin G, Patgiri B, Prajapati PK, Krishnaiah AB, Basavaiah R. Anti-inflammatory and analgesic activities of Dashanga Ghana: An Ayurvedic compound formulation. Int J Nutr Pharmacol Neurol Dis 2013;3:303-8.
Zhong Z, Jones S, Thurman RG. Glycine minimizes reperfusion injury in a low-flow, reflow liver perfusion model in the rat. Am J Physiol 1996;270:G332-8.
Iimuro Y, Bradford BU, Forman DT, Thurman RG. Glycine prevents alcohol-induced liver injury by decreasing alcohol in the rat stomach. Gastroenterology 1996;110:1536-42.
Deters M, Siegers CP, Strubelt O. Influence of glycine on the damage induced in isolated perfused rat liver by five hepatotoxic agents. Toxicology 1998;128:63-72.
Zhong Z, Enomoto N, Connor HD, Moss N, Mason RP, Thurman RG. Glycine improves survival after hemorrhagic shock in the rat. Shock 1999;12:54-62.
Stachlewitz RF, Seabra V, Bradford B, Bradham CA, Rusyn I, Germolec D, et al
. Glycine and uridine prevent D-galactosamine hepatotoxicity in the rat: Role of Kupffer cells. Hepatology 1999;29:737-45.
Thurman RG, Zhong Z, von Frankenberg M, Stachlewitz RF, Bunzendahl H. Prevention of cyclosporine-induced nephrotoxicity with dietary glycine. Transplantation 1997;63:1661-7.
Deters M, Strubelt O, Younes M. Protection by glycine against hypoxia-reoxygenation induced hepatic injury. Res Commun Mol Pathol Pharmacol 1997;97:199-213.
Nichols JC, Bronk SF, Mellgren RL, Gores GJ. Inhibition of nonlysosomal calcium-dependent proteolysis by glycine during anoxic injury of rat hepatocytes. Gastroenterology 1994;106:168-76.
Wise DR, Thompson CB. Glutamine addiction: A new therapeutic target in cancer. Trends Biochem Sci 2010;35:427-33.
Senthilkumar R, Nalini N. Effect of glycine on tissue fatty acid composition in an experimental model of alcohol-induced hepatotoxicity. Clin Exp Pharmacol Physiol 2004;31:456-61.
Senthilkumar R, Viswanathan P, Nalini N. Glycine modulates hepatic lipid accumlation in alcohol-induced liver injury. Pol J Pharmacol 2003;55:603-11.
Senthilkumar R, Nalini N. Glycine prevents hepatic fibrosis by preventing the accumulation of collagen in rats with alcoholic liver injury. Pol J Pharmacol 2004;56:121-8.
Liu J. Ethanol and liver: Recent insights into the mechanisms of ethanol-induced fatty liver. World J Gastroenterol 2014;20:14672-85.
Senthilkumar R, Nalini N. Glycine modulates lipids and lipoproteins levels in rats with alcohol-induced liver injury. Int J Pharmacol 2004;2:2.
Iimuro Y, Bradford BU, Yamashina S, Rusyn I, Nakagami M, Enomoto N. The glutathione precursor L-2-oxothiazolidine-4-carboxylic acid protects aganist liver injury due to chronic enteral ethanol exposure in the rat. Hepatology 2000;31:391-8.
Senthilkumar R, Sengottuvelan M, Nalini N. Protective effect of glycine supplementation on the levels of lipid peroxidation and antioxidant enzymes in the erythrocytes of rats with alcohol-induced liver injury. Cell Biochem Funct 2004;22:123-8.
Akao T, Kobashi K. Inhibitory effect of glycine on ethanol absorption from gastrointestinal tract. Biol Pharmacol Bull 1995;18:1653-6.