|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 Oct 25];5:1-5. Available from: https://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.
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