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Alcohol, glycine, and gastritis

Article in International Journal of Nutrition, Pharmacology, Neurological Diseases January 2015

DOI: 10.4103/2231-0738.150065

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 Vol 5 / Issue 1 / January 2015
International Journal of Nutrition, Pharmacology, Neurological Diseases Volume 5 Issue 1 January-March 2015 Pages ????
 Rev i ew A r t i cle

Alcohol, glycine, and gastritis

Shubham Singh, Supraj Raja Sangam, Venkateshwara Rao Joginapally, Senthilkumar Rajagopal

Department of Zoology, Nizam ABSTRACT

College, Hyderabad, Telangana,
India
Address for correspondence:
Dr.Senthilkumar Rajagopal,
Department of Zoology, Nizam
College, Hyderabad500001,
Telangana, India.
Email:senthilanal@yahoo.com
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, longterm use of the nonsteroidal
antiinflammatory 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 antiinflammatory immunonutrient. This article will discuss
the responsible mechanisms of protection against gastric and hepatic toxicity,
and review the beneficial effects of glycine in alcoholinduced inflammation.

Key words: Ethanol, gastritis, hepatotoxicity, inflammation, nonessential amino acids

INTRODUCTION to higher morbidity and mortality, and prolonged

Alcohol disturbs the function of several organs,
including the stomach, liver, [1] and heart, [2] in
both laboratory animals and humans. [3] 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;[46] and reduces
the responsibility of immune system infections,[7,8]
impairs the ability of the host to counteract
hemorrhagic shock, [9] augments corticosteroid
release,[10] and delays wound healing, thus leading
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recovery from trauma.[11]
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.[12,13]
Normally in adults, alcohol dehydrogenase(ADH),
aldehyde dehydrogenase(ALDH), cytochrome
P4502E1(CYP2E1), and catalase are present in the liver
and metabolizes(oxidizes) ethanol;[14] but in chronic
alcohol consumers, a second pathway, the microsomal
ethanoloxidizing 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.[15,16] This
reaction also requires oxygen and reduced nicotinamide
adenine dinucleotide phosphate(NADPH) to form
NADP and water.[17] 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(H2O2)generating system [Figure 1].[18]
Catalase does not require nicotinamide adenine
dinucleotide(NAD) as a cofactor.[19]

International Journal of Nutrition, Pharmacology, Neurological Diseases | January-March 2015 | Vol 5| Issue 1 1
 Singh, etal.: Alcoholinduced gastric inflammation
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.[18] 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, N2propanodeoxyguanosine.[18] Alcoholinduced
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 alcoholinduced
impairment of hepatic glycoprotein secretion. [20]
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,[21,22]
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.[23] 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.[24] Principal and
parietal cells become swollen and diminished due
to alcohol exposure.[24] Principal and parietal cells
are rich in mitochondria,[25] which is easily injured
as mtDNA is the major target of ethanolassociated
intracellular oxidative stress.[26] This disturbs the
morphology(becomes swollen, disaggregated, and
cristae are dissolved/disappeared)[27] 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.[28] 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.[29]
2 International Journal of Nutrition, Pharmacology, Neurological Diseases | January-March 2015 | Vol 5| Issue 1
Gastritis
Gastritis is the inflammation in the lining of the
stomach due to intake of alcohol; spicy and acidic
food; longterm consumption of nonsteroidal
antiinflammatory 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.[30] Gastric mucosal erosion(disruption
in mucosal defenses) is termed erosive gastritis.
Gastritis reduces the gastric acid secretion. Gastritis in
the corpus(corpus predominant and typeA gastritis)
and the antrum(antrum predominant or typeB
gastritis) behave differently, i.e.typeA gastritis is
more related to gastric carcinoma and typeB gastritis
is more related to ulcer disease. Pangastritis results
from antrumpredominant chronic gastritis and it
may also play a[31] pivotal role in alcoholinduced
gastritis. The metabolic product of alcoholaldehyde
is a wellknown carcinogen and plays a major role in
alcoholinduced gastritis.[32,33]
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. Antiinflammatory 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.[3336]
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(PeptoBismol) 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 medicines effectiveness.
Antacids include aluminum hydroxide(Amphojel,
AlternaGEL) magnesium hydroxide(Phillips
Milk of Magnesia), aluminum hydroxide and
magnesium hydroxide(Maalox, Mylanta) calcium
 Singh, etal.: Alcoholinduced gastric inflammation
carbonate(Rolaids, Titralac, and Tums), and sodium
bicarbonate(AlkaSeltzer).
H 2 blockers reduce gastric acid secretion. They
include cimetidine(Tagamet), ranitidine(Zantac),
nizatidine(Axid), and famotidine(Pepcid).[3741]
GLYCINE AGAINST ALCOHOLINDUCED 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.[42] Glycine and alanine reveal a special
ability to enhance alcohol metabolism.[42] Glycine
is said to activate chloride channels in Kupffer
cells that hyperpolarizes the cell membrane and
blunts intracellular Ca2+concentrations similar to its
action in neurons, and also decreases the levels of
superoxide ions from neutrophils via glycine gated
chloride channel.[43] Glycine inhibits the activation
of macrophages and tumor necrosis factor(TNF)
release and some of the herbal formulations also
reduce the inflammation. [44,45] Glycine reduces
reperfusion injury,[46] prevents liver alcoholinduced
liver damage,[47] attenuates lipid peroxidation, and
glutathione depletion induced by the different
hepatotoxins.[48]
Recently it has been reported that, when injected
intravenously prior to resuscitation, glycine reduces
organ injury and mortality in rats with hemorrhagic
shock.[49] A diet supplemented with glycine minimizes
Figure 1: Ethanol metabolism ADH = Alcohol dehydrogenase, ALDH = Aldehyde hydrogenase. Adapted from Liu, 2014
International Journal of Nutrition, Pharmacology, Neurological Diseases | January-March 2015 | Vol 5| Issue 1
injury by endotoxic shock induced by things such
as Dgalactosamine[50] or cyclosporine A.[51] Glycine
inhibits angiogenesis and endothelial cell proliferation,
hence prevents hepatic cancer and certain melanomas
like B16 in invivo studies.[52] Glycine is known to have
a cytoprotective effect during lethal cell injury, such
as anoxia, by inhibiting Ca2+dependant degradation
by nonlysosomal proteases including calpains.[53]
Glycine is a nonessential amino acid because the
body can make it from other chemicals. The normal
human diet contains about 2g of glycine per day.
Proteinrich 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.[54] 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 alcoholinduced hepatotoxicity.[5557]
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 proinflammatory cytokines
such as TNF. [58] In rat models, the protective
nature of dietary glycine against endotoxemia, liver
ischemiareperfusion, liver transplantation, and
cyclosporinetoxicity has been reported. Therefore,
3
 Singh, etal.: Alcoholinduced gastric inflammation
glycine may be effective treatment for alcoholinduced
gastritis an inflammatory disease.
We demonstrated that oral administration of
glycine confers a significant protective effect
against alcoholinduced hepatotoxicity by virtue
of its ability to optimize the activities of serum
aspartate transaminase(AST), alanine transaminase
(ALT), ALP(alkaline phosphatases) and
gglutamyltranspeptidase(GGT), as well as the tissue
fatty acid composition,[59] and glycine maintain the
integrity of membranes by optimizing the altered
lipid levels on chronic alcohol feeding.[59] We have
also observed lowered blood alcohol levels in rats
supplemented with glycine, which was in correlation
with those of Iimuro etal.[60] 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 ethanolinduced toxicity. Glycine
administration has a hypolipidemic effect in an animal
model of alcoholinduced hyperlipidemia.[59,61] Glycine
is known to lower the rate of gastric emptying of
ethanol, thereby minimizing damage.[62] 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.[60]
The supplementation with glycine offers protection
against free radicalmediated oxidative stress in the
erythrocyte membrane, plasma and hepatocytes of
animals with alcoholinduced liver injury.[61]
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
alcoholinduced 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
4 International Journal of Nutrition, Pharmacology, Neurological Diseases | January-March 2015 | Vol 5| Issue 1
radicals, proinflammatory 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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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.
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: The authors fully
declare any financial or other potential conflict of interest.
Received: 19-11-2014, Accepted: 11-12-2014
5