Glutathione,
Whey Protein and Alcohol Damage
Efficacy
of a whey protein concentrate on the inhibition of stomach ulcerative
lesions caused by ethanol ingestion
Rosaneli
CF, Bighetti AE, Antonio MA, Carvalho JE, Sgarbieri VC. [J
Med Food. 2002 Winter;5(4):221-8.] The purpose of this research
was to test the ability of a whey protein concentrate (WPC) to
inhibit gastric mucosal ulcerative lesions caused by oral administration
to rats of absolute ethanol. Acute administration (single doses)
of WPC resulted in 41% inhibition of the ulcerative lesion index
(ULI), and 73% inhibition was obtained with repetitive doses.
In a 10-days subchronic treatment study, the inhibition was 64%,
all relative to a saline treatment (negative control). Alkylation
of sulfhydryl compounds by subcutaneous injection of N-ethylmaleimide
essentially eliminated the WPC protection. Treating the rats with
an intraperitoneal injection of butathionine sulfoximine, which
inhibits glutathione synthesis, reduced WPC protection to 35%
and 52% for single and double doses, respectively. Taken
as a whole, the results indicate that WPC does protect gastric
mucosa from ethanol damage and that the protection depends on
sulfhydryl compounds present in the WPC, including its capacity
to stimulate glutathione synthesis.
N-acetylcysteine
attenuates alcohol-induced oxidative stress in the rat
(pdf)
Resat Ozaras, Veysel Tahan, Seval Aydin, Hafize Uzun, Safiye
Kaya, Hakan Senturk [World J Gastroenterol 2003;9(1):125-128]
There is increasing evidence that alcohol-induced liver damage
may be associated with increased oxidative stress. We aimed to
investigate free-radical scavenger effect of n-acetylcysteine
in rats intragastrically fed with ethanol. In this study, we tested
whether NAC attenuates alcohol-induced free radical damage in
the liver in a rat model. Reactive oxygen intermediates contributes
to the pathogenesis of various hepatic disorders such as paracetamol
intoxication, hemochromatosis, toxic hepatitis, and alcoholic
liver injury. Oxidative damage correlates with the amount of ethanol
consumed. NAC provides protection from toxic liver damage
by elevating intracellular glutathione concentrations.
Glutathione
deficiency in alcoholics: risk factor for paracetamol hepatotoxicity
Lauterburg BH and Velez ME. [Gut. 1998; volume 29, pages
1153-1157.] "The data indicate that low glutathione may be
a risk factor for [acetaminophen] hepatotoxicity in alcoholics
because a lower dose of [acetaminophen] will be necessary to deplete
glutathione below the critical threshold concentration where hepatocellular
necrosis starts to occur."
Ethanol
Ingestion Impairs Alveolar Epithelial Glutathione Homeostasis
and Function, and Predisposes to Endotoxin-Mediated Acute Lung
Injury.
David Guidot, M. Moss, F. Holguin, M. Lois, L. Brown
[Chest, July, 1999] Because ethanol impairs hepatic synthesis
and secretion of glutathione (GSH), a critical antioxidant in
the alveolar lining fluid, we hypothesized that alcohol abuse
disrupts alveolar GSH homeostasis, and that the consequent epithelial
dysfunction predisposes alcoholics to acute lung injury. These
findings support a direct role for GSH depletion in ethanol-mediated
susceptibility to lung injury. We conclude that long-term ethanol
ingestion depletes alveolar epithelial mitochondrial GSH, thereby
decreasing cell viability and function, and rendering the lung
more vulnerable to acute edematous injury. We speculate
that GSH replacement, particularly targeted to the mitochondrial
pool, may decrease the severity of acute lung injury in alcoholic
patients who are at risk for developing ARDS.
Role
of oxidative stress and antioxidant therapy in alcoholic and nonalcoholic
liver diseases
Lieber, C.S. [Adv. Pharmacol. 1997; 38: 601-28.]
Glutathione
depletion in chronic alcohol abuse makes lungs vulnerable to life-threatening
diseases
24 April, 2002; Emory University Health Sciences Center
Chronic alcohol abuse causes a profound deficiency of the antioxidant
glutathione in the lungs, generating a marked susceptibility to
serious lung diseases, according to research at Emory University
School of Medicine and the Atlanta Veterans Affairs Medical Center.
Lowered glutathione levels can be as deadly to the lungs of alcohol
abusers as alcohol itself can be to their livers and other organs,
says David Guidot, M.D., associate professor of medicine at Emory
University School of Medicine. The cure for alcohol-induced lung
damage is not as simple as just taking extra doses of glutathione,
Dr. Guidot points out, because an acute lung infection often is
the first sign of damage. "If your house is on fire, it’s
too late to install a smoke detector," he says. Glutathione
depletion cannot be quickly reversed. Only after the immediate
illness is addressed can physicians consider treating a patient
for alcoholism and consider long-term glutathione therapy. By
studying the mechanisms of glutathione damage, Dr. Guidot and
his colleagues hope to design more effective therapies for preventing
and treating the effects of chronic alcohol abuse.
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