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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