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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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