Low Dose-Ethanol Modulates Toxic Effect of Iron-Overloading in the Liver

Abstract

SummaryThe oxidant properties of iron-overload and simultaneous ethanol consump tion have received much interest, due to evidence reporting from hereditary hemochroma tosis (HC). The full form of this disease is often associated with chronic alcoholism . An additive effect of toxicity of iron and ethanol was assumed . In this study, we examined nutri tively iron-loaded Wistar rats (n=59) (TMH-Ferrocene) additionally fed with ethanol up to 8% in drinking water for 36wk. Methods: By reverse-phase HPLC we measured the concen tration of ascorbic acid, tocopherole and retinol in serum and liver homogenates as well as transaminases in the serum. Lipid peroxidation was assessed utilizing the ethane-exhalation method, Iron concentration in the liver was measured with the Bathophenanthrolin method. Liver histology was performed to investigate the iron deposits and the organ dam age (H. E., Azan and Berlin-blue-stainings). Results: 1 . Vitamin C: A linear decrease of the concentration of vitamin C in serum and liver was found independent of alcohol and iron uptake. 2. Vitamin E: Animals fed iron and alcohol showed elevated vitamin E concentra tions in the serum but not in the liver. 3. Vitamin A: Elevated levels in serum but strongly decreasing levels in liver could be measured. 4. Histology: All iron-fed animals showed mas sive deposits of iron in the liver. Iron diet caused liver cirrhosis , while an additional adminis tration of ethanol could prevent this. 5. Lipid peroxidation increased in animals fed ethanol and iron, but was significantly lower in animals only receiving an iron diet . Conclusion: Evi dence indicates that the additional exposition to ethanol in iron-loaded animals could mod ulate the organ damage and oxidative stress, The biochemical findings are positively correlated to the histology.

Anti-oxidative vitamins prevent lipid-peroxidation and apoptosis in corneal endothelial cells

“…This was then dissolved in 400 μl methanol solution, after which 100 μl of the solution was analysed by high-performance lipid chromatography (HPLC). In the case of vitamin C, the diluted filtrate obtained as above was used for direct analysis as described previously (Beutelspacher et al 2004). …”

“…Here, using iron-mediated lipid-peroxidation as an in vitro model system (Beutelspacher et al 2004), we show the direct toxicity of free radicals to CECs and the influence of anti-oxidative vitamins on CECs survival. In an attempt to attenuate cell death caused by oxidative stress induced by iron-mediated lipid-peroxidation, vitamins A, C and E have been administered to CECs undergoing apoptosis in response to sustained oxidative damage and their effect on the apoptotic rate and activation of caspase-3, an apoptosis executer enzyme, has been assessed.…”

Effect of Low-Dose Alcohol Consumption on Chronic Liver Disease

“…An in vivo study, which produced conflicting results, was conducted on 59 mice [ 100 ] and reported a lower bioavailability of vitamins (especially vitamin E) in all animals exposed to an iron-containing diet and alcohol consumption (at doses of 2%, 5%, and 8%). A significant increase in lipid peroxidation activity was found in all animals consuming alcohol, an iron-rich diet, or both.…”