Is ethanol an important antioxidant in alcoholic beverages associated with risk reduction of cataract and atherosclerosis?

Abstract

It has been reported in the epidemiological literature that cataract, stroke, and atherosclerosis risk is reduced by 50% in people consuming one alcoholic drink per day. Peroxide has been implicated as a causative agent in cataractogenesis, and LDL oxidation appears to play a role in atherosclerosis. The antioxidant activity of alcohol was measured by: (i) use of a luminescent assay developed in our laboratory, confirmed as appropriate; (ii) electron spin resonance (ESR) spin-trapping; and (iii) copper-catalysed oxidation of LDL and VLDL from hamsters fed 6% ethanol in their drinking water. Ethanol reduced the luminescent counts/min from peroxide and superoxide. It significantly reduced the spin-trapped signal of hydroxyl radical, but not the superoxide signal. Other alcohols also showed large reductions in counts from hydrogen peroxide. Plasma from hamsters fed 6% ethanol had lower lipid peroxides and the oxidizability of LDL and VLDL was significantly reduced compared to controls. These data provide a possible explanation for the effect of beverages containing ethanol in the reduction of cataract and atherosclerosis risk observed in human population studies.

Alcohol: Friend or FOE? Alcoholic Beverage Hormesis for Cataract and Atherosclerosis is Related to Plasma Antioxidant Activity

“…The luminescent assay was described previously (Trevithick and Dzialoszynski, 1994;Trevithick et al, 1999aTrevithick et al, , 1999b) using a luminometer (Lumac 1010) to measure the photons counted following addition of a standard amount of peroxide to the assay. For plasma samples, data are normalized to the initial samples, taken before the consumption of the beverages.…”

“…To obtain comparative abilities of the drinks to act as antioxidants, aliquots were assayed to see whether they could alter the luminescence resulting from the presence of a standard amount of hydrogen peroxide (37.8 mM) reacting with luminol bound to bovine albumin, as described previously (Trevithick and Dzialoszynski, 1994;Trevithick et al, 1999aTrevithick et al, , 1999b. Antioxidant activity was calculated as the decrease in counts after addition of the beverage samples, as a percent of the control.…”

“…Using these values, an IC 50 expressed as catachin equivalent concentration could be calculated to give an idea of the antioxidant availability for each beverage. The antioxidant activities of stout itself on superoxide and hydroxyl radicals were examined by electron spin resonance (ESR) spin trapping, using 5,5-dimethyl-1-pyrroline-N-oxide (DMPO; Trevithick and Dzialoszynski, 1994) in the presence of hypoxanthine and xanthine oxidase as previously described for ethanol (Trevithick et al, 1999b).…”

“…For this reason we felt it was important to use our luminescent assay (Trevithick and Dzialoszynski, 1994;Trevithick et al, 1999aTrevithick et al, , 1999b to examine the plasma oxidative status of people after they consumed one or three typical drinks of beer, stout and nonalcoholic stout, wine, or a solution of an equal amount of ethanol.…”

Is Insulin Sensitivity a Causal Intermediate in the Relationship Between Alcohol Consumption and Carotid Atherosclerosis?

“…Attempts have been made to shed light on intermediary variables through which alcohol consumption may produce this effect. Some of these intermediary variables include alterations in HDL levels (6 -8), LDL levels (8,9), LDL oxidation (10,11), blood pressure (12,13), and coagulation/ fibrinolytic factors (14,15). Alterations in insulin sensitivity (S I ), less studied than the more traditional risk factors for cardiovascular disease mentioned above, have also been postulated as a potential intermediate through which alcohol exerts its anti-and pro-atherogenic effects (16 -18).…”