Diet enriched with the Amazon fruit açaí (Euterpe oleracea) prevents electrophysiological deficits and oxidative stress induced by methyl-mercury in the rat retina.

BACKGROUND: The protective effect of a diet supplemented by the Amazonian fruit Euterpe oleracea (EO) against methylmercury (MeHg) toxicity in rat retina was studied using electroretinography (ERG) and biochemical evaluation of oxidative stress. METHOD: Wistar rats were submitted to conventional diet or EO-enriched diet for 28 days. After that, each group received saline solution or 5 mg/kg/day of MeHg for 7 days. Full-field single flash, flash and flicker ERGs were evaluated in the following groups: control, EO, MeHg, and EO+MeHg. The amplitudes of the a-wave, b-wave, photopic negative response from rod and/or cone were measured by ERGs as well as the amplitudes and phases of the fundamental component of the sine-wave flicker ERG. Lipid peroxidation was determined by thiobarbituric acid reactive species. RESULTS: All ERG components had decreased amplitudes in the MeHg group when compared with controls. EO-enriched food had no effect on the non-intoxicated animals. The intoxicated animals and those that received the supplemented diet presented significant amplitude reductions of the cone b-wave and of the fundamental flicker component when compared with non-intoxicated control. The protective effect of the diet on scotopic conditions was only observed for bright flashes eliciting a mixed rod and cone response. There was a significant increase of lipid peroxidation in the retina from animals exposed to MeHg and EO-supplemented diet was able to prevent MeHg-induced oxidative stress in retinal tissue. CONCLUSION: These findings open up perspectives for the use of diets supplemented with EO as a protective strategy against visual damage induced by MeHg.

Methylmercury neurotoxicity & antioxidant defenses.

Neurotoxicity induced by methylmercury (MeHg) increases the formation of reactive radicals and accelerates free radical reactions. This review summarizes recent findings in the MeHg-induced formation of free radicals and the role of oxidative stress in its neurotoxicity. Oxidative stress on CNS can produce damage by several interacting mechanisms, including mitochondrial damage with increase in intracellular free Ca(2+), activation and inhibition of enzymes, release of excitatory amino acids, metallothioneins expression, and microtubule disassembly. The nature of antioxidants is discussed and it is suggested that antioxidant enzymes and others antioxidants molecules may protect the central nervous system against neurotoxicity caused by MeHg.