These findings open up perspectives for the use of diets supplemented with EO as a protective strategy against visual damage induced by MeHg.

Alcohol consumption among young adults is widely accepted in modern society and may be the starting point for abusive use of alcohol at later stages of life. Chronic alcohol exposure can lead to visual function impairment. In the present study, we investigated the spatial luminance contrast sensitivity, colour arrangement ability, and colour discrimination thresholds on young adults that weekly consume alcoholic beverages without clinical concerns. Twenty-four young adults were evaluated by an ophthalmologist and performed three psychophysical tests to evaluate their vision functions. We estimated the spatial luminance contrast sensitivity function at 11 spatial frequencies ranging from 0.1 to 30 cycles/degree. No difference in contrast sensitivity was observed comparing alcohol consumers and control subjects. For the evaluation of colour vision, we used the Farnsworth-Munsell 100 hue test (FM 100 test) to test subject’s ability to perform a colour arrangement task and the Mollon-Reffin test (MR test) to measure subject’s colour discrimination thresholds. Alcohol consumers made more mistakes than controls in the FM100 test, and their mistakes were diffusely distributed in the FM colour space without any colour axis preference. Alcohol consumers also performed worse than controls in the MR test and had higher colour discrimination thresholds compared to controls around three different reference points of a perceptually homogeneous colour space, the CIE 1976 chromaticity diagram. There was no colour axis preference in the threshold elevation observed among alcoholic subjects. Young adult weekly alcohol consumers showed subclinical colour vision losses with preservation of spatial luminance contrast sensitivity. Adolescence and young adult age are periods of important neurological development and alcohol exposure during this period of life might be responsible for deficits in visual functions, especially colour vision that is very sensitive to neurotoxicants.

Anxiety is a common symptom associated with high caffeine intake. Although the neurochemical mechanisms of caffeine-induced anxiety remain unclear, there are some evidences suggesting participation of oxidative stress. Based on these evidences, the current study is aimed at evaluating the possible protective effect of alpha-tocopherol (TPH) against anxiety-like behavior induced by caffeine (CAF) in zebrafish. Adult animals were treated with CAF (100 mg/kg) or TPH (1 mg/kg)+CAF before behavioral and biochemical evaluations. Oxidative stress in the zebrafish brain was evaluated by a lipid peroxidation assay, and anxiety-like behavior was monitored using light/dark preference and novel tank diving test. Caffeine treatment evoked significant elevation of brain MDA levels in the zebrafish brain, and TPH treatment prevented this increase. Caffeine treatment also induced anxiety-like behavior, while this effect was not observed in the TPH+CAF group. Taken together, the current study suggests that TPH treatment is able to inhibit oxidative stress and anxiety-like behavior evoked by caffeine.

To evaluate the protector effect of ascorbic acid (AA) against anxiogenic-like effect induced by methylmercury (MeHg) exposure, adult zebrafish were treated with AA (2 mg g(-1), intraperitoneal [i.p.]) before MeHg administration (1.0 μg g(-1), i.p.). Groups were tested for the light/dark preference as a behavioral model of anxiety, and the content of serotonin and its oxidized metabolite tryptamine-4,5-dione (T-4,5-D) in the brain was determined by high-performance liquid chromatography. MeHg has produced a marked anxiogenic profile in both tests, and this effect was accompanied by a decrease in the extracellular levels of serotonin, and an increase in the extracellular levels of T-4,5-D. Added to this, a marked increase in the formation of a marker of oxidative stress accompanied these parameters. Interestingly, the anxiogenic-like effect and biochemical alterations induced by MeHg were blocked by pretreatment with AA. These results for the first time demonstrated the potential protector action of AA in neurobehavioral and neurochemical alterations induced by methylmecury exposure demonstrating that zebrafish model could be used as an important tool for testing substances with neuroprotector actions.

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Background: Açaí (Euterpe oleracea) has a rich nutritional composition, showing nutraceutical and protective effects in several organs. In this study, the effects of an açaí-enriched diet on motor performance, anxiety-like behavior, and memory retention were deeply investigated. Methods: Eight-week male Wistar rats were fed with an Euterpe oleracea (EO) pulp-enriched diet, an olive oil-enriched (OO) diet (polyunsaturated fatty acid [PUFA] fat control diet), or a chow diet for 31 days (28 days pre-treatment and 3 days during behavioral tests). Afterward, animals were submitted to a battery of behavioral tests to evaluate spontaneous motor behavior (open-field test), anxiety-like behavior (elevated plus maze and open-field test), and memory retention (step-down). Oxidative stress in the hippocampus was evaluated by a lipid peroxidation assay. Results: EO-enriched diet did not influence the body weight and food intake but increased the glucose plasmatic level after 31 days under this diet. However, a similar fat-enriched diet stimulated a marked weight gain and reduced the food intake, followed by changes in the plasmatic lipid markers. EO-enriched diet preserved the motor spontaneous performance, increased the exploration in the aversive environment (anxiolytic-like effects), and elevated the latency to step-down (improved memory retention). The EO-enriched diet also reduced the level of lipid peroxidation in the hippocampus. These positive effects of EO-enriched diet can greatly support the usage of this diet as a preventive therapy. Conclusion: Taken together, the current study suggests that Euterpe oleracea-enriched diet promotes anxiolytic-like effects and improves memory consolidation, possibly due to the reduced levels of lipid peroxidation in the hippocampus.

Chronic alcohol abuse can lead to a brain damages, and the health status of alcoholics even after a long-term alcohol abstinence is a public health concern. The present study investigated the color vision and spatial luminance contrast sensitivity of a group of 17 ex-alcoholics (46.3 ± 6.7 years old) in long-term alcohol abstinence after having been previously under alcohol dependence for many years. We also investigated the association of impaired psychophysical performance in different tests we applied. The mean time of alcohol consumption was 16.9 ± 5.1 years and the mean abstinence period was 12.4 ± 8.5 years. Achromatic vision of all subjects was evaluated using spatial luminance contrast sensitivity function (CSF) test and color vision was evaluated using Mollon–Reffin color discrimination test (MR) and the Farnsworth–Munsell 100 hue arrangement test (FM100). Relative to controls, the spatial luminance contrast sensitivity was lower in 10/17 of the ex-alcoholic subjects. In the color vision tests, 11/16 ex-alcoholic subjects had impaired results compared to controls in the FM100 test and 13/14 subjects had color vision deficits measured in the MR test. Fourteen subjects performed all visual tests, three subjects had impaired results for all tests, seven subjects had impaired results in two tests, three subjects had visual deficit in one test, and one had normal results for all tests. The results showed the existence of functional deficits in achromatic and chromatic vision of subjects with history of chronic alcoholism after long abstinence. Most subjects had altered result in more than one test, especially in the color vision tests. The present investigation suggests that the damage in visual functions produced by abusive alcohol consumption is not reversed after long term alcohol abstinence.

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