Considering the important role of oxidative stress in the pathogenesis of several neurological diseases, and the growing evidence of the presence of compounds with antioxidant properties in the plant extracts, the aim of the present study was to investigate the antioxidant capacity of three plants used in Brazil to treat neurological disorders: Melissa officinalis, Matricaria recutita and Cymbopogon citratus. The antioxidant effect of phenolic compounds commonly found in plant extracts, namely, quercetin, gallic acid, quercitrin and rutin was also examined for comparative purposes. Cerebral lipid peroxidation (assessed by TBARS) was induced by iron sulfate (10 microM), sodium nitroprusside (5 microM) or 3-nitropropionic acid (2 mM). Free radical scavenger properties and the chemical composition of plant extracts were assessed by 1'-1' Diphenyl-2' picrylhydrazyl (DPPH) method and by Thin Layer Chromatography (TLC), respectively. M. officinalis aqueous extract caused the highest decrease in TBARS production induced by all tested pro-oxidants. In the DPPH assay, M. officinalis presented also the best antioxidant effect, but, in this case, the antioxidant potencies were similar for the aqueous, methanolic and ethanolic extracts. Among the purified compounds, quercetin had the highest antioxidant activity followed by gallic acid, quercitrin and rutin. In this work, we have demonstrated that the plant extracts could protect against oxidative damage induced by various pro-oxidant agents that induce lipid peroxidation by different process. Thus, plant extracts could inhibit the generation of early chemical reactive species that subsequently initiate lipid peroxidation or, alternatively, they could block a common final pathway in the process of polyunsaturated fatty acids peroxidation. Our study indicates that M. officinalis could be considered an effective agent in the prevention of various neurological diseases associated with oxidative stress.

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This study evaluated extracts of Condalia buxifolia as anesthetics for the silver catfish Rhamdia quelen. The effectiveness of eugenol and of the methanolic extract (ME) of C. buxifolia during the transport of this species was also assessed. Fish of two different weights (1.50±0.02 g and 165.70±22.50 g) were transferred to aquaria containing water with the C. buxifolia ME or with fractions obtained from the ME, such as the n-hexane, dichloromethane, ethyl acetate, n-butane and aqueous fractions, at concentrations from 0-300 μL L C. buxifolia ME. The non-ionized ammonia levels were lower at the end of transport in the groups with the compounds than in that with water alone. Moreover, both compounds decreased the Na + , Cl -, and K + net effluxes; therefore, their addition to the water during transport is advisable because they reduce fish mortality and ion loss.Este estudo investigou extratos de Condalia buxifolia como anestésico para jundiá Rhamdia quelen, e também a eficiência do eugenol e do extrato metanólico (EM) de C. buxifolia para utilização durante o transporte dessa espécie. Peixes de dois diferentes pesos (1,50±0,02 g e 165,70±22,50 g) foram transferidos para aquários contendo água com o EM de C. buxifolia ou frações obtidas a partir do EM (n-hexano, acetato de diclorometano, etil n-butano e aquoso, em concentrações na faixa de 0 -300 μL L

The hypothesis that methylmercury (MeHg) potently induces formation of reactive oxygen species (ROS) in the brain is supported by observations on the neuroprotective effects of various classes of antioxidants. Flavonoids have been reported to possess divalent metal chelating properties, antioxidant activities and to readily permeate the blood-brain barrier. They can also provide neuroprotection in a wide array of cellular and animal models of neurological diseases. Paradoxically, in vivo administration of quercetin displays unexpected synergistic neurotoxic effect with MeHg. Considering this controversy and the limited data on the interaction of MeHg with other flavonoids, the potential protective effect of quercetin and two of its glycoside analogs (i.e., rutin and quercitrin) against MeHg toxicity were evaluated in rat cortical brain slices. MeHg (100 microM) caused lipid peroxidation and ROS generation. Quercitrin (10 microg/mL) and quercetin (10 microg/mL) protected mitochondria from MeHg (5 microM)-induced changes. In contrast, rutin did not afford a significant protective effect against MeHg (100 microM)-induced lipid peroxidation and ROS production in cortical brain slices. MeHg-generated ROS in cortical slices was dependent upon an increase in intracellular Ca(2+) levels, because the over-production of MeHg-induced H(2)O(2) in mitochondria occurred with a concomitant increase in Ca(2+) transient. Here, we have extended the characterization of mechanisms associated with the neuroprotective effects of quercetin against MeHg-induced toxicity in isolated mitochondria, by performing an array of parallel studies in brain slices. We provide novel data establishing that (1) Ca(2+) plays a central role in MeHg toxicity and (2) in brain slices MeHg induces mitochondrial oxidative stress both via direct interaction with mitochondria (as previously reported in in vitro studies) as well as via mitochondria-independent (or indirect) mechanisms.

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