Ascorbic acid has many nonenzymatic actions and is a powerful water-soluble antioxidant. It protects low density lipoproteins from oxidation and reduces harmful oxidants in the central nervous system. Pilocarpine-induced seizures have been suggested to be mediated by increases in oxidative stress. Current studies have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures. The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ascorbic acid (500 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of ascorbic acid (AA plus pilocarpine group). After the treatments all groups were observed for 6 h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of ascorbic acid were also evaluated on the same parameters. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite level. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the superoxide dismutase and catalase activities in hippocampus of adult rats after seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that a strong protective effect could be achieved using ascorbic acid.

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Other natural products U 0800Cytotoxic Activity of Nepetin, a Flavonoid from Eupatorium ballotaefolium HBK. -Nepetin (I) and quercetin-3-O-glucoside (II) are isolated from the title plant and evaluated for their cytotoxic activity. (I) inhibits the proliferation of the tumor cell lines tested. -(MILITAO, G. C. G.; ALBUQUERQUE, M. R. J. R.; PESSOA, O. D. L.; PESSOA, C.; MORAES, M. E. A.; DE MORAES, M. O.; COSTA-LOTUFO, L. V.; Pharmazie 59 (2004) 12, 965-966; Dep. Physiol. Pharmacol., Med. Sch., Fed. Univ.

Chresta martii (Asteraceae), found in the Xingó region, northeastern Brazil, is used in the treatment of gastrointestinal (GIT) and liver disorders and malaria. However, there are few studies regarding efficacy and safety of use for this species. Thus, the objective of this study was to determine in vivo acute toxicity and in vitro cytotoxicity of organic extracts of C. martii as well as in vivo genotoxicity of its semipurified fraction. Dried aerial parts of C. martii were extracted using three organic solvents (cyclohexane [ECCm], ethyl acetate [EACm], and ethanol [EECm]), and these extracts were examined for acute toxicity (50-2000 mg/kg ip or po) and cytotoxicity (50 μg/ml) in carcinogenic human cell lines (HL-60, NCIH-292, and MCF-7). The EACm, which showed evidence of toxicity (in vivo and in vitro), was fractionated on a silica column, yielding four fractions (F1-F4). The F1 was utilized for genotoxicity (50 mg/kg ip), by in vivo micronucleus (MN) assay. ECCm showed no indication of acute toxicity or occurrence of death, while the LD50 estimated for the extracts (EACm and EECm) was 500 mg/kg po and 200 mg/kg ip. The EACm (50 μg/ml) inhibited growth of tumor cells HL-60 (96.54%), NCIH-292 (73.43%), and MCF-7 (15%). The F1 fraction induced MN formation in polychromatic erythrocytes of Swiss Webster mice. Organic extracts from C. martii exhibited acute toxicity classified as mild to moderate, in addition to cytotoxicity (in vitro), while the F1 semipurified fraction induced genotoxicity (in vivo).