In present study, selenium was selected for evaluating effect of selenium on aluminum chloride (AlCl3)-induced Alzheimer's disease in rats. Thirty Wistar rats were divided into five groups of six in each. Group I (control) received distilled water, group II-AlCl3 (100 mg/kg, p.o.), group III-selenium (1 mg/kg, p.o.), group IV-AlCl3 + vitamin E (100 mg/kg, p.o. + 100 mg/kg, p.o.), and group V-AlCl3 + selenium (100 mg/kg, p.o. + 1 mg/kg, p.o.) for 21 days. At end of experiment, various behavioral, biochemical, and histopathological assessments were carried out. The animals showed increase in time to reach platform in Morris water maze and decreased step-down latencies in passive avoidance test indicating learning and memory impairment in aluminum chloride-treated group, but administration of selenium decreased time to reach platform in Morris water maze, increased step-down latencies, and strengthened its memory action in drug-treated animals. There was decrease in muscle strength measured by rotarod test indicating motor incoordination and decrease in locomotor activity assessed by actophotometer test in AlCl3 control group, whereas in selenium-AlCl3 group, there was improvement in muscle strength and locomotion. Biochemical analysis of the brain revealed that chronic administration of AlCl3 significantly increased lipid peroxidation and decreased levels of acetyl cholinesterase, catalase, reduced glutathione and glutathione reductase, an index of oxidative stress process. Administration of selenium attenuated lipid peroxidation and ameliorated the biochemical changes. There were marked changes at subcellular level observed by histopathology studies in AlCl3 group, and better improvement in these changes was observed in selenium + AlCl3group. Therefore, this study strengthens the hypothesis that selenium helps to combat oxidative stress produced by accumulation of AlCl3 in the brain and helps in prophylaxis of Alzheimer's diseases.

Free radical mediated genetic instability is widely thought to be a major etiological factor for initiation of carcinogenesis. Mushrooms represent a largely untapped source of powerful new pharmaceutical products. In the present study, we examined the antiperoxidative, anti-inflammatory, and antimutagenic activities of the ethanol extract of the mycelium of a medicinal mushroom, Ganoderma lucidum, occurring in south India. Antiperoxidative activity was evaluated using Fe(2+)-ascorbate-induced lipid peroxidation in rat liver homogenate and a phorbol ester (croton oil)-induced lipid peroxidation in mouse skin. Antiinflammatory activity was evaluated against carrageenan-induced acute and formalin-induced chronic inflammatory paw edema in mouse and phorbol ester-induced mouse skin inflammation. Antimutagenic activity was determined by the Ames mutagenicity assay using histidine mutant of Salmonella typhimurium strains TA 98, TA100, and TA102. Sodium azide (NaN(3)), N-methyl-N-nitro-N-nitrosoguanidine (MNNG), 4-nitro-o-phenylenediamine (NPD), and benzo[a]pyrene (B[a]P) were used as the mutagens. The extract showed significant inhibition of Fe(2+)-induced peroxidation of lipid in rat liver (IC(50) 510 +/- 22 microg/ml) and 37% inhibition of croton oil-induced peroxidation on the mouse skin at 20 mg/0.1 ml/skin. Carrageenan-induced acute and formalin-induced chronic inflammatory edema were inhibited by 56 and 60%, respectively, by the extract at 1,000 mg/kg body wt (i.p). The extract at a concentration of 5 mg/plate showed inhibition of mutagenicity elicited by direct acting mutagens, NaN(3) (55.5 and 75.7%) and MNNG (50.0 and 57.5%) for S. typhymurium strains TA100 and TA102, respectively. The extract at the same concentration also inhibited mutagenicity elicited by NPD (52.4 and 64.2%) and B[a]P (60.7 and 59.6%) for TA98 and TA100 strains, respectively. The B[a]P was activated in the presence of rat liver microsomal (S9) fraction. The results of our study revealed that ethanol extract of Ganoderma lucidum mycelium possessed significant antiperoxidative, antiinflammatory, and antimutagenic activities. The findings suggest a medicinal use for the ethanol extract of the mycelium of G. lucidum occurring in South India.

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This study was undertaken to evaluate cardio protective effect of rutin against sodium fluoride (NaF)-induced oxidative stress-mediated cardiotoxicity and blood toxicity. Cardiac injury was induced by daily administration of NaF 600 ppm in distilled water for four weeks. The animals exposed to NaF exhibited a significant increase in levels of cardiac serum markers, lipid peroxidative markers, serum total cholesterol, LDL, triglycerides and decrease in HDL levels. Decrease in hematological parameters, namely hemoglobin, red blood cells, mean corpuscular volume, mean corpuscular hemoglobin (MCH), MCH count and increase in white blood cells and erythrocyte sedimentation levels were also observed. Marked histopathological lesions and increased DNA fragmentation in cardiac tissues were observed. Activity of antioxidants-catalase, superoxide dismutase and reduced glutathione contents were decreased (p < 0.01), whereas lipid peroxidation product (malondialdehyde) was increased. A significant decrease in body and heart weight was also observed. Treatment with rutin effectively ameliorated the alterations in the studied parameters of rat through its antioxidant nature. There was also significant improvement in hematological parameters. Thus, results of this study clearly demonstrated that treatment with rutin against NaF intoxication has a significant role in protecting F-induced cardiotoxicity, blood toxicity and dyslipidemia in rats.

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