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Vitamin E exists in eight different forms, four tocopherols and four tocotrienols. It forms an important component of our antioxidant system. The structure of Vitamin E makes it unique and indispensable in protecting cell membranes. α-tocopherol, one of the forms of Vitamin E, is also known to regulate signal transduction pathways by mechanisms that are independent of its antioxidant properties. Vitamin E compounds reduce the production of inflammatory compounds such as prostaglandins. Swollen, dystrophic axons are considered as the hallmark of Vitamin E deficiency in the brains of rats, monkeys, and humans. The present work aimed to study the Vitamin E- (α-tochopherol acetate-) induced alterations of enzymes involved in metabolism of Glutamate and GABA during developmental neurogenesis of cerebrum. Therefore, cytosolic and crude mitochondrial enzyme activities of glutamine synthetase, aspartate transaminase, alanine transaminase, GABA transaminase, succinic Semialdehyde dehydrogenase, glutamic dehydrogenase, and α-Ketoglutarate dehydrogenase were analysed. Vitamin E induced significant changes in these enzymes thus altering the normal levels of glutamate and GABA during developmental neurogenesis. Such changes are surely to disturb the expression and/or intensity of neurotransmitter signaling during critical periods of brain development.

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The use of plants as a source of sedative or treatment for cancer is reasonably widespread worldwide. Annona muricata Linn exhibits a vast array of medicinal and ethno-pharmaceutical benefits, attributed by different plant parts. The activity of this plant is regarded to the bio-production of secondary metabolites like alkaloids, phenols, flavonoids, and most unique group of compounds, namely, annonaceous acetogenins. Whilst this plant is gaining popularity as an anticancer treating plant, this study was undertaken to verify the plausible anticancer effect of leaf methanol extracts of A. muricata (LEAM). Acute toxicity study was carried to obtain safe dose in mice models using haematological, biochemical, and histological evaluations in Swiss albino mice. In-vitro cytotoxicity towards Dalton's Lymphoma Ascites (DLA) and Ehrlich Ascites Carcinoma (EAC) cell lines were determined by trypan blue exclusion method. In-vivo antitumour activity of LEAM (100, 200, and 500mg/kg b.wt.) was evaluated using DLA induced solid carcinoma and EAC induced ascites carcinoma models and its comparison with standard drug Cisplatin. Acute toxicity studies did not exhibit significant variations in treated mice suggesting diminutive side effects of LEAM. Statistical analysis revealed the IC 50 values for DLA and EAC cell lines as 85.56 ± 5.28 and 68.07 ± 7.39 µg/mL, respectively, indicating better cytotoxic activity against EAC than DLA cells. LEAM decreased the tumour burden in dose-dependent manner. In comparison, with different concentrations tested, treatment with LEAM (200 mg/kg b.wt. and 500 mg/kg b.wt.) significantly reduced the solid tumour volume development by 58.11% and 65.70%, respectively. While lifespan was prolonged up to 51.43% in 500 mg/kg b.wt. LEAM treated ascites tumour-induced mice. This study thus indicates that LEAM possesses potent cytotoxic and antineoplastic activity and calls for more methodical safety assessments and other end-points of anti-tumourigenesis.

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