Prasunpriya Nayak

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It has been postulated that the neurotoxic effects of aluminium could be mediated through glutamate, an excitatory amino acid. Hence the effects of aluminium administration (at a dose of 4.2mg/kg body weight daily as aluminium chloride, hexahydrate, intraperitoneally, for 4 weeks) on glutamate and gamma-amino butyrate (GABA), an inhibitory amino acid, and(More)
Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for(More)
BACKGROUND The mechanism of aluminum-induced neurotoxicity is not clear. The involvement of glutamate in the aluminium-induced neurocomplications has been suggested. Brain glutamate levels also found to be altered in protein malnutrition. Alterations in glutamate levels as well as glutamate-alpha-decarboxylase in different regions of rat brain has been(More)
A variety of laboratory tests are available to assist in the diagnosis of alcohol consumption and related disorders. The levels of intake at which laboratory results become abnormal vary from person to person. Laboratory tests are particularly useful in settings where cooperativeness is suspected or when a history is not available. Several biochemical and(More)
BACKGROUND Alteration of glutamate and gamma-aminobutyrate system have been reported to be associated with neurodegenerative disorders and have been postulated to be involved in aluminum-induced neurotoxicity as well. Aluminum, an well known and commonly exposed neurotoxin, was found to alter glutamate and gamma-aminobutyrate levels as well as activities of(More)
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