Please use this identifier to cite or link to this item: http://localhost:80/xmlui/handle/123456789/16110
Title: Change in metabolic status of glutathione by palladium nitrate in blood components
Authors: Muhammad Mukhtiar
Khan, Muhammad Farid
Jan, Syed Umer
Khan, Haroon
Naseem Ullah
Amir Badshah
Keywords: Palladium Nitrate [Pd (NO3)2]
Glutathione (GSH)
Di,thiobis-dinitrobenzoic acid (DTNB)
Blood Components
Plasma
Cytosolic Fraction (CF)
palladium ( Pd+2)
palladium Glutathione complex (Pd-SG).
Issue Date: 20-Jan-2013
Publisher: Karachi: Pakistan Botanical Society, University of Karachi
Citation: Mukhtiar, M., Khan, M. F., Jan, S. U., Khan, H., Ullah, N., & Badshah, A. (2013). Change in metabolic status of glutathione by palladium nitrate in blood components. Pakistan Journal of Pharmaceutical Sciences, 26(1), 131-135.
Abstract: This piece of research work present the toxicological impact of varied concentrations of Palladium Nitrate [Pd (NO3)2] by changing the chemical status of glutathione and the way how glutathione plays its role in detoxification and conjugation processes of [Pd (NO3)2] in whole blood components (plasma and Cytosolic fraction). The impact of different concentration of [Pd (NO3)2] on reduced glutathione level in whole blood component(Plasma and Cytosolic fraction) were measured spectrophotometrically following Standard Ellman’s method. Compared with control sample, significant decrease in the GSH content in whole blood components (plasma and Cytosolic fraction) was obtained with various concentrations (100µM-1000µM) of Palladium Nitrate. Depleted GSH level was more pronounced with time incubation period (0-90) minutes. These finding shows that changes in the GSH status produced by palladium nitrate could either be due to palladium nitrate and glutathione( Pd-SG) complex formation or by conversion of reduce glutathione (2GSH + Pd+2 → GSSG). This change in the GSH metabolic status provides information regarding the mechanism of palladium, in blood components.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/16110
ISSN: 1011-601X
Appears in Collections:Issue 01

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