Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/105
Full metadata record
DC FieldValueLanguage
dc.contributor.authorDas, K.K.-
dc.contributor.authorDas, S.N.-
dc.contributor.authorDhundasi, S.A.-
dc.date.accessioned2021-03-25T06:50:28Z-
dc.date.available2021-03-25T06:50:28Z-
dc.date.issued2008-03-
dc.identifier.urihttp://hdl.handle.net/123456789/105-
dc.description.abstractNickel-induced toxicity and carcinogenicity, with an emphasis on the generation and role of reactive oxygen species is reviewed. Nickel is a known haematotoxic, immunotoxic, neurotoxic, genotoxic, reproductive toxic, pulmonary toxic, nephrotoxic , hepatotoxic and carcinogenic agent. This article presents a selective review on nickel and effect of its acute, subchronic and chronic doses on certain metabolically active tissues in human as well as animals. Nickel exposure causes formation of free radicals in various tissues in both human and animals which lead to various modifications to DNA bases, enhanced lipid peroxidation, and altered calcium and sulphhydryl homeostasis. The primary route for nickel toxicity is depletion of glutathione and bonding to sulphhydryl groups of proteins. Nickel homeostasis, nickel-induced activation of signaling pathways and the protective role of enzymatic and non-enzymatic antioxidants against nickel toxicity and carcinogenicity are also discussed.en_US
dc.language.isoen_USen_US
dc.relation.ispartofseries412-425;-
dc.subjectAcute toxicity - antioxidant defense - chronic toxicity - nickel - oxidative stress - subchronic toxicityen_US
dc.titleNickel, its adverse health effects & oxidative stressen_US
dc.typeArticleen_US
Appears in Collections:F P

Files in This Item:
File Description SizeFormat 
2008_1.pdf159.88 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.