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Cytotoxicity of A β with redox active metals in neuronal cells has been implicated in the progression of Alzheimer’s disease (AD).Zn_7MT-3 protects cell against Aβ-Cu~(2+) toxicity.The roles of single domain proteins(α/β) andα-βdomain-domain interaction of Zn_7MT-3 in its anti-Aβ_(1-42)-Cu~(2+) toxicity activity were investigated herein.Aβ_(1-42) and four mutants of human MT3 (α/βdomain,β(MT3)-α(MTl) and A31-34) were prepared and characterized.Aβ_(1-42)-Cu~(2+) induced hydroxyl radical and ROS production with/without Zn-MTs were measured by fluorescence spectroscopy and DCFH-DA in living cells,respectively.These results indicate that the two domains form a co-operative unit and each of them is indispensable in conducting its bioactivity.
Cytotoxicity of A β with redox active metals in neuronal cells has been implicated in the progression of Alzheimer’s disease (AD) .Zn_7 MT-3 protects cells against Aβ-Cu 2+ toxicity. These roles of single domain proteins (α / β ) and α-βdomain-domain interaction of Zn_7MT-3 in its anti-Aβ_ (1-42) -Cu ~ (2 +) toxicity activity were examined herein.Aβ 1-42 and four mutants of human MT3 (α / , β (MT3) -α (MT1) and A31-34) were prepared and characterized.Aβ 1- (1-42) -Cu 2+ induced hydroxyl radical and ROS production with / without Zn-MTs were measured by fluorescence spectroscopy and DCFH-DA in living cells, respectively. These results that that the two domains form a co-operative unit and each of them is indispensable in conducting its bioactivity.