Biochemistry of Copper

Linder, Maria C.

doi:10.1007/978-1-4757-9432-8

Cited by 411 publications

(523 citation statements)

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“…Importantly, the effect was observed with physiological concentrations of Cu, as body fluid and synaptic Cu levels have been reported at -10 and 250 pM, respectively (Kardos et al, 1989). In addition, the concentration of Cu in the cerebrospinal fluid has been measured as 78 pA4 (Linder, 1991). Similar levels of Cu toxicity were achieved using biologically bound Cu (Cul glycine complex) (data not shown), further supporting the physiological relevance of our findings.…”

Section: Discussionsupporting

confidence: 84%

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

White

Bush

Beyreuther

et al. 1999

Journal of Neurochemistry

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Perturbations to glutathione (GSH) metabolism may play an important role in neurodegenerative disorders such as Alzheimer's, Parkinson's, and prion diseases. A primary function of GSH is to prevent the toxic interaction between free radicals and reactive transition metals such as copper (Cu). Due to the potential role of Cu in neurodegeneration, we examined the effect of GSH depletion on Cu toxicity in murine primary neuronal cultures. Depletion of cellular GSH with L-buthionine-[S,R]-sulfoximine resulted in a dramatic potentiation of Cu toxicity in neurons without effect on iron (Fe) toxicity. Similarly, inhibition of glutathione reductase (GR) activity with 1,3-bis(2-chloroethyl)-l -nitrosurea also increased Cu toxicity in neurons. To determine if the Alzheimer's amyloid-p (Ap) peptide can affect neuronal resistance to transition metal toxicity, we exposed cultures to nontoxic concentrations of Ap25-35 in the presence or absence of Cu or Fe. Ap25-35 pretreatment was found to deplete neuronal GSH and increase GR activity, confirming the ability of Ap to perturb neuronal GSH homeostasis.Ap25-35 pretreatment potently increased Cu toxicity but had no effect on Fe toxicity. These studies demonstrate an important role for neuronal GSH homeostasis in selective protection against Cu toxicity, a finding with widespread implications for neurodegenerative disorders.

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Section: Discussionsupporting

confidence: 84%

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

White

Bush

Beyreuther

et al. 1999

Journal of Neurochemistry

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“…C opper is an essential element for all living organisms, where it constitutes the prosthetic, active group of many proteins and enzymes (1). Copper is also very toxic in the free form because of its ability to produce radicals by cycling between oxidized Cu(II) and reduced Cu(I).…”

mentioning

confidence: 99%

A redox switch in CopC: An intriguing copper trafficking protein that binds copper(I) and copper(II) at different sites

Arnesano

Banci

Bertini

et al. 2003

Proc. Natl. Acad. Sci. U.S.A.

169

180

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“…Copper functions as an important cofactor for a variety of enzymes that are required for essential biochemical processes such as cytochrome c oxidase, Cu,Zn superoxide dismutase, lysyl oxidase, and dopamine-␤-hydroxylase (32). On the other hand, Cu can participate in Fenton-like reactions that can generate extremely reactive hydroxyl radicals which cause cellular damage such as the oxidation of proteins, cleavage of DNA and RNA molecules, and membrane damage due to lipid peroxidation (18).…”

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confidence: 99%

Dynamic Regulation of Copper Uptake and Detoxification Genes in Saccharomyces cerevisiae

Peña

Koch

Thiele

1998

Molecular and Cellular Biology

171

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The essential yet toxic nature of copper demands tight regulation of the copper homeostatic machinery to ensure that sufficient copper is present in the cell to drive essential biochemical processes yet prevent the accumulation to toxic levels. In Saccharomyces cerevisiae, the nutritional copper sensor Mac1p regulates the copper-dependent expression of the high affinity Cu(I) uptake genes CTR1, CTR3, and FRE1, while the toxic copper sensor Ace1p regulates the transcriptional activation of the detoxification genes CUP1, CRS5, and SOD1 in response to copper. In this study, we characterized the tandem regulation of the copper uptake and detoxification pathways in response to the chronic presence of elevated concentrations of copper ions in the growth medium. Upon addition of CuSO 4 , mRNA levels of CTR3 were rapidly reduced to eightfold the original basal level whereas the Ace1p-mediated transcriptional activation of CUP1 was rapid and potent but transient.

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Biochemistry of Copper

Cited by 411 publications

References 0 publications

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

Exacerbation of Copper Toxicity in Primary Neuronal Cultures Depleted of Cellular Glutathione

A redox switch in CopC: An intriguing copper trafficking protein that binds copper(I) and copper(II) at different sites

Dynamic Regulation of Copper Uptake and Detoxification Genes in Saccharomyces cerevisiae

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