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Toxicological Sciences 2006 91(1):1-3; doi:10.1093/toxsci/kfj149
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

TOXICOLOGICAL HIGHLIGHT

Metallothionein and Anti-Metallothionein, Complementary Elements of Cadmium-Induced Renal Disease

Michael A. Lynes1 and Xiuyun Yin

Department of Molecular and Cell Biology, University of Connecticut, Storrs, Connecticut 06269-3125

1 To whom correspondence should be addressed at Department of Molecular and Cell Biology, 91 N. Eagleville Road, University of Connecticut, Storrs, CT 06269-3125. E-mail: michael.lynes@uconn.edu.

Received March 1, 2006; accepted March 2, 2006

Key Words: metallothionein; nephropathy; immune complex; inflammation; cadmium.

The first 150 words of the full text of this article appear below.

Metallothionein (MT) is a low–molecular weight, cysteine-rich stress response protein with a high affinity for divalent heavy metals. MT was originally identified as a cadmium-rich protein in the equine renal cortex. A large amount of subsequent work has shown MT to serve in many cell types in the management of essential divalent metal cations, to interfere with the toxic effects of xenobiotics, heavy metals, and free radicals, and to serve as a regulator of specific transcription factors. As a consequence of these various activities, MT synthesis has an impact on developmental processes and on the cellular responses to stressful conditions (reviewed in (Klaassen et al., 1999Go; Vasak, 2005Go)).

MT is primarily synthesized on free polysomes (Shapiro et al., 1980). Based on these observations, MT has often been considered to function exclusively as an intracellular protein. While MT lacks the signal peptide sequences or other protein trafficking . . . [Full Text of this Article]


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