Skip Navigation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by BAUMAN, J. W.
Right arrow Articles by KLAASSEN, C. D.
Right arrow Search for Related Content
PubMed
Right arrow Articles by BAUMAN, J. W.
Right arrow Articles by KLAASSEN, C. D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1993 Oxford University Press

research-article

Production of Metallothionein and Heat-Shock Proteins in Response to Metals1

JOHN W. BAUMAN2, JIE LIU and CURTIS D. KLAASSEN3

Environmental Health and Occupational Medicine Center, Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center Kansas City, Kansas 66160-7417

Received September 29, 1992; accepted March 22, 1993

Acute stress, such as heat, and some metals, such as arsenite, will induce a specific group of stress proteins referred to as heat-shock proteins. The heat-shock proteins contribute to the survival of cells following a variety of stresses. Similarly, metals such as cadmium and zinc, will increase the levels of metallothionein (MT). The metal-binding protein, MT, has also been found to have a protective role in the cellular response to acute stresses like heavy metals. The purpose of the present study was to examine the production of these proteins in response to metals. Rat hepatocytes were maintained in monolayer culture for 22 hr, and subsequently treated with various concentrations of metals for 4 hr, or incubated at 43.5°C for 15–60 min. Following two washes with fresh media, the cells were labeled with [35S]-methionine (25 µCi/ml) in methionine-free media for 4 hr for determination of heat-shock protein production, or reincubated in fresh media for 20 hr for MT determination. Heat-shock protein production was determined by SDS-polyacrylamide gel electrophoresis followed by autoradiography. The autoradiograms were quantified by densitometric scanning. MT was determined by the Cd/hemoglobin affinity assay. Three metals (arsenite, cadmium, and zinc) strongly increased the heat-shock proteins. Whereas arsenite was a much less effective inducer of MT than was cadmium or zinc, arsenite was as effective as the other metals in inducing heat-shock proteins. Nickel was a good inducer of MT; however, it resulted in only a slight increase in the levels of heat-shock proteins. Heat-shock treatment was found to cause a major elevation in heat-shock proteins levels while actually decreasing the levels of MT. In conclusion, while similarities exist between induction of heat-shock protein and MT, there is not always a good correlation between the various stresses that induce heat-shock proteins and those that induce MT.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.