Accession Number : ADA192439
Title : The Role of Chemical Inhibition of Gap Junctional Intercellular Communication in Toxicology.
Descriptive Note : Annual rept. 15 Feb 87-14 Feb 88,
Corporate Author : MICHIGAN STATE UNIV EAST LANSING DEPT OF PEDIATRICS/HUMAN DEVELOPMENT
Personal Author(s) : Trosko, James E
PDF Url : ADA192439
Report Date : 14 Feb 1988
Pagination or Media Count : 27
Abstract : Our goal has been to study the mechanism by which non-genotoxic chemicals act. To this end, we are testing the hypothesis that chemical modulation of gap junctional intercellular communication can lead to many toxic endpoints, such as teratogenesis, tumor promotion, immune-, reproductive and neurotoxicities. Our aims have been (a) to study the biochemical mechanisms by which inhibitors of gap junctions work; (b) to develop and apply new in vitro techniques to measure gap junction function; and (c) to test if known non-genotoxic chemicals inhibit gap junctions in various cell types. Results to data have validated the 'fluorescence recovery after photobleaching' and scrape-loading/dye transfer techniques for measuring gap junction function. In addition, we have shown that protein kinase C, the ras oncogene and the neurotoxicant, heptachlor, all seem to work via different mechanisms to block intercellular communication. Results described in this report have been communicated at several meetings, while abstracts, preprints and reprints of these reports are attached to the progress report.
Descriptors : *CYTOCHEMISTRY, *TOXICOLOGY, BIOCHEMISTRY, CELLS(BIOLOGY), CHEMICAL REACTIONS, CHEMICALS, COMMUNICATION AND RADIO SYSTEMS, FLUORESCENCE, HYPOTHESES, IN VITRO ANALYSIS, INHIBITION, MODULATION, NEOPLASMS, PROMOTION(ADVANCEMENT), RECOVERY, REPRINTS, TERATOGENIC COMPOUNDS, TOXICITY, TRANSPORT PROPERTIES, HOMEOSTASIS, PHOSPHORUS TRANSFERASES, PROTEINS
Subject Categories : Biochemistry
Distribution Statement : APPROVED FOR PUBLIC RELEASE