The Role of Chemical Inhibition of Gap Junctional Intercellular Communication in Toxicology.
Abstract
Progress during this past grant period (3/1/92 - 4/30/93) has continued to mount, with new findings, new techniques to achieve our aims and objectives, and new support for our original working hypothesis that chemical modulation of gap junctional intercellular communication (GJIC) is involved in multiple formats of toxicity. We now have evidence on how certain tumor promoting chemicals, neurotoxicants, reproductive toxicants, teratogens or immunotoxicants can affect GJIC at either the transcriptional, translational or posttranslational levels. Using cells (a) mutated for altered GJIC; (b) transfected with various oncogenes; or (c) treated with different kinds of chemical toxicants, We have now elucidated the different mechanisms by which GJIC can be effected.. This new mechanistic understanding should contribute to a more biologically-based risk assessment model and an understanding of how epigenetic toxicants work. Gap junctions, Cell communication, Epigenetic toxicology, Neurotoxicants, Tumor promoters, Oncogenes, Chemical toxicity.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 19, 1993
- Accession Number
- ADA269251
Entities
People
- Burra V. Madhukar
- James E. Trosko
Organizations
- Michigan State University