Accession Number : ADA323482

Title :   Oxidative Stress, Signal Transductions, Cell-Cell Communication.

Descriptive Note : Final rept. 15 May-14 Oct 96,

Corporate Author : MICHIGAN STATE UNIV EAST LANSING COLL OF HUMAN MEDICINE

Personal Author(s) : Trosko, James E.

PDF Url : ADA323482

Report Date : 27 FEB 1997

Pagination or Media Count : 9

Abstract : The objective of this research project was to study the mechanisms by which non-genotoxic or epigenetic chemicals induce multiple disease endpoints such as birth defects, tumor promotion, reproductive and neurotoxicities. The purpose is to develop a 'biologically-based' risk assessment model for human exposure to this class of toxic chemicals. The working hypothesis to have been tested was non-genotoxic chemicals disrupted homeostatic control of cell proliferation, differentiation and adaptive responses of differentiated cells. Three specific aims were designed to be tested (e.g., test a series of toxicants of interest to the USAFOSR for their ability to inhibit gap junctional function; to examine if these toxic chemicals alter the redox state of the cells; to determine if these chemicals alter apoptosis frequency via some oxidative damage-induced signal transduction mechanism). Results showed a structure-function relationship between PAH molecules and inhibition of gap junctions; jet fuels JP8 and JP4 were inhibitory to gap junctions; and perfluorinated fatty acids with chain length of 7 to 10 carbons were inhibitory to gap junctions.

Descriptors :   *STRESS(PHYSIOLOGY), *DEFECTS(MATERIALS), *ADAPTIVE SYSTEMS, *EXPOSURE(PHYSIOLOGY), *OXIDATION REDUCTION REACTIONS, *BIRTH, *REPRODUCTION(PHYSIOLOGY), *NEUROTOXINS, CHEMICALS, TOXICITY, NEOPLASMS, OXIDATION, TOXIC AGENTS, HUMAN BODY, HYPOTHESES, RESPONSE(BIOLOGY), CELLS(BIOLOGY), JET ENGINE FUELS, PROMOTION(ADVANCEMENT), FLUORINATION, HOMEOSTASIS, FATTY ACIDS.

Subject Categories : Biochemistry
      Medicine and Medical Research
      Toxicology

Distribution Statement : APPROVED FOR PUBLIC RELEASE