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Inhibited intercellular communication as a mechanistic link between teratogenesis and carcinogenesis.

Authors
Loch-Caruso-R; Trosko-JE
Source
Crit Rev Toxicol 1985 Jan; 16(2):157-183
NIOSHTIC No.
00164360
Abstract
The potential role of inhibited intercellular communication as a mechanism of disruptive differentiation in teratogenesis and carcinogenesis was explored. Gap structure between adjacent cells can be monitored by measurements of electrocoupling, junctional permeability, fluorescent dye transfer, intercellular exchange of metabolites through direct cell contact, and electronmicrograph visualization. The communicating junction appears to be modulated by calcium concentration, acidity, hormones, phosphorylation, and level of cyclic adenosine-monophosphate. Carcinogenic initiators are agents or conditions which can induce stable and irreversible genomic changes, while promoters act as selective mitogens. Chemicals which influence carcinogenesis do not seem to fit into neat categories of pure initiators and promoters. There seems to be a good correlation between depressed junctional communication and cancerous growth. In carcinogenesis, the initiated cell remains inactive until stimulated to proliferate by a tumor promoter. Direct interruption of junctional communication may be a common mechanism of action for tumor promoters that are also teratogens. Parameters that influence teratogenesis are dose, route of delivery, metabolism, embryonic stage of development, and genetic predisposition. Mechanisms involved in teratogenesis include cell death, abnormal membrane characteristics, and altered amounts of metabolic components. Formation and disappearance of gap junctions have been associated with major morphogenic events in several embryonic species and tissues. Inhibition of gap junction mediated communication may interfere with embryonic development. Direct intercellular communication is a likely method to control distribution of small morphogenic substances. Inhibitory signal may be transmitted through the gap junction. Several teratogens interfere with gap junction mediated metabolic cooperation.
Keywords
Carcinogenicity; Teratogenicity; Mutagenicity; Embryotoxicity; Cytotoxicity; Cell-differentiation; Cell-wall-permeability; Tumor-inhibition; Cellular-structures; Physiological-chemistry; NIOSH-Publication; NIOSH-Grant
CODEN
CRTXB2
Publication Date
19850101
Document Type
Journal Article
Funding Amount
44380.00
Funding Type
Grant
Fiscal Year
1985
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-K01-OH-00024
Issue of Publication
2
ISSN
1040-8444
Source Name
Critical Reviews in Toxicology
State
MI
Performing Organization
Pediatrics and Human Devel Michigan State University B238 Life Science Building East Lansing, Mich 48824
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