Cargando…

Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.

Chemical pollutants in the Great Lakes have found their way through the food chain into humans because of their environmental persistence and lipophilicity. Some epidemiological studies have claimed an association between metabolites of 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT), polychlori...

Descripción completa

Detalles Bibliográficos
Autores principales: Kang, K S, Wilson, M R, Hayashi, T, Chang, C C, Trosko, J E
Formato: Texto
Lenguaje:English
Publicado: 1996
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1469268/
https://www.ncbi.nlm.nih.gov/pubmed/8820588
_version_ 1782127575179460608
author Kang, K S
Wilson, M R
Hayashi, T
Chang, C C
Trosko, J E
author_facet Kang, K S
Wilson, M R
Hayashi, T
Chang, C C
Trosko, J E
author_sort Kang, K S
collection PubMed
description Chemical pollutants in the Great Lakes have found their way through the food chain into humans because of their environmental persistence and lipophilicity. Some epidemiological studies have claimed an association between metabolites of 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT), polychlorinated biphenyls (PCBs), and polybrominated biphenyls (PBBs) and breast cancer, but others have reported no such association. We examined various halogenated hydrocarbons for their capacity to inhibit gap junctional intercellular communication (GJIC) in normal human breast epithelial cells (HBEC) when given as single compounds or as mixtures. The scrape-loading/dye transfer and fluorescent redistribution after photobleaching techniques were used to measure GJIC; immunostaining and Western and Northern analyses were performed on connexin 43 (Cx43) gap junction protein and message to determine how halogenated hydrocarbons might affect GJIC. DDT, dieldrin, and toxaphene inhibited GJIC in a dose-responsive manner after 90 min treatments. Dieldrin suppressed GJIC within 30 min with no recovery after 24 hr. Inhibition of GJIC by DDT and toxaphene was partially restored after 12 hr and fully restored after 24 hr. Several PCB and PBB congeners inhibited GJIC in a dose-responsive and time-dependent manner, but GJIC was almost restored to control values 24 hr after exposure. The highest concentrations of the individual chemicals that did not inhibit GJIC was determined, and mixtures containing two of these chemicals were tested for their ability to inhibit GJIC. Significant inhibition of GJIC was observed when cells were treated with a mixture of DDT and 2,4,5-hexachlorobiphenyl (2,4,5-HCB), dieldrin and 2,4,5-HCB, or dieldrin and 2,4,5-hexabromobiphenyl (2,4,5-HBB). These results indicate that halogenated hydrocarbons, alone or in specific combinations, can alter GJIC at the post-translational level. These results are consistent with the hypothesis that DDT, dieldrin, toxaphene, 2,3,4-HCB, 2,4,5-HCB, and 2,4,5-HBB could have tumor-promoting potential in human breast tissue.
format Text
id pubmed-1469268
institution National Center for Biotechnology Information
language English
publishDate 1996
record_format MEDLINE/PubMed
spelling pubmed-14692682006-06-01 Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures. Kang, K S Wilson, M R Hayashi, T Chang, C C Trosko, J E Environ Health Perspect Research Article Chemical pollutants in the Great Lakes have found their way through the food chain into humans because of their environmental persistence and lipophilicity. Some epidemiological studies have claimed an association between metabolites of 2,2-bis(p-chlorophenyl)-1,1,1-trichloroethane (DDT), polychlorinated biphenyls (PCBs), and polybrominated biphenyls (PBBs) and breast cancer, but others have reported no such association. We examined various halogenated hydrocarbons for their capacity to inhibit gap junctional intercellular communication (GJIC) in normal human breast epithelial cells (HBEC) when given as single compounds or as mixtures. The scrape-loading/dye transfer and fluorescent redistribution after photobleaching techniques were used to measure GJIC; immunostaining and Western and Northern analyses were performed on connexin 43 (Cx43) gap junction protein and message to determine how halogenated hydrocarbons might affect GJIC. DDT, dieldrin, and toxaphene inhibited GJIC in a dose-responsive manner after 90 min treatments. Dieldrin suppressed GJIC within 30 min with no recovery after 24 hr. Inhibition of GJIC by DDT and toxaphene was partially restored after 12 hr and fully restored after 24 hr. Several PCB and PBB congeners inhibited GJIC in a dose-responsive and time-dependent manner, but GJIC was almost restored to control values 24 hr after exposure. The highest concentrations of the individual chemicals that did not inhibit GJIC was determined, and mixtures containing two of these chemicals were tested for their ability to inhibit GJIC. Significant inhibition of GJIC was observed when cells were treated with a mixture of DDT and 2,4,5-hexachlorobiphenyl (2,4,5-HCB), dieldrin and 2,4,5-HCB, or dieldrin and 2,4,5-hexabromobiphenyl (2,4,5-HBB). These results indicate that halogenated hydrocarbons, alone or in specific combinations, can alter GJIC at the post-translational level. These results are consistent with the hypothesis that DDT, dieldrin, toxaphene, 2,3,4-HCB, 2,4,5-HCB, and 2,4,5-HBB could have tumor-promoting potential in human breast tissue. 1996-02 /pmc/articles/PMC1469268/ /pubmed/8820588 Text en
spellingShingle Research Article
Kang, K S
Wilson, M R
Hayashi, T
Chang, C C
Trosko, J E
Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title_full Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title_fullStr Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title_full_unstemmed Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title_short Inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, PCBs, and PBBs, alone or in mixtures.
title_sort inhibition of gap junctional intercellular communication in normal human breast epithelial cells after treatment with pesticides, pcbs, and pbbs, alone or in mixtures.
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1469268/
https://www.ncbi.nlm.nih.gov/pubmed/8820588
work_keys_str_mv AT kangks inhibitionofgapjunctionalintercellularcommunicationinnormalhumanbreastepithelialcellsaftertreatmentwithpesticidespcbsandpbbsaloneorinmixtures
AT wilsonmr inhibitionofgapjunctionalintercellularcommunicationinnormalhumanbreastepithelialcellsaftertreatmentwithpesticidespcbsandpbbsaloneorinmixtures
AT hayashit inhibitionofgapjunctionalintercellularcommunicationinnormalhumanbreastepithelialcellsaftertreatmentwithpesticidespcbsandpbbsaloneorinmixtures
AT changcc inhibitionofgapjunctionalintercellularcommunicationinnormalhumanbreastepithelialcellsaftertreatmentwithpesticidespcbsandpbbsaloneorinmixtures
AT troskoje inhibitionofgapjunctionalintercellularcommunicationinnormalhumanbreastepithelialcellsaftertreatmentwithpesticidespcbsandpbbsaloneorinmixtures