Exposure to polychlorinated biphenyls causes endothelial cell dysfunction.

Michal J Toborek, S. W. Barger, M. P. Mattson, P. Espandiari, L. W. Robertson, B. Hennig

Research output: Contribution to journalArticle

110 Citations (Scopus)

Abstract

Environmental chemicals, such as polychlorinated biphenyls (PCBs), may be atherogenic by disrupting normal functions of the vascular endothelium. To investigate this hypothesis, porcine pulmonary artery-derived endothelial cells were exposed to 3,3',4,4'-tetrachlorobiphenyl (PCB 77), 2,3,4,4',5-pentachlorobiphenyl (PCB 114), or 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) for up to 24 hours. These PCBs were selected for their varying binding avidities with the aryl hydrocarbon (Ah) receptor and differences in their induction of cytochrome P450. PCB 77 and PCB 114 significantly disrupted, in a dose-dependent manner, endothelial barrier function by allowing an increase in albumin transfer across endothelial monolayers. These PCBs also contributed markedly to cellular oxidative stress, as measured by 2,7-dichlorofluorescin (DCF) fluorescence and lipid hydroperoxides, and caused a significant increase in intracellular calcium ([Ca2+]i) levels. Enhanced oxidative stress and [Ca2+]i in PCB 77- and PCB 114-treated cells were accompanied by increased activity and content of cytochrome P450 1A and by a decrease in the vitamin E content in the culture medium. In contrast to the effects of PCB 77 and PCB 114, cell exposure to PCB 153 had no effect on cellular oxidation, [Ca2+]i, or endothelial barrier function. These results suggest that certain PCBs may play a role in the development of atherosclerosis by causing endothelial cell dysfunction and a decrease in the barrier function of the vascular endothelium. It is possible that interaction of PCBs with the Ah receptor and activation of the cytochrome P450 1A subfamily are involved in this pathology.

Original languageEnglish
Pages (from-to)219-226
Number of pages8
JournalJournal of Biochemical Toxicology
Volume10
Issue number4
StatePublished - Aug 1 1995
Externally publishedYes

Fingerprint

Polychlorinated Biphenyls
Endothelial cells
Endothelial Cells
Cytochrome P-450 Enzyme System
Aryl Hydrocarbon Receptors
3,4,3',4'-tetrachlorobiphenyl
Oxidative stress
2,4,5,2',4',5'-hexachlorobiphenyl
Vascular Endothelium
Oxidative Stress
Lipid Peroxides
Pathology
Vitamin E
Pulmonary Artery
Culture Media
Albumins
Monolayers

ASJC Scopus subject areas

  • Toxicology

Cite this

Toborek, M. J., Barger, S. W., Mattson, M. P., Espandiari, P., Robertson, L. W., & Hennig, B. (1995). Exposure to polychlorinated biphenyls causes endothelial cell dysfunction. Journal of Biochemical Toxicology, 10(4), 219-226.

Exposure to polychlorinated biphenyls causes endothelial cell dysfunction. / Toborek, Michal J; Barger, S. W.; Mattson, M. P.; Espandiari, P.; Robertson, L. W.; Hennig, B.

In: Journal of Biochemical Toxicology, Vol. 10, No. 4, 01.08.1995, p. 219-226.

Research output: Contribution to journalArticle

Toborek, MJ, Barger, SW, Mattson, MP, Espandiari, P, Robertson, LW & Hennig, B 1995, 'Exposure to polychlorinated biphenyls causes endothelial cell dysfunction.', Journal of Biochemical Toxicology, vol. 10, no. 4, pp. 219-226.
Toborek MJ, Barger SW, Mattson MP, Espandiari P, Robertson LW, Hennig B. Exposure to polychlorinated biphenyls causes endothelial cell dysfunction. Journal of Biochemical Toxicology. 1995 Aug 1;10(4):219-226.
Toborek, Michal J ; Barger, S. W. ; Mattson, M. P. ; Espandiari, P. ; Robertson, L. W. ; Hennig, B. / Exposure to polychlorinated biphenyls causes endothelial cell dysfunction. In: Journal of Biochemical Toxicology. 1995 ; Vol. 10, No. 4. pp. 219-226.
@article{21112f89c57143e198b291405fff0888,
title = "Exposure to polychlorinated biphenyls causes endothelial cell dysfunction.",
abstract = "Environmental chemicals, such as polychlorinated biphenyls (PCBs), may be atherogenic by disrupting normal functions of the vascular endothelium. To investigate this hypothesis, porcine pulmonary artery-derived endothelial cells were exposed to 3,3',4,4'-tetrachlorobiphenyl (PCB 77), 2,3,4,4',5-pentachlorobiphenyl (PCB 114), or 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) for up to 24 hours. These PCBs were selected for their varying binding avidities with the aryl hydrocarbon (Ah) receptor and differences in their induction of cytochrome P450. PCB 77 and PCB 114 significantly disrupted, in a dose-dependent manner, endothelial barrier function by allowing an increase in albumin transfer across endothelial monolayers. These PCBs also contributed markedly to cellular oxidative stress, as measured by 2,7-dichlorofluorescin (DCF) fluorescence and lipid hydroperoxides, and caused a significant increase in intracellular calcium ([Ca2+]i) levels. Enhanced oxidative stress and [Ca2+]i in PCB 77- and PCB 114-treated cells were accompanied by increased activity and content of cytochrome P450 1A and by a decrease in the vitamin E content in the culture medium. In contrast to the effects of PCB 77 and PCB 114, cell exposure to PCB 153 had no effect on cellular oxidation, [Ca2+]i, or endothelial barrier function. These results suggest that certain PCBs may play a role in the development of atherosclerosis by causing endothelial cell dysfunction and a decrease in the barrier function of the vascular endothelium. It is possible that interaction of PCBs with the Ah receptor and activation of the cytochrome P450 1A subfamily are involved in this pathology.",
author = "Toborek, {Michal J} and Barger, {S. W.} and Mattson, {M. P.} and P. Espandiari and Robertson, {L. W.} and B. Hennig",
year = "1995",
month = "8",
day = "1",
language = "English",
volume = "10",
pages = "219--226",
journal = "Journal of Biochemical and Molecular Toxicology",
issn = "1095-6670",
publisher = "John Wiley and Sons Inc.",
number = "4",

}

TY - JOUR

T1 - Exposure to polychlorinated biphenyls causes endothelial cell dysfunction.

AU - Toborek, Michal J

AU - Barger, S. W.

AU - Mattson, M. P.

AU - Espandiari, P.

AU - Robertson, L. W.

AU - Hennig, B.

PY - 1995/8/1

Y1 - 1995/8/1

N2 - Environmental chemicals, such as polychlorinated biphenyls (PCBs), may be atherogenic by disrupting normal functions of the vascular endothelium. To investigate this hypothesis, porcine pulmonary artery-derived endothelial cells were exposed to 3,3',4,4'-tetrachlorobiphenyl (PCB 77), 2,3,4,4',5-pentachlorobiphenyl (PCB 114), or 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) for up to 24 hours. These PCBs were selected for their varying binding avidities with the aryl hydrocarbon (Ah) receptor and differences in their induction of cytochrome P450. PCB 77 and PCB 114 significantly disrupted, in a dose-dependent manner, endothelial barrier function by allowing an increase in albumin transfer across endothelial monolayers. These PCBs also contributed markedly to cellular oxidative stress, as measured by 2,7-dichlorofluorescin (DCF) fluorescence and lipid hydroperoxides, and caused a significant increase in intracellular calcium ([Ca2+]i) levels. Enhanced oxidative stress and [Ca2+]i in PCB 77- and PCB 114-treated cells were accompanied by increased activity and content of cytochrome P450 1A and by a decrease in the vitamin E content in the culture medium. In contrast to the effects of PCB 77 and PCB 114, cell exposure to PCB 153 had no effect on cellular oxidation, [Ca2+]i, or endothelial barrier function. These results suggest that certain PCBs may play a role in the development of atherosclerosis by causing endothelial cell dysfunction and a decrease in the barrier function of the vascular endothelium. It is possible that interaction of PCBs with the Ah receptor and activation of the cytochrome P450 1A subfamily are involved in this pathology.

AB - Environmental chemicals, such as polychlorinated biphenyls (PCBs), may be atherogenic by disrupting normal functions of the vascular endothelium. To investigate this hypothesis, porcine pulmonary artery-derived endothelial cells were exposed to 3,3',4,4'-tetrachlorobiphenyl (PCB 77), 2,3,4,4',5-pentachlorobiphenyl (PCB 114), or 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) for up to 24 hours. These PCBs were selected for their varying binding avidities with the aryl hydrocarbon (Ah) receptor and differences in their induction of cytochrome P450. PCB 77 and PCB 114 significantly disrupted, in a dose-dependent manner, endothelial barrier function by allowing an increase in albumin transfer across endothelial monolayers. These PCBs also contributed markedly to cellular oxidative stress, as measured by 2,7-dichlorofluorescin (DCF) fluorescence and lipid hydroperoxides, and caused a significant increase in intracellular calcium ([Ca2+]i) levels. Enhanced oxidative stress and [Ca2+]i in PCB 77- and PCB 114-treated cells were accompanied by increased activity and content of cytochrome P450 1A and by a decrease in the vitamin E content in the culture medium. In contrast to the effects of PCB 77 and PCB 114, cell exposure to PCB 153 had no effect on cellular oxidation, [Ca2+]i, or endothelial barrier function. These results suggest that certain PCBs may play a role in the development of atherosclerosis by causing endothelial cell dysfunction and a decrease in the barrier function of the vascular endothelium. It is possible that interaction of PCBs with the Ah receptor and activation of the cytochrome P450 1A subfamily are involved in this pathology.

UR - http://www.scopus.com/inward/record.url?scp=0029349247&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029349247&partnerID=8YFLogxK

M3 - Article

C2 - 8568836

AN - SCOPUS:0029349247

VL - 10

SP - 219

EP - 226

JO - Journal of Biochemical and Molecular Toxicology

JF - Journal of Biochemical and Molecular Toxicology

SN - 1095-6670

IS - 4

ER -