2,3,7,8-TCDD exposure, endothelial dysfunction and impaired microvascular reactivity

Vascular function was examined in subjects with long-term high level of serum 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) during their follow-up visits. Their earlier mean peak TCDD level at the time of exposure in 1965—1968 was estimated in the range of 3300—74 000 pg/g lipids. Ten former pesticide...

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Veröffentlicht in:Human & experimental toxicology 2007-09, Vol.26 (9), p.705-713
Hauptverfasser: Pelclová, Daniela, Prázný, Martin, Škrha, Jan, Fenclová, Zdenka, Kalousová, Marta, Urban, Pavel, Navrátil, Tomáš, Šenholdová, Zdenka, Šmerhovský, Zdeněk
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container_end_page 713
container_issue 9
container_start_page 705
container_title Human & experimental toxicology
container_volume 26
creator Pelclová, Daniela
Prázný, Martin
Škrha, Jan
Fenclová, Zdenka
Kalousová, Marta
Urban, Pavel
Navrátil, Tomáš
Šenholdová, Zdenka
Šmerhovský, Zdeněk
description Vascular function was examined in subjects with long-term high level of serum 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) during their follow-up visits. Their earlier mean peak TCDD level at the time of exposure in 1965—1968 was estimated in the range of 3300—74 000 pg/g lipids. Ten former pesticide production workers heavily exposed to TCDD (age 57 ± 2 years, TCDD about 170 pg/g lipids) were examined in 2001. Extended group of 15 TCDD-exposed men (age 59 ± 3 years, TCDD about 130 pg/g lipids) underwent the same examination in 2004. Findings were compared with a control group of 14 healthy men (age 54 ± 2 years). Skin microvascular reactivity (MVR) was measured by laser Doppler perfusion monitoring in the forearm during post-occlusive reactive hyperemia (PORH) and thermal hyperemia (TH). Several parameters of MVR in men exposed to TCDD were significantly impaired, compared with the control group and further progression of the impairment of MVR has been observed between years 2001 and 2004. Serum concentration of E-selectin and inhibitor of tissue plasminogen activator 1 (PAI-1) was significantly higher in exposed subjects (56.0 ± 18.4 ng/mL versus 40.0 ± 12.0 ng/mL, P = 0.022 and 90.9 ± 33.3 ng/mL versus 45.0 ± 18.0, P = 0.002, respectively). In addition, PORH in the forearm was significantly negatively associated with SOD activity (r = —0.77, P = 0.009) as well as the velocity of perfusion increase during TH (r = —0.68, P = 0.03) and TH% (r = —0.78, P = 0.008). Our data document the presence of endothelial dysfunction in TCDD-exposed men. Human & Experimental Toxicology (2007) 26, 705—713
doi_str_mv 10.1177/0960327107083971
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Serum concentration of E-selectin and inhibitor of tissue plasminogen activator 1 (PAI-1) was significantly higher in exposed subjects (56.0 ± 18.4 ng/mL versus 40.0 ± 12.0 ng/mL, P = 0.022 and 90.9 ± 33.3 ng/mL versus 45.0 ± 18.0, P = 0.002, respectively). In addition, PORH in the forearm was significantly negatively associated with SOD activity (r = —0.77, P = 0.009) as well as the velocity of perfusion increase during TH (r = —0.68, P = 0.03) and TH% (r = —0.78, P = 0.008). Our data document the presence of endothelial dysfunction in TCDD-exposed men. 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Their earlier mean peak TCDD level at the time of exposure in 1965—1968 was estimated in the range of 3300—74 000 pg/g lipids. Ten former pesticide production workers heavily exposed to TCDD (age 57 ± 2 years, TCDD about 170 pg/g lipids) were examined in 2001. Extended group of 15 TCDD-exposed men (age 59 ± 3 years, TCDD about 130 pg/g lipids) underwent the same examination in 2004. Findings were compared with a control group of 14 healthy men (age 54 ± 2 years). Skin microvascular reactivity (MVR) was measured by laser Doppler perfusion monitoring in the forearm during post-occlusive reactive hyperemia (PORH) and thermal hyperemia (TH). Several parameters of MVR in men exposed to TCDD were significantly impaired, compared with the control group and further progression of the impairment of MVR has been observed between years 2001 and 2004. Serum concentration of E-selectin and inhibitor of tissue plasminogen activator 1 (PAI-1) was significantly higher in exposed subjects (56.0 ± 18.4 ng/mL versus 40.0 ± 12.0 ng/mL, P = 0.022 and 90.9 ± 33.3 ng/mL versus 45.0 ± 18.0, P = 0.002, respectively). In addition, PORH in the forearm was significantly negatively associated with SOD activity (r = —0.77, P = 0.009) as well as the velocity of perfusion increase during TH (r = —0.68, P = 0.03) and TH% (r = —0.78, P = 0.008). Our data document the presence of endothelial dysfunction in TCDD-exposed men. Human &amp; Experimental Toxicology (2007) 26, 705—713</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>17984141</pmid><doi>10.1177/0960327107083971</doi><tpages>9</tpages></addata></record>
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subjects Aged
Biological and medical sciences
Blood Flow Velocity - drug effects
Cardiovascular Diseases - blood
Cardiovascular Diseases - chemically induced
Cardiovascular Diseases - physiopathology
Chemical and industrial products toxicology. Toxic occupational diseases
E-Selectin - blood
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiopathology
Follow-Up Studies
Forearm - blood supply
Health risk assessment
Human exposure
Humans
Hyperemia - physiopathology
Intercellular Adhesion Molecule-1 - blood
Laser-Doppler Flowmetry
Lipids - blood
Male
Medical sciences
Men
Microcirculation - drug effects
Occupational Diseases - blood
Occupational Diseases - chemically induced
Occupational Diseases - physiopathology
Occupational Exposure
Occupational hazards
Pesticides
Pesticides - blood
Pesticides - toxicity
Plasminogen Activator Inhibitor 1 - blood
Polychlorinated Dibenzodioxins - blood
Polychlorinated Dibenzodioxins - toxicity
Regional Blood Flow - drug effects
Skin - blood supply
Superoxide Dismutase - blood
Time Factors
Toxicity
Toxicology
Various organic compounds
Vein & artery diseases
title 2,3,7,8-TCDD exposure, endothelial dysfunction and impaired microvascular reactivity
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