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Titolo:
Agglomerates of ultrafine particles of elemental carbon and TiO2 induce generation of lipid mediators in alveolar macrophages
Autore:
Beck-Speier, I; Dayal, N; Karg, E; Maier, KL; Roth, C; Ziesenis, A; Heyder, J;
Indirizzi:
GSF, Natl Res Ctr Environm & Hlth, Inst Inhalat Biol, D-85758 Neuherberg, Germany GSF Neuherberg Germany D-85758 Inhalat Biol, D-85758 Neuherberg, Germany
Titolo Testata:
ENVIRONMENTAL HEALTH PERSPECTIVES
, volume: 109, anno: 2001, supplemento:, 4
pagine: 613 - 618
SICI:
0091-6765(200108)109:<613:AOUPOE>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
PARTICULATE AIR-POLLUTION; PLATELET-ACTIVATING-FACTOR; EICOSANOID PRODUCTION; HUMAN NEUTROPHILS; PROSTAGLANDINS; RELEASE; CELLS; LEUKOTRIENES; INVOLVEMENT; INHIBITION;
Keywords:
alveolar macrophages; cyclooxygenase; leukotrienes; 5-lipoxygenase; phospholipase A(2); prostaglandins; ultrafine particles;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Beck-Speier, I GSF, Natl Res Ctr Environm & Hlth, Inst Inhalat Biol, POB 1129, D-85758 Neuherberg, Germany GSF POB 1129 Neuherberg Germany D-85758 euherberg, Germany
Citazione:
I. Beck-Speier et al., "Agglomerates of ultrafine particles of elemental carbon and TiO2 induce generation of lipid mediators in alveolar macrophages", ENVIR H PER, 109, 2001, pp. 613-618

Abstract

Agglomerates of ultrafine particles (AUFPs) may cause adverse health effects because of their large surface area. To evaluate physiologic responses of immune cells, we studied whether agglomerates of 77-nm elemental carbon [(EC); specific surface area 750 m(2)/g] and 21 nm titanium dioxide (TiO2) particles (specific surface area 50 m(2)/g) affect the release of lipid mediators by alveolar macrophages (AMs), After 60-min incubation with 1 mug/mL AUFP-EC (corresponding to 7.5 cm(2) particle surface area), canine AMs (1 x10(6) cells/mL) released arachidonic acid (AA) and the cyclooxygenase (COX) products prostaglandin E-2 (PGE(2)), thromboxane B-2, and 12-hydroxyheptadecatrienoic acid but not 5-lipoxygenase (5-LO) products. AUFP-TiO2 with a 10-fold higher mass (10 mug/mL) than AUFP-EC, but a similar particle surface area (5 cm(2)) also induced AMs to release AA and COX products. Agglomerates of 250 nm TiO2 particles (specific surface area 6.5 m(2)/g) at 100 mug/mL mass concentration (particle surface area 6.5 cm2) showed the same response. Interestingly, 75 cm(2)/mL surface area of AUFP-EC and 16 cm(2)/mL surface area of AUFP-TiO2 additionally induced the release of the 5-LO products leukotriene B-4 and 5-hydroxyeicosatetraenoic acid. Respiratory burst activity of stimulated canine neutrophils was partially suppressed by supernatants of AMs treated with various mass concentrations of the three types of particles. Inhibition of neutrophil activity was abolished by supernatants of AMs treated with COX inhibitors prior to AUFP-incubation. This indicatesthat anti-inflammatory properties of PGE2 dominate the overall response oflipid mediators released by AUFP-affected AMs. In conclusion, our data indicate that surface area rather than mass concentration determines the effect of AUFPs, and that activation of phospholipase A(2) and COX pathway occurs at a lower particle surface area than that of 5-LO-pathway. We hypothesize a protective role of PGE2 in downregulating potential inflammatory reactions induced by ultrafine particles.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 00:06:34