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Titolo:
PULMONARY PROINFLAMMATORY GENE INDUCTION FOLLOWING ACUTE EXPOSURE TO RESIDUAL OIL FLY-ASH - ROLES OF PARTICLE-ASSOCIATED METALS
Autore:
KODAVANTI UP; JASKOT RH; COSTA DL; DREHER KL;
Indirizzi:
US EPA,NHEERL,ETD,PTB,MD-82 RES TRIANGLE PK NC 27711 US EPA,NHEERL,ETD,PTB RES TRIANGLE PK NC 27711
Titolo Testata:
Inhalation toxicology
fascicolo: 7, volume: 9, anno: 1997,
pagine: 679 - 701
SICI:
0895-8378(1997)9:7<679:PPGIFA>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; ADHESION MOLECULE-1 EXPRESSION; NORMAL HUMAN KERATINOCYTES; FACTOR-KAPPA-B; ALVEOLAR MACROPHAGES; FACTOR-ALPHA; ENDOTHELIAL ACTIVATION; NUCLEOTIDE-SEQUENCE; DUST EXPOSURE; TNF-ALPHA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
U.P. Kodavanti et al., "PULMONARY PROINFLAMMATORY GENE INDUCTION FOLLOWING ACUTE EXPOSURE TO RESIDUAL OIL FLY-ASH - ROLES OF PARTICLE-ASSOCIATED METALS", Inhalation toxicology, 9(7), 1997, pp. 679-701

Abstract

Residual oil fly ash (ROFA), an emission source particulate, has beenshown to induce acute icing injury and fibrosis in the rat. However, the mechanism(s) and the identities of various inflammatory mediators induced by ROFA are not known. Also the extent to which ROFA-associated metals contribute to proinflammatory gene induction is yet to be determined. To examine the mechanism of ROFA-induced lung injury, male Sprague-Dawley rats (60 days old) were intratracheally instilled with 0.3 ml of either acidified saline (brought to pH 2.5 using H2SO4, similar to the pH of the ROFA suspension in saline), ROFA (2.5 mg/rat in saline, yields pH of 2.5), or predominant ROFA-associated metals such as Fe-2(SO4)(3) (Fe, 0.54 mu mol/rat), VSO4 (V, 1.7 mu mol/rat), and NiSO4 (Ni, 1.0 mu mol/rat), individually or as a mixture (Fe + V + Ni). The quantity of metals instilled reflected the amount present in the leachable material of ROFA. Histopathological findings indicated marked and progressive acute focal lung injury characterized by inflammation, edema, alveolar cell hyperplasia, thickening of the alveolar and airway walls, and bronchiolar secretory cell hypertrophy following ROFA exposure. The metal mixture induced similar pathology; however, the severity of lesions appeared less pronounced than with ROFA. Ni by itself caused the most severe damage, hemorrhage and inflammation, while V andFe alone at a concentration present in ROFA produced less severe pathology. ROFA-instilled rats showed denudation of airway epithelium at 3h that was less severe with individual metals and the metal mixture. Focal alveolar fibrosis was round in the case of ROFA and the metal mixture, and alveolar wall hyperplasia in the case of Ni, which pre dominated at 96 h postinstillation. Results obtained from semiquantitativereverse transcription-polymerase chain reaction (RT-PCR) analyses indicated that interleukin 1 beta (IL-1 beta) and IL-5 were induced as early as 3 h and returned to control levels by 24 h following ROFA exposure. The metal mixture as well as Fe and V produced similar induction of IL-1 beta and IL-5 at 3 h. Although the extent of IL-1 beta and IL-5 induction by Ni was similar to ROFA at 3 h, unlike ROFA or the othermetals, this induction persisted for up to 96 h postexposure. Macrophage inflammatory protein 2 (MIP-2) and IL-6 mRNA were induced by ROFA,the metal mixture, and individual metals, as early as 3 h after instillation. Both cytokines remained elevated especially in ROFA-, metal mixture-, and Ni-instilled rats at 24 h. MIP-2 expression remained elevated through 96 h in Ni-instilled rats. Surprisingly, tumor necrosis factor alpha (TNF-alpha) mRNA was not affected by ROFA or metals at anytime points examined. Vascular cell adhesion molecule-1 (VCAM-1) expression was increased slightly by ROFA, the metal mixture, and Ni, but not by Fe or V, at 3 h and returned to control levels by 24 h postexposure, E-selectin mRNA increased following ROFA, metal mix, V, and Ni instillation at 3 h, again returning to control levels by 24 h postexposure. These studies suggest that ROFA could induce a number of proinflammatory cytokine genes very early and that much of this induction wasdue to ROFA-associated metals. Overall, the persistency and the extent of cytokine induction over 96 h by ROFA and metals were in the orderof Ni > ROFA greater than or equal to metal mix greater than or equalto V greater than or equal to Fe. The persistency cytokine induction rather than degree was more closely associated with the histopathologyinduced by ROFA and associated metals.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/04/20 alle ore 12:06:24