Time course of systemic oxidative stress and inflammatory response induced by an acute exposure to Residual Oil Fly Ash.

MARCHINI, TIMOTEO; MAGNANI, NATALIA; VANASCO, VIRGINIA; PAZ, MARIELA; TASAT, DEBORAH; GONZALEZ MAGLIO, DANIEL; ALVAREZ, SILVIA; EVELSON, PABLO

TOXICOLOGY AND APPLIED PHARMACOLOGY

ACADEMIC PRESS INC ELSEVIER SCIENCE

Lugar: Amsterdam; Año: 2014 vol. 274 p. 274 - 282

0041-008X

Abstract: It is suggested that systemic oxidative stress and inflammation play a central role in the onsetand progression of cardiovascular diseases associated with the exposure to particulate matter (PM).The aim of this work was to evaluate the time changes of systemic markers of oxidative stress andinflammation, after an acute exposure to Residual Oil Fly Ash (ROFA). Female Swiss mice wereintranasally instilled with a ROFA suspension (1.0 mg/kg body weight) or saline solution, and plasmalevels of oxidative damage markers [thiobarbituric acid reactive substances (TBARS) and proteincarbonyls], antioxidant status [reduced (GSH) and oxidized (GSSG) glutathione, ascorbic acid levels,and superoxide dismutase (SOD) activity], cytokines levels, and intravascular leukocyte activationwere evaluated after 1, 3 or 5 h of exposure. Oxidative damage to lipids and decreased GSH/GSSG ratiowas observed in ROFA-exposed mice as early as 1 h. Afterwards, increased protein oxidation,decreased ascorbic acid content and SOD activity was found in this group at 3 h. The onset of anadaptive response was observed at 5 h after the ROFA exposure, as indicated by decreased TBARSplasma content and increased SOD activity. The observed increase in oxidative damage to plasmamacromolecules, together with systemic antioxidants depletion, may be a consequence of a systemicinflammatory response triggered by the ROFA exposure, since increased TNF-α and IL-6 plasma levelsand polymorphonuclear leukocytes activation was found at every evaluated time-point. These findingscontribute to the understanding of the increase in cardiovascular morbidity and mortality, inassociation with environmental PM inhalation.