This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.

Along the aluminum refining process, alumina (Al2O3) constitutes the main source of dust. Although aluminum refinery workers present respiratory symptoms with lung functional changes, no conclusive data about lung function impairment after alumina exposure has been so far reported. We examined the pulmonary alterations of exposure to material collected in an aluminum refinery in Brazil. BALB/c mice were exposed in a whole-body chamber for 1 h to either saline (CTRL, n = 11) or to a suspension (in saline) of 8 mg/m(3) of the dust (ALUM, n = 11) both delivered by an ultrasonic nebulizer. Twenty-four hours after exposure lung mechanics were measured by the end-inflation method. Lungs were prepared for histology. ALUM showed significantly higher static elastance (34.61 +/- 5.76 cmH2O/mL), elastic component of viscoelasticity (8.16 +/- 1.20 cmH2O/mL), pressure used to overcome the resistive component of viscoelasticity (1.62 +/- 0.24 cmH2O), and total resistive pressure (2.21 +/- 0.49 cmH2O) than CTRL (27.95 +/- 3.63 cmH2O/mL, 6.12 +/- 0.99 cmH2O/mL, 1.23 +/- 0.19 cmH2O, and 1.68 +/- 0.23 cmH2O, respectively). ALUM also presented significantly higher fraction area of alveolar collapse (69.7 +/- 1.2%) and influx of polymorphonuclear cells (27.5 +/- 1.1%) in lung parenchyma than CTRL (27.2 +/- 1.1% and 14.6 +/- 0.7%, respectively). The composition analysis of the particulate matter showed high concentrations of aluminum. For the first time it was demonstrated in an experimental model that an acute exposure to dust collected in an aluminum producing facility impaired lung mechanics that could be associated with inflammation.

Chronic obstructive pulmonary disease (COPD) typical features may be induced by administration of exogenous proteases, Rationale: such as papain. Despite the extensive description of the cellular and molecular aspects involved, much remains to be explored in these models.To disclose a putative gender-related pulmonary functional response in a mice model of papain-induced emphysema. Aim:30 male (M) and female (F) BALB/c mice (20-25 g) were randomly divided into four groups. The animals received Materials and methods: intratracheally 50 μL of saline (groups SALF and SALM) or 0.2 U/μL of papain diluted in 50 μL of saline (groups PAPF and PAPM) once a week, for 2 weeks. The animals were weighed once a week. 2 wks after the last intratracheal instillation, the animals were sedated, anesthetized and paralyzed. Lung mechanics (resistive, viscoelastic and total pressures, static elastance and elastic component of viscoelasticity) were measured. The lungs were prepared for histology and biochemical tests were run to evaluate oxidative stress.Pulmonary functional changes were more pronounced in males, with increased elastic, resistive and viscoelastic components of Results: pulmonary mechanics: Est (SALM 19.7 ± 1.7; PAPM 25.5 ± 1.4 cmH O/ml), ΔP1 (0.43±0.04; 0.76 ±0.03 cmH O), ΔP2 (0.94 ±0.08; 1.23 ±0.06 2 2 cmH O), ΔE (4.7± 0.4; 6.2±0.3 cmH O/ml), while females showed only higher elastic and resistive components: Est (SALF 21.9±1.7; PAPF 2 2 29.6±1.4), ΔP1 (0.50±0.04; 0.67±0.03). Increased influx of polymorphonuclear cells was detected in lung parenchyma. The reduction in collagen and elastic fibers confirmed a serious injury at 14 days after exposure. Males presented increase significantly higher in functional residual capacity (SALM 0.20±0.01; PAPM 0.41±0.02 ml) and mean alveolar diameter (SALM 39.4±0.7; PAPM 58.8±0.6 mm), than females (SALF 0.21±0.02; PAPF 0.29±0.01 ml) and (SALF 37.61±0.7; PAPF 47.27±0.6ï€ mm). Male and female mice exposed to papain gained weight to a lesser extent. Antioxidant enzymes were altered suggesting the existence of a mechanism for pulmonary defense against reactive oxygen species. Papain impaired respiratory system functional and inflammatory profiles, and induced oxidative stress. Conclusions:Males displayed more severe lung injuries than females.FAPERJ, CNPq, PRONEX, MCT.