Abstract

We have previously shown that newborn male (but not female) mice exposed to the air pollutant 1,2-naphthoquinone (1,2-NQ), a compound usually adsorbed on fine particulate matter such as diesel exhaust particles, show an exacerbated lung allergic response at youth. In the present study, we investigated the consequences of the early exposure of mice to 1,2- NQ on the in vitro vasomotor activity of pulmonary artery. Vessels were isolated and mounted in a wire-myograph system in order to evaluate the vasomotor response (contractility and vasorelaxation) to different agents. Activities of the antioxidant enzymes superoxide dismutase (SOD), catalase, glutathione (G) peroxidase (GPx), reductase (GR) and transferase (GST), and nitrotyrosine content in pulmonary arteries and serum samples from both groups were also measured. The exposure of male mice to 1,2-NQ during the neonatal period resulted in impairment of the in vitro pulmonary artery function, in terms of both contraction (induced by phenylephrine and compound U-46619) and relaxation (induced by acetylcholine, sodium nitroprusside, isoproterenol and hydrogen peroxide). In addition, reduced SOD and catalase activities were measured in the vessels in comparison with the control animals. We thus conclude that, parallel to diminished antioxidant enzyme defences, the exposure of male newborn mice to the pollutant 1,2-NQ results in impairment of pulmonary artery vasomotricity during puberty, thus suggesting that increased cardiovascular risk may occur upon the early exposure to the air pollutant.

Keywords

pulmonary artery, 1,2-naphthoquinone, vascular reactivity, oxidative stress, mice