Formaldehyde inhalation reduces respiratory mechanics in a rat model with allergic lung inflammation by altering the nitric oxide/cyclooxygenase-derived products relationship

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• 作者：Adriana Lino-dos-Santos-Franco ; Jo?o Antonio Gimenes-J¨²nior ; Ana Paula Ligeiro-de-Oliveira ; Ana Cristina Breithaupt-Faloppa ; Beatriz Goleg? Acceturi ; Luana Beatriz Vitoretti ; Isabel Daufenback Machado ; Ricardo Martins Oliveira-Filho ; S ; ra Helena Poliselli Farsky ; Henrique Takachi Moriya ; Wothan Tavares-de-Lima
• 关键词：Pollution ; Allergic lung disease ; Bronchial responsiveness ; Pulmonary mechanics ; Nitric oxide ; Cyclooxygenase products
• 刊名：Food and Chemical Toxicology
• 出版年：2013
• 出版时间：September, 2013
• 年：2013
• 卷：59
• 期：Complete
• 页码：731-738
• 全文大小：511 K

文摘

Bronchial hyperresponsiveness is a hallmark of asthma and many factors modulate bronchoconstriction episodes. A potential correlation of formaldehyde (FA) inhalation and asthma has been observed; however, the exact role of FA remains controversial. We investigated the effects of FA inhalation on Ovalbumin (OVA) sensitisation using a parameter of respiratory mechanics. The involvement of nitric oxide (NO) and cyclooxygenase-derived products were also evaluated.

The rats were submitted, or not, to FA inhalation (1 % , 90 min/day, 3 days) and were OVA-sensitised and challenged 14 days later. Our data showed that previous FA exposure in allergic rats reduced bronchial responsiveness, respiratory resistance (Rrs) and elastance (Ers) to methacholine. FA exposure in allergic rats also increased the iNOS gene expression and reduced COX-1. L-NAME treatment exacerbated the bronchial hyporesponsiveness and did not modify the Ers and Rrs, while Indomethacin partially reversed all of the parameters studied. The L-NAME and Indomethacin treatments reduced leukotriene B₄ levels while they increased thromboxane B₂ and prostaglandin E₂. In conclusion, FA exposure prior to OVA sensitisation reduces the respiratory mechanics and the interaction of NO and PGE₂ may be representing a compensatory mechanism in order to protect the lung from bronchoconstriction effects.