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

• Published in: Food and chemical toxicology Vol. 59; pp. 731 - 738
• Main Authors: Lino-dos-Santos-Franco, Adriana, Gimenes-Júnior, João Antonio, Ligeiro-de-Oliveira, Ana Paula, Breithaupt-Faloppa, Ana Cristina, Acceturi, Beatriz Golegã, Vitoretti, Luana Beatriz, Machado, Isabel Daufenback, Oliveira-Filho, Ricardo Martins, Farsky, Sandra Helena Poliselli, Moriya, Henrique Takachi, Tavares-de-Lima, Wothan
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.09.2013; Elsevier
• Subjects: Administration, Inhalation; Airway Resistance - drug effects; Allergic lung disease; animal models; Animals; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; asthma; Biological and medical sciences; breathing; Bronchial Hyperreactivity - drug therapy; Bronchial Hyperreactivity - immunology; Bronchial Hyperreactivity - metabolism; Bronchial Hyperreactivity - physiopathology; Bronchial responsiveness; bronchoconstriction; Bronchoconstrictor Agents - pharmacology; Cyclooxygenase 1 - genetics; Cyclooxygenase 1 - metabolism; Cyclooxygenase products; Dinoprostone - agonists; Dinoprostone - metabolism; Disease Models, Animal; Eicosanoids - metabolism; formaldehyde; Formaldehyde - administration & dosage; Formaldehyde - toxicity; gene expression; Gene Expression Regulation, Enzymologic - drug effects; indomethacin; inducible nitric oxide synthase; Leukotriene B4 - antagonists & inhibitors; Leukotriene B4 - metabolism; Male; mechanics; Medical sciences; Membrane Proteins - antagonists & inhibitors; Membrane Proteins - genetics; Membrane Proteins - metabolism; Nitric oxide; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - biosynthesis; Nitric Oxide Synthase Type II - genetics; Nitric Oxide Synthase Type II - metabolism; ovalbumin; pneumonia; Pollution; prostaglandins; Pulmonary mechanics; Rats; Rats, Wistar; Respiratory Insufficiency - etiology; Respiratory Insufficiency - prevention & control; Respiratory Mucosa - drug effects; Respiratory Mucosa - immunology; Respiratory Mucosa - metabolism; Respiratory Mucosa - physiopathology; Thromboxane B2 - agonists; Thromboxane B2 - metabolism; Toxicology; Allergic lung disease; Pollution; Cyclooxygenase products; Bronchial responsiveness; Nitric oxide; Pulmonary mechanics; Allergy; Animal model; Prostaglandin-endoperoxide synthase; Rat; Toxicity; Lung; Formaldehyde; Derived product; Immunopathology; Lung disease; Enzyme; Respiratory disease; EC 1.14.99.1; Rodentia; Inflammation; Inhalation; Vertebrata; Mammalia; Animal; Oxidoreductases
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2013.07.027

•Exposure to FA previous OVA-sensitisation reduces respiratory mechanics.•FA exposure prior OVA-sensitisation increases iNOS gene expression and reduces COX-1 without change COX-2 in lung tissue.•Exposure to FA prior OVA-sensitisation modifies nitric oxide/eicosanoids relationship. 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%, 90min/day, 3days) and were OVA-sensitised and challenged 14days 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.