Ascorbic acid attenuates acute pulmonary oxidative stress and inflammation caused by zinc oxide nanoparticles. Issue 2 (25th April 2015)

• Record Type: Journal Article
• Authors: Fukui, Hiroko; Iwahashi, Hitoshi; Endoh, Shigehisa; Nishio, Keiko; Yoshida, Yasukazu; Hagihara, Yoshihisa; Horie, Masanori
• Is Part Of: Journal of occupational health. Volume 57:Issue 2(2015)
• Page Start: 118
• Page End: 125
• Publication Date: 2015-04-25
• Subjects: Antioxidants -- Inflammation -- Metals -- Nanoparticles -- Oxidative stress; Medicine, Industrial -- Periodicals; Industrial hygiene -- Periodicals; Medicine, Industrial; Occupational Diseases; Occupational Exposure; Occupational Health; Occupational Medicine; Periodicals; Periodical; Electronic journals; 613.62
• DOI: 10.1539/joh.14-0161-OA
• Languages: English
• ISSNs: 1341-9145

Abstract

Abstract : Ascorbic acid attenuates acute pulmonary oxidative stress and inflammation caused by zinc oxide nanoparticles: Hiroko Fukui, et al . United Graduate School of Agricultural Science, Gifu University Objective: It is known that inhalation of zinc oxide nanoparticles (ZnO NPs) induces acute pulmonary dysfunction, including oxidative stress, inflammation, and injury, but there are no reports on how to prevent these adverse effects. We have previously reported that the pulmonary symptoms caused by ZnO NPs were associated with oxidative stress; in the present study, we therefore investigated the use of ascorbic acid (AA), which is known as vitamin C, to prevent these toxic effects. Methods: AZnO NP dispersion was introduced into rat lungs by intratracheal injection, and thereafter a 1% aqueous AA solution was given as drinking water. Bronchoalveolar lavage fluid was collected at 1 day and 1 week after injection, and lactate dehydrogenase (LDH) activity, heme oxygenase‐1 (HO1), and interleukin‐6 (IL‐6) levels were measured. In addition, expression of the chemokine cytokine‐induced neutrophil chemoattractants (CINCs), HO‐1, and metallothionein‐1 (MT‐1) genes in the lungs were determined. Results: Acute oxidative stress induced by ZnO NPs was suppressed by supplying AA. Increases in LDH activity and IL‐6 concentration were also suppressed by AA, as was the expression of the CINC1, CINC‐3, and HO‐1 genes. Conclusions: Oral intake of AA prevents acute pulmonary oxidative stress and inflammation caused by ZnO NPs. Intake of AA after unanticipated exposure to ZnO NPs is possibly the first effective treatment for the acute pulmonary dysfunction they cause.