Ascorbic acid attenuates acute pulmonary oxidative stress and inflammation caused by zinc oxide nanoparticles.
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
A ZnO 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 (HO-1), 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 CINC-1, 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.
Health Research Institute (HRI), National Institute of Advanced Industrial Science and Technology (AIST).
Hiroko
H
Fukui
Hitoshi
H
Iwahashi
Shigehisa
S
Endoh
Keiko
K
Nishio
Yasukazu
Y
Yoshida
Yoshihisa
Y
Hagihara
Masanori
M
Horie
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D054360:Chemokine CXCL1 / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000378:metabolism; D019570:Inhalation Exposure / Q000009:adverse effects*; D015850:Interleukin-6 / Q000378:metabolism; D045022:Lactate Dehydrogenases / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008297:Male; D008668:Metallothionein / Q000378:metabolism; D053758:Nanoparticles / Q000737:chemistry / Q000633:toxicity*; D018384:Oxidative Stress / Q000187:drug effects*; D011014:Pneumonia / Q000139:chemically induced / Q000517:prevention & control*; D051381:Rats; D017208:Rats, Wistar; D015034:Zinc Oxide / Q000633:toxicity*
D000975:Antioxidants; D054360:Chemokine CXCL1; C513297:Cxcl1 protein, rat; D015850:Interleukin-6; C491055:Mt2A protein, rat; D008668:Metallothionein; D045022:Lactate Dehydrogenases; D051547:Heme Oxygenase-1; D001205:Ascorbic Acid; D015034:Zinc Oxide