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Overexpression of manganese superoxide dismutase by N-acetylcysteine in hyperoxic lung injury.
Respir Med. 2007 Apr; 101(4):800-7.RM

Abstract

BACKGROUND

Exposure of animals to hyperoxia causes lung injury, characterized by diffuse alveolar damage and exudation of plasma into the alveolar space. Reactive oxygen species (ROS) play an important role in the development of hyperoxic lung injury. Mitochondrial oxidative phosphorylation is one of the major sources of ROS. N-acetylcysteine (NAC) is a precursor of glutathione (GSH), which functions as an antioxidant by reducing hydrogen peroxide to water and alcohols. NAC has been shown to diminish lung injury in a large variety of animal models.

AIM

We elucidated the mechanism underlying the protective effects of NAC in hyperoxia-induced lung injury.

METHODS

Male BALB/c mice were exposed to 98% oxygen for 72 h. The mice inhaled NAC or saline twice a day from 72 h before oxygen exposure to the end of experiment.

RESULTS

Inhaled NAC increased the GSH level in lung homogenate. NAC also attenuated cellular infiltrations in both bronchoalveolar lavage fluid (BALF) and lung tissue. The total protein level in BALF and the level of 8-isoprostane, a marker of lipid peroxidation, in lung homogenate were decreased by inhalation of NAC. Inhaled NAC induced the overexpression of Mn superoxide dismutase (MnSOD) mRNA and protein, but did not alter the expressions of other antioxidant enzymes, including CuZnSOD, extracellular SOD, and glutathione peroxydase 1.

CONCLUSION

These findings suggest that the antioxidant properties of NAC in hyperoxic lung injury involve a decrease in mitochondrial ROS in association with the induction of MnSOD, in addition to its role as a precursor of GSH.

Authors+Show Affiliations

Department of Respiratory Medicine, Kyoto Prefectural University of Medicine, 465 Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602-8566, Japan. nagata@koto.kpu-m.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17010595

Citation

Nagata, Kazuhiro, et al. "Overexpression of Manganese Superoxide Dismutase By N-acetylcysteine in Hyperoxic Lung Injury." Respiratory Medicine, vol. 101, no. 4, 2007, pp. 800-7.
Nagata K, Iwasaki Y, Yamada T, et al. Overexpression of manganese superoxide dismutase by N-acetylcysteine in hyperoxic lung injury. Respir Med. 2007;101(4):800-7.
Nagata, K., Iwasaki, Y., Yamada, T., Yuba, T., Kono, K., Hosogi, S., Ohsugi, S., Kuwahara, H., & Marunaka, Y. (2007). Overexpression of manganese superoxide dismutase by N-acetylcysteine in hyperoxic lung injury. Respiratory Medicine, 101(4), 800-7.
Nagata K, et al. Overexpression of Manganese Superoxide Dismutase By N-acetylcysteine in Hyperoxic Lung Injury. Respir Med. 2007;101(4):800-7. PubMed PMID: 17010595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Overexpression of manganese superoxide dismutase by N-acetylcysteine in hyperoxic lung injury. AU - Nagata,Kazuhiro, AU - Iwasaki,Yoshinobu, AU - Yamada,Tadaaki, AU - Yuba,Tatsuya, AU - Kono,Kenji, AU - Hosogi,Shigekuni, AU - Ohsugi,Shuji, AU - Kuwahara,Hiroomi, AU - Marunaka,Yoshinori, Y1 - 2006/09/28/ PY - 2006/01/05/received PY - 2006/07/13/revised PY - 2006/07/28/accepted PY - 2006/10/3/pubmed PY - 2007/6/26/medline PY - 2006/10/3/entrez SP - 800 EP - 7 JF - Respiratory medicine JO - Respir Med VL - 101 IS - 4 N2 - BACKGROUND: Exposure of animals to hyperoxia causes lung injury, characterized by diffuse alveolar damage and exudation of plasma into the alveolar space. Reactive oxygen species (ROS) play an important role in the development of hyperoxic lung injury. Mitochondrial oxidative phosphorylation is one of the major sources of ROS. N-acetylcysteine (NAC) is a precursor of glutathione (GSH), which functions as an antioxidant by reducing hydrogen peroxide to water and alcohols. NAC has been shown to diminish lung injury in a large variety of animal models. AIM: We elucidated the mechanism underlying the protective effects of NAC in hyperoxia-induced lung injury. METHODS: Male BALB/c mice were exposed to 98% oxygen for 72 h. The mice inhaled NAC or saline twice a day from 72 h before oxygen exposure to the end of experiment. RESULTS: Inhaled NAC increased the GSH level in lung homogenate. NAC also attenuated cellular infiltrations in both bronchoalveolar lavage fluid (BALF) and lung tissue. The total protein level in BALF and the level of 8-isoprostane, a marker of lipid peroxidation, in lung homogenate were decreased by inhalation of NAC. Inhaled NAC induced the overexpression of Mn superoxide dismutase (MnSOD) mRNA and protein, but did not alter the expressions of other antioxidant enzymes, including CuZnSOD, extracellular SOD, and glutathione peroxydase 1. CONCLUSION: These findings suggest that the antioxidant properties of NAC in hyperoxic lung injury involve a decrease in mitochondrial ROS in association with the induction of MnSOD, in addition to its role as a precursor of GSH. SN - 0954-6111 UR - https://www.unboundmedicine.com/medline/citation/17010595/Overexpression_of_manganese_superoxide_dismutase_by_N_acetylcysteine_in_hyperoxic_lung_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0954-6111(06)00390-8 DB - PRIME DP - Unbound Medicine ER -