Format

Send to

Choose Destination
See comment in PubMed Commons below
Inhal Toxicol. 2013 Jan;25(1):9-16. doi: 10.3109/08958378.2012.750405.

Docosahexaenoic acid (DHA) attenuated paraquat induced lung damage in mice.

Author information

1
Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong Province 250012, China.

Abstract

CONTEXT:

Accumulating evidences have proposed the critical roles of oxidative stress in the etiology of lung injury caused by paraquat (PQ). Docosahexaenoic acid (DHA) is an essential n-3 polyunsaturated fatty acid (PUFA), which has been proved to possess prominent antioxidative and anti-inflammatory effects.

OBJECTIVE:

The aim of this study was to evaluate effects of DHA against acute lung injury (ALI) induced by PQ in mice.

MATERIALS AND METHODS:

Male Kunming mice were randomly divided into three groups: control group, PQ group, and PQ+DHA group (n = 24). The mice of PQ+DHA group received 500 mg/kg bodyweight DHA by gavage daily for consecutive 14 days. On day 8, the mice in PQ and PQ+DHA groups received a single oral dose of 50 mg/kg bodyweight PQ. All the mice were sacrificed on day 15. The myeloperoxidase (MPO) activities, levels of the malondialdehyde (MDA) and glutathione (GSH), and the 4-hydroxynonenal (4-HNE) and MDA modified proteins of lung were investigated.

RESULTS:

DHA treatment significantly increased the survival rate of mice treated with PQ. Pulmonary MPO activities and MDA contents were elevated in the mice of the PQ group, while the GSH level was reduced. Furthermore, levels of 4-HNE and MDA modified protein in lungs of the PQ group mice were significantly increased. All the above changes were significantly inhibited by DHA pretreatment. Morphological examination revealed that DHA effectively attenuated the hyperemia, edema of ALI induced by PQ.

CONCLUSION:

These results demonstrated that DHA could effectively attenuate PQ-induced ALI in mice probably via its antioxidant activity.

PMID:
23293968
DOI:
10.3109/08958378.2012.750405
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center