期刊
ANTIOXIDANTS
卷 11, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/antiox11040681
关键词
lung; acute respiratory distress syndrome; arachidonic acid; D-PUFA; eicosanoids; isotope effect
Arachidonic acid (ARA) is easily oxidized and its oxidation products induce inflammatory responses. This study found that deuterated ARA (D-ARA) can protect lungs from adverse effects of inflammation and reduce lung damage caused by acute lung injury, suggesting a potential therapeutic avenue for severe infections and inflammatory diseases.
Arachidonic acid (ARA) is a major component of lipid bilayers as well as the key substrate for the eicosanoid cascades. ARA is readily oxidized, and its non-enzymatic and enzymatic oxidation products induce inflammatory responses in nearly all tissues, including lung tissues. Deuteration at bis-allylic positions substantially decreases the overall rate of ARA oxidation when hydrogen abstraction is an initiating event. To compare the effects of dosing of arachidonic acid (H-ARA) and its bis-allylic hexadeuterated form (D-ARA) on lungs in conventionally healthy mice and in an acute lung injury model, mice were dosed with H-ARA or D-ARA for six weeks through dietary supplementation and then challenged with intranasal lipopolysaccharide (LPS) for subsequent analysis of bronchoalveolar lavage fluid and lung tissue. Dosing on D-ARA resulted in successful incorporation of D-ARA into various tissues. D-ARA significantly reduced LPS-induced adverse effects on alveolar septal thickness and the bronchoalveolar area. Oral deuterated ARA is taken up efficiently and protects against adverse LPS-induced pathology. This suggests novel therapeutic avenues for reducing lung damage during severe infections and other pathological conditions with inflammation in the pulmonary system and other inflammatory diseases.
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