脂质过氧化
肺
多不饱和脂肪酸
药理学
百草枯
化学
磷脂
生物化学
生物
脂肪酸
氧化应激
内科学
医学
膜
作者
Yuki Tomitsuka,Hirotsugu Imaeda,Haruka Ito,Isaki Asou,Masayuki Ohbayashi,Fumihiro Ishikawa,Hiroshi Kuwata,Shuntaro Hara
出处
期刊:Redox biology
[Elsevier]
日期:2023-10-01
卷期号:66: 102850-102850
标识
DOI:10.1016/j.redox.2023.102850
摘要
Long-chain acyl-CoA synthetase (ACSL) 4 converts polyunsaturated fatty acids (PUFAs) into their acyl-CoAs and plays an important role in maintaining PUFA-containing membrane phospholipids. Here we demonstrated decreases in various kinds of PUFA-containing phospholipid species in ACSL4-deficient murine lung. We then examined the effects of ACSL4 gene deletion on lung injury by treating mice with two pulmonary toxic chemicals: paraquat (PQ) and methotrexate (MTX). The results showed that ACSL4 deficiency attenuated PQ-induced acute lung lesion and decreased mortality. PQ-induced lung inflammation and neutrophil migration were also suppressed in ACSL4-deficient mice. PQ administration increased the levels of phospholipid hydroperoxides in the lung, but ACSL4 gene deletion suppressed their increment. We further found that ACSL4 deficiency attenuated MTX-induced pulmonary fibrosis. These results suggested that ACSL4 gene deletion might confer protection against pulmonary toxic chemical-induced lung injury by reducing PUFA-containing membrane phospholipids, leading to the suppression of lipid peroxidation. Inhibition of ACSL4 may be promising for the prevention and treatment of chemical-induced lung injury.
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