CONTACT US: Contact info
|
Citation |
Marashi SM, Hosseini SF, Hosseinzadeh M, Qadir MF, Khodaei F. J. Biochem. Mol. Toxicol. 2019; 33(9): e22370. |
|
Copyright |
(Copyright © 2019, John Wiley and Sons) |
|
DOI |
|
PMID |
31348582 |
|
Abstract |
Paraquat (PQ) has accounted for numerous suicide attempts in developing countries. Aspirin (ASA) as an adjuvant treatment in PQ poisoning has an ameliorative role. And, it's uncoupling of mitochondrial oxidative phosphorylation role has been well established. The current study aimed at examining the aspirin mechanism on lung mitochondria of rats exposed to PQ. Male rats were randomly allocated in five groups: Control group, PQ group (50 mg/kg; orally, only on the first day), and PQ + ASA (100, 200, and 400 mg/kg; i.p.) groups for 3 weeks. Mitochondrial indices and respiratory chain-complex activities were determined. PQ induced lung interstitial fibrosis; however, ASA (400 mg/kg) led to decrease in this abnormal alteration. In comparison with PQ group, complex II and IV activity, and adenosine triphosphate content in ASA groups had significantly increased; however, reactive oxygen species production, mitochondrial membrane permeabilization, and mitochondrial swelling were significantly reduced. In conclusion, aspirin can alleviate lung injury induced by PQ poisoning by improving mitochondrial dynamics. Language: en |
|
Keywords |
Male; Animals; Lung; Rats; Paraquat; Dose-Response Relationship, Drug; Rats, Sprague-Dawley; Aspirin; Mitochondria; Herbicides; paraquat poisoning; lung injury; aspirin; Reactive Oxygen Species; Membrane Potential, Mitochondrial; mitochondrial respiratory chain; oxidative stress biomarkers |