The effects of edaravone, a free-radical scavenger in lung injury induced by valproic acid demonstrated via different biochemical parameters


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Bayrak B. B. , Yilmaz S., Hacihasanoglu Cakmak N., Yanardağ R.

JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, vol.35, no.9, 2021 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 35 Issue: 9
  • Publication Date: 2021
  • Doi Number: 10.1002/jbt.22847
  • Journal Name: JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Applied Science & Technology Source, BIOSIS, Biotechnology Research Abstracts, Chemical Abstracts Core, EMBASE, Environment Index, Food Science & Technology Abstracts, MEDLINE
  • Keywords: n-dipropyl acetic acid, lung damage, oxidative stress, synthetic antioxidant, ANTIOXIDANT CAPACITY, PULMONARY-FIBROSIS, OXIDATIVE STRESS, LIPID-PEROXIDATION, ENZYME-ACTIVITY, TISSUE, LIVER, ARGINASE, SERUM, HYDROXYPROLINE
  • Istanbul University-Cerrahpasa Affiliated: Yes

Abstract

In this study, we aimed to evaluate whether edaravone (EDA) has a protective role against valproic acid (VPA)-induced lung damage via its antioxidative activity. Male Sprague-Dawley rats were split into four groups. Control (n = 8) rats; rats given EDA (30 mg kg(-1) day(-1); n = 10); rats given only (VPA, 500 mg kg(-1) day(-1); n = 10); rats given VPA + EDA (in the same dose and time) for 7 days. EDA and VPA were applied intraperitoneally. After 8 days, lung tissues were immediately taken from the rats. In lung homogenates, reduced glutathione, total antioxidant status levels, and superoxide dismutase, glutathione peroxidase, sodium/potassium ATPase, paraoxonase1, and carbonic anhydrase activities significantly abated, whereas catalase, glutathione reductase, glutathione-S-transferase activities insignificantly decreased in the VPA-treated group. In contrast, lipid peroxidation, reactive oxygen species, and total oxidant status levels, glycoprotein and protein carbonyl contents, nitric oxide, hydroxyproline levels, and xanthine oxidase, lactate dehydrogenase, arginase, and prolidase activities significantly increased in the VPA-given group. Administration of EDA caused the reverse effects. As a consequence, EDA prevented oxidative stress-mediated lung injury via its robust antioxidant effects.