Melatonin scavenges hydroxyl radical and protects isolated rat hearts from ischemic reperfusion injury

Shinji Kaneko, Kenji Okumura, Yasushi Numaguchi, Hideo Matsui, Kichiro Murase, Shinji Mokuno, Itsuro Morishima, Kenji Hira, Yukio Toki, Takayuki Ito, Tetsuo Hayakawa

研究成果: Article査読

95 被引用数 (Scopus)

抄録

During postischemic reperfusion, free radicals are produced and have deleterious effects in isolated rat hearts. We investigated whether melatonin (MEL) reduces the production of hydroxyl radical (·OH) in the effluent and aids in recovery of left ventricular (LV) function. Hearts were subjected to 30 min of ischemia followed by 30 min of reperfusion. Salicylic acid (SAL) was used as the probe for ·OH, and its derivatives 2,5- and 2,3- dihydroxybenzoic acid (DHBA) were quantified using HPLC. In addition, thiobarbituric acid reactive substances (TBARS) in the myocardium was measured. Plateaus in the measurement of 2,5- and 2,3-DHBA were seen from 3 to 8 min after reperfusion in each group. The group that received 100 μM MEL+ SAL had significantly reduced amounts of 2,5- and 2,3-DHBA by multiple folds, compared to the SAL group. TBARS was significantly decreased in the 100 μM MEL group (1.20 ± 0.36 vs 1.85 ± 0.10 μmol/g of drug-free group, p<0.001). More importantly, the 100 μM MEL group significantly recovered in LV function (LV developed pressure, +dp/dt, and -dp/dt; 63.0%, 60.3%, and 59.4% in the 100 μM MEL group; 30.2%, 29.7%, and 31.5% in the drug-free group, respectively; p<0.05). Duration of ventricular tachycardia or ventricular fibrillation significantly decreased in the 100 μM MEL group (100 μM MEL, 159 ± 67 sec; drug-free, 1244 ± 233 sec; p<0.05). As a result of scavenging ·OH and reducing the extent of lipid peroxidation, MEL is an effective agent for protection against postischemic reperfusion injury. (C) 2000 Elsevier Science Inc.

本文言語English
ページ(範囲)101-112
ページ数12
ジャーナルLife Sciences
67
2
DOI
出版ステータスPublished - 02-06-2000
外部発表はい

All Science Journal Classification (ASJC) codes

  • 生化学、遺伝学、分子生物学(全般)
  • 薬理学、毒性学および薬学(全般)

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