Metallothionein inhibits ischemia-reperfusion injury in mouse heart

Yujian Kang, Guangqiu Li, Jack T. Saari

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

Oxidative stress is believed to play a major role in ischemia- reperfusion injury to the heart. Metallothionein (MT), a potential free radical scavenger, may function in cardiac protection against ischemia- reperfusion damage. To test this hypothesis, a specific cardiac MT- overexpressing transgenic mouse model was used. The hearts isolated from these animals were subjected to 50 min of warm (37°C) zero-flow ischemia followed by 60- or 90-min reflow. Compared with the nontransgenic controls, the transgenic mouse hearts with MT concentrations ~10-fold higher than normal showed significantly improved recovery of contractile force postischemia (69.2 ± 4.2 vs. 26.0 ± 6.0% at the end of 60-min reperfusion, P < 0.01). Efflux of creatine kinase from these transgenic hearts was reduced by more than 50% (P < 0.01). In addition, the zone of infarction induced by ischemia-reperfusion at the end of 90-min reperfusion was suppressed by ~40% (P < 0.01) in the transgenic hearts. The results strongly indicate that MT provides protection against ischemia-reperfusion-induced heart injury.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume276
Issue number3 45-3
StatePublished - Jan 1 1999
Externally publishedYes

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Metallothionein
Reperfusion Injury
Reperfusion
Ischemia
Transgenic Mice
Heart Injuries
Free Radical Scavengers
Creatine Kinase
Infarction
Oxidative Stress

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Metallothionein inhibits ischemia-reperfusion injury in mouse heart. / Kang, Yujian; Li, Guangqiu; Saari, Jack T.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 276, No. 3 45-3, 01.01.1999.

Research output: Contribution to journalArticle

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