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Vol. 276, Issue 3, H993-H997, March 1999

Metallothionein inhibits ischemia-reperfusion injury in mouse heart

Y. James Kang¹, Guangqiu Li^,1, and Jack T. Saari²

¹ Departments of Medicine, and Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky 40292; and ² United States Department of Agriculture, Agricultural Research Service, Human Nutrition Research Center, Grand Forks, North Dakota 58202

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.

contractile force; creatine kinase; infarction; Langendorff; myocardium

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Deceased 12 November 1996.

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