Kentucky State University

Poster Title

Hepatic Ischemia and Reperfusion Injury in Copper-Deficient Rats

Institution

Kentucky State University

Abstract

Dietary copper is known to have a significant role in the normal structure and function of the cardiovascular system. In particular, animals fed diets that are deficient in copper have shown augmented inflammatory responses in the heart, lungs, and systematic circulation. The current study was designed to determine whether a marginal restriction of copper would promote inflammatory damage in the liver. Male Sprague-Dawley rats were fed purified basal diets which were either copper adequate (Cu-A; 6.0 mg Cu/kg diet) or copper marginal (Cu-M; 1.5 mg Cu/kg diet) for four weeks. The rats were anesthetized, a midline laparotomy was performed and a clamp was used to suspend blood flow to 70% of the liver. The rats were subjected to hepatic ischemia for 90 minutes, which was followed by 8 hours of reperfusion. Myeloperoxidase as an index of neutrophil accumulation, was significantly greater in the Cu-M group but hepatocellular damage as indicated by serum ALT was not different. We conclude that a marginal copper deficiency is proinflammatory with a significant effect on the neutrophil function.

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Hepatic Ischemia and Reperfusion Injury in Copper-Deficient Rats

Dietary copper is known to have a significant role in the normal structure and function of the cardiovascular system. In particular, animals fed diets that are deficient in copper have shown augmented inflammatory responses in the heart, lungs, and systematic circulation. The current study was designed to determine whether a marginal restriction of copper would promote inflammatory damage in the liver. Male Sprague-Dawley rats were fed purified basal diets which were either copper adequate (Cu-A; 6.0 mg Cu/kg diet) or copper marginal (Cu-M; 1.5 mg Cu/kg diet) for four weeks. The rats were anesthetized, a midline laparotomy was performed and a clamp was used to suspend blood flow to 70% of the liver. The rats were subjected to hepatic ischemia for 90 minutes, which was followed by 8 hours of reperfusion. Myeloperoxidase as an index of neutrophil accumulation, was significantly greater in the Cu-M group but hepatocellular damage as indicated by serum ALT was not different. We conclude that a marginal copper deficiency is proinflammatory with a significant effect on the neutrophil function.