Modulation of creatine kinase activity by ruthenium complexes

摘要

Creatine kinase is a crucial enzyme for brain, heart and skeletal muscle energy homeostasis, and a decrease of its activity has been associated with cell death. Many biological properties have been attributed to ruthenium complexes. In this context, this work was performed in order to evaluate creatine kinase activity from rat brain, heart and skeletal muscle (quadriceps) after administration of ruthenium complexes, trans- [RuCl2(nic)(4)] (nic = 3-pyridinecarboxylic acid) 180.7 mu mol/kg (complex 1), trans-[RuCl2(i-nic)(4)] (i-nic = 4-pyridinecarboxylic acid) 13.6 mu mol/kg (complex 11), trans-[RuCl2(dinic)(4)] (dinic = 3,5-pyridinedicarboxylic acid) 180.7 mu mol/kg (complex 111) and trans-[RuCl2(i-dinic)(4)] G-dinic = 3,4-pyridinedicarboxylic acid) 180.7 mu mol/kg (complex IV). Our results showed that complex I caused inhibition of creatine kinase activity in hippocampus, striatum, cerebral cortex, heart and skeletal muscle. Besides, complex 11 did not affect the enzyme activity. complexes III and IV increased creatine kinase activity in hippocampus, striatum, cerebral cortex and heart, but not in skeletal muscle. Besides, none of the complexes in vitro altered creatine kinase activity, suggesting that enzymatic activity is indirectly affected by complexes 1, 111 and IV. It is believed that diminution of creatine kinase in brain of rats caused by complex I may be related to results from other study reporting memory impairment caused by the same complex. Further research is necessary in order to elucidate the effects of ruthenium complexes in other important metabolic enzymes. (c) 2006 Elsevier Inc. All rights reserved.