Biochemical and Biophysical Research Communications
Pyrroloquinoline quinone preserves mitochondrial function and prevents oxidative injury in adult rat cardiac myocytes
Section snippets
Materials and methods
Cardiac myocytes. Adult cardiac myocytes were isolated and cultured from 250–300 g male rats (Charles River) as previously described in our laboratory for murine myocytes [16]. The animal protocol was approved by the San Francisco Veterans Affairs Medical Center Animal Studies Committee. The investigation conforms to the Guide for the Care and Use of Laboratory Animals published by the US National Institutes of Health (NIH Publication No. 85-23, revised 1996). Chemicals and reagents for
Cell death
We performed concentration-response experiments to obtain a working concentration of H2O2 that routinely causes approximately 50% cell death (Fig. 1A). In experimental buffer lacking bovine serum albumin (BSA), 100 μM H2O2 caused approximately 60% cell death. In the presence of BSA, which is necessary for maintaining viable cultured myocytes in experimental media, cell death was significantly prevented. Therefore, we increased H2O2 to 1 mM to reach the goal of 50% cell mortality. Viable cells
Discussion
The first major finding of this study is that PQQ substantially reduced cell death in cultured adult rat cardiac myocytes subjected to oxidative damage with H2O2. PQQ protection against oxidant-induced cell death is consistent with our previous reports demonstrating that PQQ is highly effective in reducing infarct size and in improving hemodynamics in intact rats subjected to I/R injury [14], [15]. As a dietary supplement, PQQ has also been found to be neuroprotective in a rodent stroke model
Acknowledgments
Grant support: NIH PO1 HL68738 (J.S.K.), VA Merit Awards (C.C.A.), Charitable Leadership Foundation (J.S.K.), and American Heart Association (C.C.A. and J.Z.).
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