Are oxygen radicals implicated in the calcium paradox of the rat heart?

Abstract

No reduction in creatine kinase (CK) release during standard Ca2+ paradox in the Langendorff-perfused rat heart was afforded by anoxic perfusion, nor by addition of the radical scavengers superoxide dismutase (150,000 U/L), catalase (150,000 U/L), mannitol (15 or 50 mM), dimethylthiourea (DMTU, 10 mM), the antioxidant vitamin E (0.25 or 0.75 mM), or the iron chelator desferrioxamine (0.8 mM). Even under mild Ca(2+)-paradox conditions, achieved by (a) reducing the duration of the Ca(2+)-free period, (b) increasing [Ca2+]0 during the "Ca(2+)-free" period, or (c) reperfusing with 0.1 mM Ca2+, no protection was achieved by mannitol, DMTU, or desferrioxamine. Perfusion with N2 did not cause a reduction in CK release caused by caffeine or dinitrophenol or Ca2+ paradox. We conclude that no evidence supports the hypothesis that oxygen radicals are implicated in release of CK in Ca2+ paradox.