ABSTRACT
This chapter presents the role of redox-active transition metals as potential mediators of postischemic cardiac oxidative injury, and how zinc, may be used as an antagonist to preserve postischemic function. Virtually all of the data supporting the concept that zinc is cardioprotective in the postischemic heart is derived from studies conducted in laboratory. The earliest reports to demonstrate possible antioxidant effects of zinc on oxidative cardiac damage were related to catecholamine-induced myocardial injury, a process thought to involve production of reactive oxygen intermediates. Numerous studies have demonstrated that the redox-active transition metals play a critical role in initiation and propagation of lipid peroxidation. Sulfhydryl oxidation along the same protein chain results in intraprotein disulfide cross-linking, which can alter the conformation of the enzyme. In addition, zinc has been shown to antagonize copper-mediated free radical formation in several chemical systems including from hydrogen peroxide and ascorbate oxidation.
