Metal ions in stroke pathophysiology

Abstract

Metal ions are used in biology in many ways and are integrated parts of numerous enzymes and proteins. They function as cofactors in cellular and genetic signaling and, therefore, have important roles in biochemistry ranging from essential to toxic. Perturbed homeostasis of metal ions in stroke has been well recognized for several decades. In cellular and biochemical responses following stroke, metal ion imbalance in neurons is in the center of these cellular events, which is immediate results of stroke and, in turn, leads to the overactivation of several deleterious enzymes and signaling process that impairs neuronal function or lead to cell death. The most studies and well-characterized metal ion in stroke-associated ionic imbalance is calcium (Ca). Almost as soon as Ca was recognized as a factor in the ischemic cell death, considerable evidence has emerged regarding the role of iron (Fe), zinc (Zn), potassium (K), sodium (Na), magnesium (Mg), copper (Cu), manganese (Mn), or selenium (Se) in neurotoxicity as well as neuroprotection after stroke. Several exogenous metal ions such as cadmium (Cd), nickel (Ni), arsenic (As), mercury (Hg), and aluminum (Al) are also linked to stroke pathophysiology. For the first time, the dyshomeostasis and pathophysiological actions of these metals in stroke are discussed systematically in one volume.