Farber J L
Department of Pathology, Thomas Jefferson University, Philadelphia, PA 19107.
Environ Health Perspect. 1990 Mar;84:107-11. doi: 10.1289/ehp.9084107.
Calcium ions have been increasingly implicated as a mediator of the mechanisms generating lethal cell injury under a variety of pathologic circumstances. An overview of the various roles suggested for such alterations in cellular calcium homeostasis is presented. The central role of plasma membrane damage in the genesis of irreversible cell injury is used to divide the postulated roles for calcium ions into two major mechanisms. On the one hand, calcium ions have been proposed as mediators of the functional consequences of plasma membrane injury. An influx of extracellular calcium ions across a damaged permeability barrier and down a steep concentration gradient may convert potentially reversible injury into irreversible injury. On the other hand, alterations in intracellular calcium homeostasis are postulated to participate in the mechanisms generating potentially lethal plasma membrane injury. The release of calcium stores sequestered within intracellular organelles raises the cytosolic concentration of free calcium, a process that may activate, in turn, a number of membrane-disruptive processes. The data supporting these two distinct actions of calcium are reviewed and discussed.
在各种病理情况下，钙离子越来越多地被认为是导致致命性细胞损伤机制的介质。本文概述了细胞钙稳态改变所具有的各种作用。利用质膜损伤在不可逆性细胞损伤发生过程中的核心作用，将钙离子的假定作用分为两种主要机制。一方面，钙离子被认为是质膜损伤功能后果的介质。细胞外钙离子通过受损的通透性屏障并顺着陡峭的浓度梯度内流，可能会将潜在可逆性损伤转变为不可逆性损伤。另一方面，据推测细胞内钙稳态的改变参与了导致潜在致命性质膜损伤的机制。细胞内细胞器中储存的钙的释放会提高胞质游离钙的浓度，这一过程可能进而激活许多破坏膜的过程。本文对支持钙离子这两种不同作用的数据进行了综述和讨论。
