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Oxidative Stress, Intracellular Calcium Signals and Apoptotic Processes

  • Chapter
Apoptosis: Involvement of Oxidative Stress and Intracellular Ca2+ Homeostasi

Abstract

Apoptosis, an essential physiological process that is required for the normal development and maintenance of tissue homeostasis, is mediated by active intrinsic mechanisms, although extrinsic factors can also contribute. Aerobic metabolism induces the production of reactive oxygen species (ROS), which are able to induce oxidative stress that promotes cellular apoptosis. The mechanisms of ROS-induced modifications in ion transport pathways involves oxidation of sulphydryl groups located in the ion transport proteins, peroxidation of membrane phospholipids, inhibition of membrane-bound regulatory enzymes and modification of the oxidative phosphorylation and ATP levels. Alterations in the ion transport mechanisms lead to changes in a second messenger system, primary Ca2+ homeostasis. Ca2+ disregulation induces mitochondrial depolarization, which further augments the abnormal electrical activity and disturbs signal transduction, causing cell dysfunction and apoptosis. Control of ROS levels in cells is important, because cellular dysfunction triggered by ROS is a major factor contributing to the development of many diseases. Available evidences show that ROS can induce increases in cytosolic free Ca2+ concentration ([Ca2+]c) by release of the divalent cation from internal stores and impairment of Ca2+ clearance systems. In fact, [Ca2+]c increase is a constant feature of pathological states associated with oxidative stress and apoptosis.

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  1. Department of Physiology, University of Extremadura, Avda. Universidad s/n, 10071 Caceres, Spain

    G.M. Salido

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    Gines Maria Salido  & Juan Antonio Rosado  & 

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Salido, G. (2009). Oxidative Stress, Intracellular Calcium Signals and Apoptotic Processes. In: Salido, G.M., Rosado, J.A. (eds) Apoptosis: Involvement of Oxidative Stress and Intracellular Ca2+ Homeostasi. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-9873-4_1

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