Abstract
A number of disorders, such as Alzheimer disease and diabetes mellitus, have in common the alteration of the redox balance, resulting in an increase in reactive oxygen species (ROS) generation that might lead to the development of apoptosis and cell death. It has long been known that ROS can significantly alter Ca2+ mobilization, an intracellular signal that is involved in the regulation of a wide variety of cellular functions. Cells have a limited capability to counteract the effects of oxidative stress, but evidence has been provided supporting the beneficial effects of exogenous ROS scavengers. Here, we review the effects of oxidative stress on intracellular Ca2+ homeostasis and the role of antioxidants in the prevention and treatment of disorders associated to abnormal Ca2+ mobilization induced by ROS.
Highlights
A number of disorders, such as Alzheimer disease and diabetes mellitus, have in common the alteration of the redox balance, resulting in an increase in reactive oxygen species (ROS) generation that might lead to the development of apoptosis and cell death
This versatility derives from the fact that Ca2+ signalling works in a variety of ways, Molecules 2010, 15 and the processes involved in Ca2+ mobilization are widely dynamic in range and amplitude
In the cardiac myocyte, Ca2+ entering through L-type Ca2+ channels leads to a signal known as ‘spark’ that triggers contraction within microseconds; on the other hand, the duration of processes like gene transcription or cell proliferation ranges from minutes to hours
Summary
Ca2+ is the most versatile signal involved in the control of cellular processes and functions [1,2,3]. Cytosolic Ca2+ concentration ([Ca2+]c) is determined by a balance between the mechanisms that introduce Ca2+ into the cytoplasm, termed “on”, and those that remove it, termed “off” These processes combine the action of a variety of channels, both in the plasma membrane and in the membrane of the intracellular stores, such as the endoplasmic or sarcoplasmic reticulum, including. Agonist-activated Ca2+ “on” mechanisms includes Ca2+ release from the intracellular pools and entry through plasma membrane channels. Channels in the plasma membrane depending on the cell type, which are gated by voltage (only in electrically excitable cells), agonists or second messengers [14,15] In addition to these signals, other physical stimuli, such as mechanical stretch, are able to induce Ca2+ entry [16]. When a decrease in [Ca2+]L occurs, Ca2+ dissociates from the EF hand motif and STIM1 activates Ca2+ channels [32,36,38,39]
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