Ion channels in toxicology.
Ion channels play essential roles in human physiology and toxicology. Cardiac contraction, neural transmission, temperature sensing, insulin release, regulation of apoptosis, cellular pH and oxidative stress, as well as detection of active compounds from chilli, are some of the processes in which ion channels have an important role. Regulation of ion channels by several chemicals including those found in air, water and soil represents an interesting potential link between environmental pollution and human diseases; for instance, de novo expression of ion channels in response to exposure to carcinogens is being considered as a potential tool for cancer diagnosis and therapy. Non-specific binding of several drugs to ion channels is responsible for a huge number of undesirable side-effects, and testing guidelines for several drugs now require ion channel screening for pharmaceutical safety. Animal toxins targeting human ion channels have serious effects on the population and have also provided a remarkable tool to study the molecular structure and function of ion channels. In this review, we will summarize the participation of ion channels in biological processes extensively used in toxicological studies, including cardiac function, apoptosis and cell proliferation. Major findings on the adverse effects of drugs on ion channels as well as the regulation of these proteins by different chemicals, including some pesticides, are also reviewed. Association of ion channels and toxicology in several biological processes strongly suggests these proteins to be excellent candidates to follow the toxic effects of xenobiotics, and as potential early indicators of life-threatening situations including chronic degenerative diseases.
Restrepo-Angulo
Iván
I
Department of Pharmacology, Centro de Investigación y de Estudios Avanzados, Avenida Instituto Politécnico Nacional 2508, México D. F. 07360, México.
De Vizcaya-Ruiz
Andrea
A
Camacho
Javier
J
D000818:Animals; D017209:Apoptosis; D015220:Calcium Channels / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D018118:Chloride Channels / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D064420:Drug-Related Side Effects and Adverse Reactions; D004785:Environmental Pollutants / Q000633:toxicity*; D006801:Humans; D007473:Ion Channels / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D009369:Neoplasms / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D015221:Potassium Channels / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D011485:Protein Binding; D015222:Sodium Channels / Q000096:biosynthesis / Q000378:metabolism / Q000502:physiology; D014116:Toxicology / Q000379:methods*; D014118:Toxins, Biological / Q000633:toxicity*
D015220:Calcium Channels; D018118:Chloride Channels; D004785:Environmental Pollutants; D007473:Ion Channels; D015221:Potassium Channels; D015222:Sodium Channels; D014118:Toxins, Biological