Biological effects of electric shock and heat denaturation and oxidation of molecules, membranes, and cellular functions.
Direct exposure of cells in suspension to intense electric pulses is known to produce damages to cell membranes and supramolecular organizations of cells, and denaturation of macromolecules, much like injuries and tears seen in electric trauma patients. Thus, the system has been used as a laboratory model for investigating the biochemical basis of electric injury. An intense electric pulse can produce two major effects on cells--one caused by the field, or the electric potential, and the other by current, or the electric energy. The field-induced transmembrane potential can produce electro-conformational changes of ion channels and ion pumps and, when the potential exceeds the dielectric strength of the cell membrane (approximately 500 mV for a pulse width of a few ms), electro-conformational damages and electroporations of membrane proteins and lipid bilayers. These events lead to passage of electric current through the membrane-porated cells and to heating of cell membranes and cytoplasmic contents. The subsequent denaturation of cell membranes and cytoplasmic macromolecules brings about many complex biochemical reactions, including oxidation of proteins and lipids. The combined effects may cripple the cells beyond repair. This communication will focus on the thermal effects of electric shock. After a brief review of the current state of knowledge on thermal denaturation of soluble enzymes and muscle proteins, this paper will describe experiments on the thermal denaturation of cellular components and functions, such as nucleosomes, and the electron transport chain and ATP synthetic enzymes of the mitochondrial inner membranes. Data will show that lipid peroxidation and the subsequent loss of the energy-transducing ability of the cells may occur even at moderate temperatures between 40 degrees C and 45 degrees C. However, lipid peroxidation may be prevented with reducing reagents such as mercaptoethanol, dithiothreitol, and ascorbic acid. Reactivation of denatured cellular proteins and functions may also be possible and a strategy for doing so is discussed.
Tsong
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Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota College of Biological Sciences, St. Paul 55108, USA.
Su
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D000818:Animals; D002462:Cell Membrane / Q000502:physiology; D002477:Cells / Q000378:metabolism*; D004556:Electric Injuries / Q000378:metabolism*; D004594:Electrophysiology; D018274:Electroporation; D006358:Hot Temperature; D006801:Humans; D066298:In Vitro Techniques; D007473:Ion Channels / Q000378:metabolism; D017136:Ion Transport; D008564:Membrane Potentials; D010084:Oxidation-Reduction; D011489:Protein Denaturation
D007473:Ion Channels