The effect of metabolic inhibition on ion contents and sodium exchange in human lymphocytes.
Lymphocytes depleted of ATP by incubation in iodoacetate (IAA) and nitrogen (N2) lost K and gained Na. Isotopic Na exchange showed a fast fraction and a slower exponential fraction, the latter conventionally assumed to reflect surface membrane properties. The gain of cell Na was not accounted for by a decrease in 22Na efflux in either the slow or the fast fraction. After 3-5 hours, Na efflux increased. These results led us to question the concept that normal cell ion levels are maintained by an ATPase pump and could not be explained by exchange diffusion, co-transport, countertransport, or other inherently dissipative mechanisms. The data are, on the other hand, consistent with the concept that cell ion contents are determined by their relative exclusion from cell water coupled with selective adsorption onto fixed macromolecular anionic sites within the cell. In this view, the IAA,N2-induced rise in cell Na is due to the occupancy of adsorption sites losing K, while the increased isotopic exchange is due to a decreased activation energy for ion-site interaction.
D000255:Adenosine Triphosphate / Q000097:blood*; D001693:Biological Transport, Active / Q000187:drug effects; D006801:Humans; D007461:Iodoacetates / Q000494:pharmacology; D019807:Iodoacetic Acid; D007473:Ion Channels; D008214:Lymphocytes / Q000378:metabolism*; D009584:Nitrogen / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology; D011188:Potassium / Q000097:blood*; D012964:Sodium / Q000097:blood*
D007461:Iodoacetates; D007473:Ion Channels; D000255:Adenosine Triphosphate; D012964:Sodium; D009584:Nitrogen; D011188:Potassium; D010100:Oxygen; D019807:Iodoacetic Acid