Increased heat production proportional to oxygen consumption in human neutrophils activated with phorbol-12-myristate-13-acetate.
The heat produced by neutrophils was measured with a flow microcalorimeter. 02 consumption, ATP concentration, lactic acid production and 14CO2 production from oxidation of [1-(14)C]-glucose [6-(14)C]-glucose and [U-14C]-glucose were evaluated. Experiments were also carried out in the presence of the metabolic inhibitors, N-ethylmaleimide and NaF. Heat effects were correlated to the enthalpy change of aerobic and anaerobic glucose catabolism. Two different heat contributions related to two different nonmitochondrial 02 reduction pathways are present during the metabolic burst. Theoretical and experimental data indicate that the reducing power is derived from the catabolism of glucose both through the hexose monophosphate shunt and glycolysis.
D000255:Adenosine Triphosphate / Q000097:blood; D002151:Calorimetry; D005033:Ethylmaleimide / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects; D006358:Hot Temperature; D006801:Humans; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects*; D010704:Phorbols / Q000494:pharmacology*; D012969:Sodium Fluoride / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D010704:Phorbols; D000255:Adenosine Triphosphate; D012969:Sodium Fluoride; D013755:Tetradecanoylphorbol Acetate; D005033:Ethylmaleimide