Nicotine Effects on Alveolar Macrophage Respiration and Adenosine Triphosphatase Activity

Abstract

Pulmonary alveolar macrophage cells (PAMs) manifest a high endogenous respiration (0.16μmols/liter of O₂ per milligram of protein per second) and a Mg⁺⁺ dependent Na,⁺K⁺ stimulated adenosinetriphosphatase (ATPase) activity at the cellular level (2.2μmols of phosphate per milligram of protein per hour). Nicotine adversely affected the PAM respiration and ATPase systems. Concentrations above 0.5 millimols/liter inhibited PAM ATPase activity; a 33% inhibition occurred at 5 millimols/liter of nicotine. Prein cubation exposure of PAMs to nicotine for one to two hours deteriorated the ATPase system further; a 50% to 60% inhibition occurred at 5 millimols/liter of nicotine. Low concentrations of this alkaloid (< 5 millimols/liter) stimulated cell respiration by 20%; high concentrations (>10 millimols/liter) were inhibitory. Preincubation of cells for one to four hours in the presence of 0.1 to 5.0 millimols/liter of nicotine caused abolishment of biphasic response and greater respiratory inhibition.