Inhibition of the respiratory burst in mouse macrophages by ultra-low doses of an opioid peptide is consistent with a possible adaptation mechanism

• Published in: FEBS letters 1994-11, Vol.355 (2), p.114-116
• Main Authors: Efanov, A.M., Koshkin, A.A., Sazanov, L.A., Borodulina, O.I., Varfolomeev, S.D., Zaitsev, S.V.
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological; Animals; DAMEA, [d-Ala2]methionine enkephalinamide; Dose-Response Relationship, Drug; Enkephalin, Methionine - administration & dosage; Enkephalin, Methionine - analogs & derivatives; Enkephalin, Methionine - pharmacology; In Vitro Techniques; Kinetic mechanism; Kinetics; Macrophage; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - metabolism; Male; Mice; Mice, Inbred CBA; Opioid peptide; PMA, phorbol 12-myristate 13 acetate; Respiratory burst; Respiratory Burst - drug effects; ROS, reactive oxygen species; Tetradecanoylphorbol Acetate - pharmacology; Ultra-low dose
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/0014-5793(94)01109-5

The respiratory burst induced by phorbol myristate acetate in mouse macrophages was inhibited by ultra-low doses (10 −15 −10 −13 M) of an opioid peptide [ d-Ala 2] methionine enkephalinamide. The effect disappeared at concentrations above and below this range. The inhibition approached 50% and was statistically significant ( P < 0.001). Increasing the time of the opioid incubation with cells brought about a shift in the maximal effect to lower concentrations of the opioid (from 10 −13 to 5 · 10 −15 M) and led to a decrease in the value of the effect, fully in accord with the previously proposed adaptation mechanism of the action of ultra-low doses.