Acetaminophen inhibits the human polymorphonuclear leukocyte function in vitro

The Thermal Potentiation of Acetaminophen-Inhibited PMN Oxidative Metabolismin Vitro

“…Degranulation of isolated human PMNs was also reported after treatment with AM.5 In this laboratory, AM was found to inhibit the CL response of PMNs, superoxide production, and phagocytosis of opsonized dead yeast cells. 6 The present study extends these observations further. Thus the addition of AM not only counteracted the stimulating effect of 39 "C on isolated PMNs, but also increased the percentage of inhibition of OFR production compared with the control (37°C).…”

“…Also, AM exerted some inhibitory effect on the ability of PMNs to generate superoxide anions and to phagocytose opsonized dead yeast cells in a dose-dependent fashion. 6 Modulation of PMN functions by high temperature was reported by several authors. A significant enhancement of bactericidal activity of human PMNs at 40 against 37 "C was noted by Roberts and Steigbigel.7 In addition, Koller et a1.…”

“…Besides, at a higher temperature (42 "C) the viability of PMNs was markedly reduced. 6 Elevation of the body temperature is usually associated with viral or bacterial infections, and, since AM is a widely used antipyretic drug, the present study was undertaken to examine the effect of low concentration of AM (10-7M) on the oxidative metabolism of whole blood as well as isolated human PMNs incubated at temperatures less than 37 "C for various time intervals, using the luminol-dependent CL technique. Additionally, the effect of temperature on AM-induced inhibition of superoxide generation by isolated PMN was investigated using the ferricytochrome C reduction method.…”

Risk factors and mechanisms of anaphylactoid reactions to acetylcysteine in acetaminophen overdose

“…Supra-therapeutic concentrations of acetaminophen inhibit leukocytes and platelets via reversible cyclo-oxygenase inhibition and reduce prostaglandin and thromboxane synthesis (31,32). Therefore, acetaminophen might minimize the severity of NAC adverse effects by inhibiting the inflammatory cascade, as previously suggested (8).…”

Comparison of oral and i.v. acetylcysteine in the treatment of acetaminophen poisoning

“…[38][39][40] This is thought to be due to acetaminophen-induced inhibition of cyclooxygenase and the subsequent inhibition of prostaglandin and thromboxane synthesis. Schmidt and Dalhoff 36 postulated that acetaminophen inhibits the function of basophils and mast cells, resulting in decreased anaphylactoid reactions to acetylcysteine in patients with toxic acetaminophen serum levels.…”