Propofol and intralipid interact with reactive oxygen species: a chemiluminescence study

Abstract

We have studied the ability of propofol and Intralipid to inhibit reactive oxygen species generated either by stimulated human leucocytes or cell-free systems using luminol chemiluminescence. Human leucocytes were stimulated by a chemotactic peptide, FMLP 1 mumol litre-1, or by a phorbol ester, PMA (protein kinase C activator) 0.1 mumol litre-1. In cell-free experiments, superoxide-hydrogen peroxide, hypochlorous acid or hydroxyl radical-induced chemiluminescence responses were initiated by xanthine 0.1 mmol litre-1 with xanthine oxidase 10 mu. ml-1, NaOCl 70 mumol litre-1 and FeSO4 3 mumol litre-1, respectively. Propofol with Intralipid, and to a lesser degree Intralipid alone, produced a concentration-dependent reduction in chemiluminescence from stimulated leucocytes. Similar attenuations were also observed using propofol with Intralipid on xanthine with xanthine oxidase-, HOCl- and ferrous iron-induced chemiluminescence. However, Intralipid produced a reduction only at high concentrations. Intralipid produced marked decreases in ferrous iron-induced chemiluminescence. This study suggests that propofol had a direct scavenging activity against HOCl, superoxide-hydrogen peroxide and hydroxyl radical in the concentrations used. These direct scavenging effects may contribute to the effect of propofol on human leucocyte chemiluminescence.

Therapeutic concentrations of propofol protects mouse macrophages from nitric oxide-induced cell death and apoptosis

“…In a human leukocyte chemiluminescence study, Demiryurek et al reported that PPF possesses a direct scavenging effect on hydroxyl chloride, superoxide, hydrogen peroxide and hydroxyl radical. 10 Our data suggest that PPF has no such effects on the direct scavenging of nitric oxide. Therefore, the protective mechanism of PPF against nitric oxide-mediated cellular damage may be through other signal transduction pathways rather than direct scavenging of nitric oxide.…”

Hematologic changes in propofol-anesthetized dogs with or without tramadol administration

“…Additionally, catecholamines and glucocorticoids, released during anesthesia, impaired the immune system (Elenkov and Chrousos, 2002) because the lymphocyte production and function decreased (Inada et al, 2004). However, we suggested that these factors did not influence white blood cell counts because propofol provides an enhancement in antioxidant efficacies (Murphy et al, 1992;Demiryurek et al, 1998) and promotes lower release of catecholamines (Elenkov and Chrousos, 2002).…”

The Effect of Dexmedetomidine and Propofol on Oxidative Stress and Antioxidizing System Studied on Liver Ischemia-reperfusion Model on Rats

“…Ko et al has reported that propofol has a preventive effect on ventricles after a global ischemia of the heart [18]. And other similar models of I/R injury on neurons [19], leucocytes [4] and erythrocytes [20] prooved that propofol has a preventive effect against I/R injury. Aarts et al has reported that propofol has a preventive role in cases such as coronary artery transplantation surgery, sepsis and burns, which of all lead into a decreased ontioxidising defense mechanism [13].…”

“…Chemical structure of propofol (2,6-diisoproyl phenol) mimics butilised hydroxy toluen (BHT) and endogenous antioxidising agent alpha-tocopherol (vitamin E) which are phenol containing free oxygen radical scavengers and contains a phenolic hydroxy group [13]. All these molecules form complexes with either the cellular membranes or its structural components resulting in a less reactive molecules and each single propofol molecule can scavenger two free oxygen radicals [3,4]. Its also reported that propofol functions as both peroxynitrite scavenger which is produced by superoxide radicals binding to nitric oxide physiologically and inhibiting lipid peroxidation on cellular membranes [14,15].…”

“…One of these agents, its antioxidant activity proven in many studies is propofol. Its proven that each molecule of propofol can scavange two free radicals and prevent the lipid peroxidation inducted by oxidative stress [3,4]. The alfa 2 adrenoreceptor agonist dexmedetomidin used as an anxiolytic and sedative agent in intensive care units decreases the cathecolamine decharge inducted by ischemia and decreases the damage caused by reperfusion [5,6].…”