Modification of anti-inflammatory drug effectiveness by ambient lipid peroxides
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Cited by (79)
Inhibition of mitochondrial function: An alternative explanation for the antipyretic and hypothermic actions of acetaminophen
2023, Life SciencesCitation Excerpt :Historically the antipyretic properties of acetaminophen have been attributed to the inhibition of the cyclooxygenase-2 (COX-2) enzyme [6,7] or a putative cyclooxygenase protein termed COX-3 [8]. However, linking the temperature regulatory actions of acetaminophen to the inhibition of cyclooxygenase enzymes has always been problematic, as it is a weak inhibitor of cyclooxygenases which is out of step with its ability to lower body temperature [6,9–11]. In our previous study, we showed that acetaminophen attenuated both lipolysis and mitochondrial function which are both essential for heat generation and thermoregulation [12].
Lipid nutrition: “In silico” studies and undeveloped experiments
2022, Progress in Lipid ResearchCitation Excerpt :Two excellent reviews describe how NSAIDs decrease prostaglandin formation [109,110]. When glutathione peroxidase was added to decrease hydroperoxide amplification in in vitro assays of NSAID inhibition of PGHS activity, it made some NSAIDS more potent while others were not enhanced [111]. The result led to a concept that hyperalgesic conditions may occur at nM levels of peroxide, less than occurs in more intense inflammatory conditions [112].
Part I. Mechanisms of actions and metabolism of acetaminophen related to the neonatal brain
2021, Early Human DevelopmentLoss of hypothermic and anti-pyretic action of paracetamol in cyclooxygenase-1 knockout mice is indicative of inhibition of cyclooxygenase-1 variant enzymes
2019, European Journal of PharmacologyCitation Excerpt :It has been argued by several groups that both the antipyretic and analgesic target for paracetamol is COX-2. Hinz and colleagues in 2007 demonstrated a 4.4 fold selectivity by paracetamol for the inhibition of human COX-2 (IC50 = 25.8 μmol/L) over COX-1 (IC50 = 113.7 μmol/L) and argued that the weak inhibitory effect by paracetamol on COX-2 activity during inflammation and hence its weak anti-inflammatory activity is dictated by its lower potency for COX inhibition under elevated intracellular lipid hydroperoxide tone (Hanel and Lands, 1982). It is noteworthy that to date the link between the lipid hydroperoxide tone and the inhibition of COX enzymes by paracetamol has only been demonstrated in vitro (Boutaud et al., 2002; Lucas et al., 2005; Ouellet and Percival, 2001) and not shown in vivo.
Acetaminophen: Old Drug, New Issues
2015, Journal of EndodonticsCitation Excerpt :In the brain, liver, and lung, monoacylglycerol lipase hydrolyzes the endocannabinoid 2-arachidonoylglycerol to liberate arachidonic acid (16). Therapeutic concentrations of acetaminophen inhibit COX activity when the levels of arachidonic acid and peroxide are low but have little effect when the levels of arachidonic acid or peroxide are high as seen in severe inflammatory conditions such as rheumatoid arthritis (17, 18). In addition to its direct effect on COX, acetaminophen also inhibits prostaglandin synthesis by scavenging peroxynitrite, an activator of COX (19).