Cyclooxygenase-3 (COX-3): Filling in the gaps toward a COX continuum?

Warner, Timothy D.; Mitchell, Jane A.

doi:10.1073/pnas.222543099

Cited by 253 publications

(191 citation statements)

References 34 publications

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“…Interestingly, among low COX inhibitors, acetaminophen was most commonly incriminated, followed by nimesulide, meloxicam, and less frequently, the coxibs, the more selective drugs sparing COX-1 (Figure 2). This is in agreement with the rates of inhibition of COX-1 in vitro,[11] with the exception of acetaminophen that inhibits another isoenzyme, COX-3, which is closely related to COX-1 [12-14]. …”

Section: Discussionsupporting

confidence: 84%

A Novel Phenotype of Nonsteroidal Anti-Inflammatory Drug Hypersensitivity

Sánchez‐Borges¹,

Capriles‐Hulett

Caballero‐Fonseca

2009

World Allergy Organization Journal

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BackgroundSome nonsteroidal anti-inflammatory drug (NSAID)-hypersensitive patients develop adverse reactions when challenged with weak cyclooxygenase 1 (COX-1) inhibitors.ObjectivesTo investigate the prevalence and clinical features of this high-risk population.Materials and methodsPatients from 2 outpatient allergy clinics consulting between October 2005 and October 2007 because of adverse reactions to classic NSAIDs were submitted to confirmatory double-blind oral challenges with the suspected NSAID and with acetaminophen, preferential and/or specific COX-2 inhibitors. Patients were then classified as low-risk and high-risk groups according to the results of provocation tests.ResultsThree hundred three patients were studied: 179 (59.0%) were tolerant to acetaminophen and the selective COX-2 inhibitors (low-risk group), whereas 124 (40.9%) developed reactions to at least one of the ''low COX-1 inhibitors'' (high-risk group). No distinctive demographic or clinical characteristics were present when both groups of patients were compared.ConclusionsA large proportion of patients sensitive to classic NSAIDs cannot tolerate the weak COX-1 inhibitors. Oral challenges should be performed by trained specialists to advise these patients about the use of NSAIDs.

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Section: Discussionsupporting

confidence: 84%

A Novel Phenotype of Nonsteroidal Anti-Inflammatory Drug Hypersensitivity

Sánchez‐Borges¹,

Capriles‐Hulett

Caballero‐Fonseca

2009

World Allergy Organization Journal

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“…COX-2, on the other hand, has been found to be rapidly expressed in inflammatory conditions and is the target for a new group of nonsteroidal anti-inflammatory drugs such as celecoxib and rofecoxib that have negligible effects on the constitutive COX-1 (Hawkey, 1999). The recent controversial finding of a third type of COX, COX-3, derived from the COX-1 gene that is expressed in the cerebral cortex and heart, and is sensitive to analgesic/antipyretic drugs such as acetaminophen (Chandrasekharan et al, 2002), has given new insights into the mechanism of action of such agents (Chandrasekharan et al, 2002;Warner and Mitchell, 2002). It remains to be established if variants of COX-2 will be discovered (Chandrasekharan et al, 2002).…”

Section: Prostanoid Biosynthetic Pathways In Mammalsmentioning

confidence: 99%

Prostaglandins in non-insectan invertebrates: recent insights and unsolved problems

Rowley

Vogan

Taylor

et al. 2005

Journal of Experimental Biology

122

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Prostaglandins, together with thromboxanes (collectively termed prostanoids), are fatty acid derivatives of significant importance in many physiological processes. These compounds are formed following the action of cyclooxygenases (COX) and associated enzymes on C20 polyunsaturated fatty acid precursors released from phospholipids in membranes. Nearly all mammalian cell types have the biosynthetic machinery to produce at least one type of prostanoid. The same C20 fatty acid substrates can also be acted upon by lipoxygenases to produce mono-di-and trihydroxy derivatives such as leukotrienes, lipoxins and resolvins. The final route is the cytochrome P 450 pathway that can convert C20 fatty acids to hydroxylated derivatives.Collectively these compounds are called eicosanoids; the term derived from the Greek eikosi that refers to the C20 backbone in the parent fatty acid.Prostaglandins (PGs) were first discovered in the 1930s by von Euler and colleagues, who found a substance produced by the prostate gland that caused smooth muscle contraction. They christened the active substance 'prostaglandin', but it was over 30 years until the structure and mode of biosynthesis of these fatty acid derivatives became fully understood. PGs have many basic physiological functions where they act as 'local' hormones. For example, thromboxane (Tx) A 2 and prostacyclin (PGI 2 ) generated by platelets and endothelial cells, respectively, regulate the aggregatory behaviour of

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“…Aspirin was the first discovered member of nonsteroidal anti-inflammatory drugs (NSAIDs) (Warner, 2002). Aspirin, also known as acetylsalicylic acid, is a salicylate drug, is a synthetic compound with antipyretic, analgesic, anti-inflammatory, and antiplatelet properties (Awtry and Loscalzo, 2007).…”

Section: Introductionmentioning

confidence: 99%

Aspirin Associated Liver Toxicity – The Optimal Dose of Aspirin in Liver Insufficiency

Rafeeq¹,

Najam²,

Hussain³

2016

IJSRK

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Abstract. Acetylsalicylic acid (Aspirin) belongs to nonsteroidal anti-inflammatory drugs (NSAIDs). Numerous studies have proven that aspirin reduces the signs and symptoms of inflammation and exhibited a broad range of pharmacological activities, including analgesic, antipyretic and antiplatelet properties. Previous studies suggested that beside the pharmacological activities aspirin was also associated with the side effects and toxicity of various doses and in various formulations. The present study is performed to explore the effects of aspirin in various doses (75mg (EC), 100mg, 150 (EC)mg and 300mg) in different preparation (enteric coated (EC), non-enteric coated) on liver enzymes (Serum glutamic oxaloacetate transaminase (SGOT) and Serum glutamic pyruvic transaminase (SGPT)) followed by daily administration for 10 days and for 30 days. We found that the SGOT level was increased by all doses of aspirin after 30 days of treatment, this effect was most significant at 75mg (EC) and 100mg dose, whereas at 150mg (EC) and 300mg was not very significant. The level of SGPT was decreased by all doses regardless of duration of treatment, only 75mg (EC) dose increased its level after 30 days of treatment, suggesting 75mg (EC) aspirin could be hepatotoxic due to lessen of anti-oxidant effects, furthermore suggests that patients with hepatic insufficiency should not receive 75mg (EC) dose of aspirin.

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Cyclooxygenase-3 (COX-3): Filling in the gaps toward a COX continuum?

Cited by 253 publications

References 34 publications

A Novel Phenotype of Nonsteroidal Anti-Inflammatory Drug Hypersensitivity

A Novel Phenotype of Nonsteroidal Anti-Inflammatory Drug Hypersensitivity

Prostaglandins in non-insectan invertebrates: recent insights and unsolved problems

Aspirin Associated Liver Toxicity – The Optimal Dose of Aspirin in Liver Insufficiency

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