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Last Updated: 3 years ago

Possible Interaction: Arachidonic Acid and Nicotine

supplement:

Arachidonic Acid

Research Papers that Mention the Interaction

In intact cells, nicotine , cotinine and methylnicotine at submicromolar concentrations inhibited the rate of conversion of both arachidonic acid and the unstable endoperoxide prostaglandin H2 into thromboxane but not into other eicosanoids.
The clinical investigator  •  2004  |  View Paper
Nicotine , compared to saline, when administrated 2 mins before [1-14C]AA infusion, significantly decreased k∗ for AA in 26 regions, including cerebral cortex, thalamus, and habenula—interpeduncular regions, by 13% to 45%.
We hypothesized that nicotine would modify brain signaling involving AA by binding to nAChRs.
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism  •  2009  |  View Paper
In addition, a 12h treatment with nicotine increased mRNA levels of trkA. Both nicotine and exogenous NGF inhibited arachidonic acid induced apoptosis of spinal cord neurons.
Neuroscience Research  •  2003  |  View Paper
In addition, because nicotine can exert a variety of neuroprotective effects, we hypothesized that it can prevent arachidonic acid induced apoptosis of spinal cord neurons.
These results indicate that nicotine can exert potent neuroprotective effects by inhibiting arachidonic acid induced apoptotic cascades of spinal cord neurons.
Journal of neurochemistry  •  2001  |  View Paper
Because nicotine is known to be a neuroprotective agent, we propose that it can prevent arachidonic acid-induced neurotoxicity.
In addition, nicotine prevented arachidonic acid-induced activation of caspase-3 activity and apoptotic cell death.
Nicotine attenuated arachidonic acid-induced compromised cell viability and cellular ATP levels in spinal cord neurons.
Nicotine exerted these protective effects when used at the concentration of 10 microM and only after a 2-h pre-treatment before a co-exposure to arachidonic acid.
Brain Research  •  2000  |  View Paper
It is suggested that the enhancement by chronic nicotine treatment of depressor responses to arachidonic acid could be due to changes in the formation and/or removal of its vaso-active metabolites (i.e. prostacyclin and/or thromboxane A2).
The vasodepressor effect of arachidonic acid was significantly enhanced in rats given nicotine 5 and 25 micrograms/ml in their drinking water for 10 days but remained unchanged in the animals treated with 1 microgram/ml nicotine for 10 days or given 1 mg/kg i.v.
Pharmacology  •  1991  |  View Paper
Components of the particulate phase of smoke (especially nicotine ) as well as the gas phase of smoke have been shown to adversely alter arachidonic acid metabolism.
Prostaglandins, leukotrienes, and essential fatty acids  •  1988  |  View Paper
Nicotine , a major constituent of smoke, has been shown to adversely alter arachidonic acid metabolism.
Artery  •  1987  |  View Paper