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Last Updated: 3 years ago

Possible Interaction: Acetylcysteine and Arachidonic Acid

supplement:

Acetylcysteine

supplement:

Arachidonic Acid

Research Papers that Mention the Interaction

The thiol antioxidant NAC reduces activation of cPLA2 (assessed by isoform gel-shift and membrane translocation), production of AA in AGE-albumin–exposed neutrophils (H3 release reduced to 104±17%, P =0.94 compared with albumin-exposed neutrophils), and the AGE-augmented neutrophil respiratory burst.
Circulation  •  2003  |  View Paper
Furthermore, … N-acetyl cysteine … arachidonic acid-induced increase in intracellular ROS and TBARS, and the activation of AP1 and NFkappaB. These results indicate that the accumulation of …-3) series elicited an intracellular oxidative stress, resulting in the activation of oxidative stress-responsive transcription factors such as AP1 and NFkappaB.
Biochemical and biophysical research communications  •  1999  |  View Paper
NAC (200 microM) decreased the number of apoptotic nuclei in normoxia in control and arachidonic acid exposed cells.
Pharmacological reports : PR  •  2009  |  View Paper
Here, we show topical AFC inhibits in vivo acute inflammation induced by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) and arachidonic acid using the mouse ear model of inflammation.
The Journal of investigative dermatology  •  2008  |  View Paper
Antioxidants such as trolox or N-acetyl cysteine prevented this synergistic toxicity of SAMe plus AA or SAMe plus BSO, respectively.
American journal of physiology. Gastrointestinal and liver physiology  •  2006  |  View Paper
We further demonstrated that the free radical scavenger N-acetylcysteine blocked arachidonic acid-induced JNK activation, while H(2)O(2), a reactive oxidative molecule, activated JNK in a dose-dependent manner, providing additional support for a redox mechanism.
Proceedings of the National Academy of Sciences of the United States of America  •  1997  |  View Paper
Furthermore, the neurotoxic action of AA was abolished by antioxidants butylated hydroxyanisole or N‐acetylcysteine.
Neuroreport  •  1995  |  View Paper
Additional experiments supported the hypothesis that n-acetylcysteine is an oxygen radical scavenger, since it reduced or prevented the free radical-dependent cerebral arteriolar dilation normally induced by the topical application of arachidonic acid or bradykinin.
Journal of neurosurgery  •  1991  |  View Paper