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Last Updated: 4 months ago

Possible Interaction: Adenosine Triphosphate and Capsaicin

Research Papers that Mention the Interaction

In addition, capsaicin stimulated the formation of reticular mitochondria, augmented mitochondrial membrane potential, increased adenosine triphosphate production, and upregulated Mfn2.
Journal of vascular surgery  •  2017  |  View Paper
CAP has been shown to improve mitochondrial biogenesis and adenosine triphosphate (ATP) production.
Nutrients  •  2016  |  View Paper
The ATP levels were drastically suppressed by capsaicin treatment in both BxPC-3 and AsPC-1 cells and attenuated by catalase or EUK-134.
PloS one  •  2011  |  View Paper
At a negative holding potential, the P2X3 receptor agonist α,β‐meATP induced less current in the presence of the TRPV1 agonist capsaicin than that in its absence.
Pain  •  2009  |  View Paper
Electrophysiology experiments show that either ATP or PIP2 prevent desensitization to repeated applications of capsaicin , i.e., tachyphylaxis, while calmodulin plays an opposing role and is necessary for tachyphylaxis.
Neuron  •  2007  |  View Paper
In cells expressing TRPV1, ATP increased the currents evoked by capsaicin or protons through activation of P2Y metabotropic receptors in a PKC-dependent manner.
Novartis Foundation symposium  •  2004  |  View Paper
CAP causes mitochondrial membrane potential loss, inhibits ATP synthesis and reduces mitochondrial Bcl-2 protein production.
In summary, these results suggest that CAP induces cytotoxicity by disturbing mitochondrial potential, and inhibits ATP synthesis in NET cells.
Cellular signalling  •  2014  |  View Paper
We demonstrated that CPS induces pre- and early apoptotic cell surface exposure of calreticulin (CRT), HSP90, and HSP70 as well as ATP release.
Cell Stress and Chaperones  •  2013  |  View Paper
The same concentration of capsaicin induced the release of about 7 fmol adenosine triphosphate per mg.
The Journal of urology  •  2009  |  View Paper
It has been reported that ATP , one of the inflammatory mediators, potentiates the VR1 currents evoked by capsaicin or protons and reduces the temperature threshold for activation of VR1 through metabotropic P2Y1 receptors in a protein Kinase C (PKC)-dependent pathway, suggesting the phosphorylation of VR1 by PKC.
The Journal of Biological Chemistry  •  2002  |  View Paper
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