Xenon—A Miracle Drug ?

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I have been curious about dissociative anaesthetics for ME/CFS for awhile. But in reading about xenon, I’m more excited by the potential applications than by ketamine, nitrous oxide, etc. The only downside seems to be cost and difficulty obtaining it.

“Xenon interacts with many different receptors and ion channels, and like many theoretically multi-modal inhalation anesthetics, these interactions are likely complementary. Xenon is a high-affinity glycine-site NMDA receptor antagonist.[136]However, xenon is different from certain other NMDA receptor antagonists in that it is not neurotoxic and it inhibits the neurotoxicity of ketamine and nitrous oxide, while actually producing neuroprotective effects.[137][138] Unlike ketamine and nitrous oxide, xenon does not stimulate a dopamine efflux in the nucleus accumbens.[139] Like nitrous oxide and cyclopropane, xenon activates the two-pore domain potassium channel TREK-1. A related channel TASK-3 also implicated in the actions of inhalation anesthetics is insensitive to xenon.[140] Xenon inhibits nicotinic acetylcholine α4β2 receptors which contribute to spinally mediated analgesia.[141][142] Xenon is an effective inhibitor of plasma membrane Ca2+ATPase. Xenon inhibits Ca2+ ATPase by binding to a hydrophobic pore within the enzyme and preventing the enzyme from assuming active conformations.[143]
Xenon is a competitive inhibitor of the serotonin 5-HT3 receptor. While neither anesthetic nor antinociceptive, this reduces anesthesia-emergent nausea and vomiting.[144]

Xenon has a minimum alveolar concentration (MAC) of 72% at age 40, making it 44% more potent than N2O as an anesthetic.[145] Thus, it can be used with oxygen in concentrations that have a lower risk of hypoxia.
...
Xenon induces robust cardioprotectionand neuroprotection through a variety of mechanisms. Through its influence on Ca2+, K+, KATP\HIF, and NMDA antagonism, xenon is neuroprotective when administered before, during and after ischemic insults.[147][148] Xenon is a high affinity antagonist at the NMDA receptor glycine site.[136] Xenon is cardioprotective in ischemia-reperfusion conditions by inducing pharmacologicnon-ischemic preconditioning. Xenon is cardioprotective by activating PKC-epsilon and downstream p38-MAPK.[149] Xenon mimics neuronal ischemic preconditioning by activating ATP sensitive potassium channels.[150]Xenon allosterically reduces ATP mediated channel activation inhibition independently of the sulfonylurea receptor1 subunit, increasing KATP open-channel time and frequency.[151]

Sports dopingEdit
Inhaling a xenon/oxygen mixture activates production of the transcription factor HIF-1-alpha, which may lead to increased production of erythropoietin. The latter hormone is known to increase red blood cell production and athletic performance. Reportedly, doping with xenon inhalation has been used in Russia since 2004 and perhaps earlier.[152] On August 31, 2014, the World Anti Doping Agency (WADA) added xenon (and argon) to the list of prohibited substances and methods, although no reliable doping tests for these gases have yet been developed.[153
So we have an nmda antagonist with some direct effects on ion channels, increases blood volume, antagonist of 5ht3 (like zofran) , neuro and cardioprotective , and I have heard from people in the industry that it’s bejng experimented with to protect from brain damage in premature babies. I also have found some info on its use in cancer. Will post below.

The ONLY real downside seems to be cost and availability.

@haidut @Travis @SB4 @Dan Wich thoughts ?
 
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energyandstruct
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I asked ray about nitrous oxide, carbogen, and xenon and his response was this:
“Nitrous oxide can be changed into nitric oxide, so I don’t think it’s safe. I think CO2 is the most practical gas, the noble gases are expensive and hard to use, but the idea of using them therapeutically is interesting because of their effects on water.
Xenon and breast cancer cell function in-vitro : 9AP6-7
Ash, S. A.1; Valchev, G.1; Crowley, P.2; Gallagher, H. G.3; Buggy, D. J.1
European Journal of Anaesthesiology: June 2014 - Volume 31 - Issue - p 160
Pharmacology
Background and Goal of Study: Breast cancer is one of the most common causes of cancer death among women, usually from metastasis. Several perioperative factors may influence the development of metastasis. Volatile agents have been implicated in metastasis-enhancing effects on cancer cell biology. The noble gas Xenon is an anaesthetic with many desirable properties, but its effects on cancer cell biology are unknown. Therefore, we investigated the effect of Xenon and Sevoflurane on proliferation, migration and expression of angiogenesis biomarkers in breast adenocarcinoma cell cultures in-vitro.
Materials and methods: MDA-MB-231 (estrogen receptor negative, ER-) and MCF-7 (estrogen and progesterone receptor positive, ER+) breast cancer cells were seeded in 96-well plates and exposed to experimental or control gas concurrently in two hermetic chambers. The Xenon cylinder contained O2 25 %, CO2 5% and Xenon 70%. The Control gas cylinder contained O2 25 %, CO2 5% and N2 75%. Sevoflurane 2.5% was administered in control gas. Methylthaizolyldiphenyl-tetrazolium-bromide (MTT) assay evaluated the effect of Xenon on cell viability. Cancer cell migration was determined using the Oris™ Cell Migration Assay, its mechanism with addition of glycine or glipizide. Human Angiogensis Array C1 quantified the expression of angiogenesis markers in the cellular supernatant.
Results: Cell exposure to each gas mixtures for 1, 3 or 5 hr had no effect on cell viability in either cell. Xenon reduced ER- migration to 59±13% following 1 hr exposure, P=0.02; to 64±10% at 3 hr, P=0.01; and 71±9% at 5 hr, P=0.04. Similar results were observed in ER+ cells. Sevoflurane had no effect on migration. Glycine, a NMDA receptor agonist, competitively reversed Xenon inhibition of migration, increasing ER- migration to 190±44%, P=0.02 and ER+ migration to 173±17%, P=0.02. No effect was observed with addition of glipizide. Examination of the angiogenisis array film in Xenon exposed media showed decreased RANTES cytokine compared with Sevoflurane and Control (mean dot density 2.05±0.20 vs 2.95±0.07 and 3.1±0.28 respectively, P=0.02).
Conclusion: Xenon inhibits breast cancer cell migration in both ER+ and ER- breast cancer cells by an NMDA receptor mediated mechanism, whereas Sevoflurane does not. Xenon decreases expression of breast cancer angiogenesis factor RANTES compared with Sevoflurane.
Acknowledgements: Funded by an unrestricted research grant from Air Liquide, manufacturers of Xenon.”
 

michael94

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zum zum zum

die profane Gemagen geht jeden an und da ist nichts zu sagen ))

girls are like drugs ( in a good way ... or bad :)
 

SB4

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@debored13 Certainitly is interesting, the effects you listed could well benefit our symptoms although it is impossible to say without trying. If you get your hands on some I will be following with interest.
 
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energyandstruct
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@debored13 Certainitly is interesting, the effects you listed could well benefit our symptoms although it is impossible to say without trying. If you get your hands on some I will be following with interest.
i doubt I will be able to obtain it. Even if I did , I would want to figure out how to recycle it somehow (it’s inert so it should be doable).
 
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energyandstruct
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It looks like you can get reasonable xenon prices on Ali Baba if you buy, say, 1000 liters lol. Group buy?
 
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energyandstruct
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I tried a noble gas store in New York, they said to call back and I’ve been calling and they won’t pick up , I’m pretty sure they may have figured this out
 

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