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      Argon: Systematic Review on Neuro- and Organoprotective Properties of an “Inert” Gas

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          Abstract

          Argon belongs to the group of noble gases, which are regarded as chemically inert. Astonishingly some of these gases exert biological properties and during the last decades more and more reports demonstrated neuroprotective and organoprotective effects. Recent studies predominately use in vivo or in vitro models for ischemic pathologies to investigate the effect of argon treatment. Promising data has been published concerning pathologies like cerebral ischemia, traumatic brain injury and hypoxic ischemic encephalopathy. However, models applied and administration of the therapeutic gas vary. Here we provide a systematic review to summarize the available data on argon’s neuro- and organoprotective effects and discuss its possible mechanism of action. We aim to provide a summary to allow further studies with a more homogeneous setting to investigate possible clinical applications of argon.

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          Competitive inhibition at the glycine site of the N-methyl-D-aspartate receptor by the anesthetics xenon and isoflurane: evidence from molecular modeling and electrophysiology.

          Nicholas P. Franks, Mervyn Maze, Paul Banks … (2007)
          Inhibition of N-methyl-D-aspartate (NMDA) receptors by anesthetic gases and vapors may play an important role in anesthesia and neuroprotection. However, the site of action of these agents on the NMDA receptor is unknown. The authors show that xenon and isoflurane compete for the binding of the coagonist glycine on the NMDA receptor NR1 subunit. Using a novel application of grand canonical Monte Carlo simulations, the authors predict the binding site of xenon on NMDA receptors. They test this prediction using electrophysiology on recombinant NMDA receptors. The authors' modeling predicts that xenon binds at the glycine site of the NMDA receptor. The authors show that inhibition of NMDA receptors by xenon and isoflurane increases as glycine concentration is decreased, consistent with the prediction of competitive inhibition at the glycine site. Lineweaver-Burk analysis shows that isoflurane inhibition seems purely competitive with glycine, but for xenon, there is an additional component of noncompetitive inhibition. The loss of inhibitory effect of xenon and isoflurane in mutant NR1(F639A)/NR2A receptors is explained by increased glycine affinity of the mutant receptors, and inhibition is restored at low glycine concentrations. Xenon and isoflurane inhibit NMDA receptors by binding at the same site as the coagonist glycine. This finding may have important implications for general anesthesia and neuroprotection. Neuroprotectants that act at the glycine site of the NMDA receptor antagonists are well tolerated in patients, being devoid of psychotomimetic side effects, and the mechanism of inhibition may play a role in their clinical profile.
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            The protective profile of argon, helium, and xenon in a model of neonatal asphyxia in rats.

            Buwei Yu, Ting-Ting Yang, António Fidalgo … (2012)
            Xenon provides neuroprotection in multiple animal models; however, little is known about the other noble gases. The aim of the current study was to compare xenon, argon, and helium neuroprotection in a neonatal asphyxia model in rats. Randomized controlled trial. Laboratory. Seven-day-old postnatal Sprague-Dawley rats. Seventy percent argon, helium, xenon, or nitrogen balanced with oxygen after hypoxic-ischemic brain injury. Control animals undergoing moderate hypoxic-ischemia endured reduced neuronal survival at 7 days with impaired neurologic function at the juvenile age compared with naïve animals. Severe hypoxic-ischemic damage produced a large cerebral infarction in controls. After moderate hypoxic-ischemia, all three noble gases improved cell survival, brain structural integrity, and neurologic function on postnatal day 40 compared with nitrogen. Interestingly, argon improved cell survival to naïve levels, whereas xenon and helium did not. When tested against more severe hypoxic-ischemic injury only, argon and xenon reduced infarct volume. Furthermore, postinjury body weight in moderate insult was lower in the helium-treated group compared with the naïve, control, and other noble gas treatment groups, whereas in the severe injurious setting, it is lower in both control and helium-treated groups than other groups. In the nondirectly injured hemisphere, argon, helium, and xenon increased the expression of Bcl-2, whereas helium and xenon increased Bcl-xL. In addition, Bax expression was enhanced in the control and helium groups. These studies indicate that argon and xenon provide neuroprotection against both moderate and severe hypoxia-ischemic brain injury likely through prosurvival proteins synthesis.
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              Argon: Neuroprotection in in vitro models of cerebral ischemia and traumatic brain injury

              Philip D Loetscher, Jan Rossaint, Rolf Rossaint … (2009)
              Introduction Recently, it has been shown in several experimental settings that the noble gases xenon and helium have neuroprotective properties. In this study we tested the hypothesis that the noble gas argon has a neuroprotective potential as well. Since traumatic brain injury and stroke are widespread and generate an enormous economic and social burden, we investigated the possible neuroprotective effect in in vitro models of traumatic brain injury and cerebral ischemia. Methods Organotypic hippocampal slice cultures from mice pups were subjected to either oxygen-glucose deprivation or to a focal mechanical trauma and subsequently treated with three different concentrations (25, 50 and 74%) of argon immediately after trauma or with a two-or-three-hour delay. After 72 hours of incubation tissue injury assessment was performed using propidium iodide, a staining agent that becomes fluorescent when it diffuses into damaged cells via disintegrated cell membranes. Results We could show argon's neuroprotective effects at different concentrations when applied directly after oxygen-glucose deprivation or trauma. Even three hours after application, argon was still neuroprotective. Conclusions Argon showed a neuroprotective effect in both in vitro models of oxygen-glucose deprivation and traumatic brain injury. Our promising results justify further in vivo animal research.
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                Author and article information

                Contributors
                Katalin Prokai-Tatrai: Role: External Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 10 October 2014
                Publication date Collection: October 2014
                Volume: 15
                Issue: 10
                Pages: 18175-18196
                Affiliations
                [1 ]Department of Neurosurgery, University RWTH Aachen, 52074 Aachen, Germany; E-Mails: ahoellig@ 123456ukaachen.de (A.H.); anschug@ 123456ukaachen.de (A.S.)
                [2 ]Department of Anesthesiology, University RWTH Aachen, 52074 Aachen, Germany; E-Mails: afahlenkamp@ 123456ukaachen.de (A.V.F.); rrosaint@ 123456ukaachen.de (R.R.)
                Author notes
                [†]

                Members are listed in Appendix.

                [* ]Author to whom correspondence should be addressed; E-Mail: mcoburn@ 123456ukaachen.de ; Tel.: +49-241-80-88179; Fax: +49-241-80-82406.
                Article
                Publisher ID: ijms-15-18175
                DOI: 10.3390/ijms151018175
                PMC ID: 4227210
                PubMed ID: 25310646
                SO-VID: 0cfb8790-82ec-4ceb-9be1-52ef1f1870c8
                Copyright © © 2014 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 14 August 2014
                Date revision received : 12 September 2014
                Date accepted : 23 September 2014
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: argon,neuroprotection,organoprotection,inert gas,hypoxia,ischemia,cytoprotection
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: argon, neuroprotection, organoprotection, inert gas, hypoxia, ischemia, cytoprotection

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