About: Biochemical insight into soman intoxication and treatment with atropine, HI-6, trimedoxime, and K203 in a rat model     Goto   Sponge   NotDistinct   Permalink

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Description
  • The present experiment is based on biochemical assessment of nerve agent soman intoxication and atropine, respectively atropine and HI-6, trimedoxime or K203 treatment in rats. Background: Nerve agents are toxic substances irreversibly inhibiting enzyme acetylcholinesterase (AChE). Treatment is typically based on application of atropine and oxime reactivator. Atropine is able to protect overstimulation of muscarinic acetylcholine receptors. Application of oxime reactivator enable return of AChE activity and full suppression of intoxication. The most striking shifts were found for blood acetylcholinesterase and plasma creatinine, glucose, inorganic phosphate as well as uric acid. Lactate dehydrogenase and aspartate aminotransferase assays were useless due to soman interference. Conclusion: It was demonstrated that treatment was able to protect poisoned animals from metabolic disorder represented by hyperglycemia and nephropathy represented by hyperuricemia and elevated creatinine. Soman exposure and treatment with the oxime reactivators and/or atropine contains quite complex and still not well understood side mechanisms (Tab. 2, Fig. 1, Ref. 25).
  • The present experiment is based on biochemical assessment of nerve agent soman intoxication and atropine, respectively atropine and HI-6, trimedoxime or K203 treatment in rats. Background: Nerve agents are toxic substances irreversibly inhibiting enzyme acetylcholinesterase (AChE). Treatment is typically based on application of atropine and oxime reactivator. Atropine is able to protect overstimulation of muscarinic acetylcholine receptors. Application of oxime reactivator enable return of AChE activity and full suppression of intoxication. The most striking shifts were found for blood acetylcholinesterase and plasma creatinine, glucose, inorganic phosphate as well as uric acid. Lactate dehydrogenase and aspartate aminotransferase assays were useless due to soman interference. Conclusion: It was demonstrated that treatment was able to protect poisoned animals from metabolic disorder represented by hyperglycemia and nephropathy represented by hyperuricemia and elevated creatinine. Soman exposure and treatment with the oxime reactivators and/or atropine contains quite complex and still not well understood side mechanisms (Tab. 2, Fig. 1, Ref. 25). (en)
Title
  • Biochemical insight into soman intoxication and treatment with atropine, HI-6, trimedoxime, and K203 in a rat model
  • Biochemical insight into soman intoxication and treatment with atropine, HI-6, trimedoxime, and K203 in a rat model (en)
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  • Biochemical insight into soman intoxication and treatment with atropine, HI-6, trimedoxime, and K203 in a rat model
  • Biochemical insight into soman intoxication and treatment with atropine, HI-6, trimedoxime, and K203 in a rat model (en)
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  • RIV/60162694:G44__/11:00002467!RIV12-MO0-G44_____
http://linked.open...avai/riv/aktivita
http://linked.open...avai/riv/aktivity
  • Z(MO0FVZ0000501), Z(MSM6215712402)
http://linked.open...iv/cisloPeriodika
  • 10
http://linked.open...vai/riv/dodaniDat
http://linked.open...aciTvurceVysledku
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  • 188249
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  • RIV/60162694:G44__/11:00002467
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  • nerve agents; sarin; oxime reactivator; acetylcholinesterase; acetylcholine; cholinergic crisis (en)
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  • SK - Slovenská republika
http://linked.open...ontrolniKodProRIV
  • [E9DE67BF8A80]
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  • Bratislava Medical Journal-Bratislavske Lekarske Listy
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http://linked.open...v/svazekPeriodika
  • 112
http://linked.open...iv/tvurceVysledku
  • Kassa, Jiří
  • Kuča, Kamil
  • Pikula, Jiří
  • Pohanka, Miroslav
http://linked.open...ain/vavai/riv/wos
  • 000294514400001
http://linked.open...n/vavai/riv/zamer
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  • 0006-9248
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  • G44
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