Ion transportation: Difference between revisions
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==Function== | ==Function== | ||
Ion transportation plays key roles in the functioning of many different [[:Category:Body systems|bodily systems]], including the [[nervous system]], the [[endocrine system]], [[Portal:Energy metabolism|energy metabolism]] and the [[cardiovascular system]]. Important ions, sometimes called [[electrolyte]]s, include [[calcium]], [[potassium]], [[sodium]], [[chlorine]], and [[magnesium]].<ref name="Ashcroftbook">{{Cite book|url=https://books.google.co.uk/books?id=LaE-PSQJRwgC&printsec=frontcover&dq=channelopathy&hl=en&sa=X#v=onepage&q=channelopathy&f=true|title=Ion Channels and Disease|last=Ashcroft|first=Frances M.|date=1999-10-20|publisher=Academic Press|isbn=9780080535210|language=en}}</ref> | Ion transportation plays key roles in the functioning of many different [[:Category:Body systems|bodily systems]], including the [[nervous system]], the [[endocrine system]], [[Portal:Energy metabolism|energy metabolism]] and the [[cardiovascular system]]. Important ions, sometimes called [[electrolyte]]s, include [[calcium]], [[potassium]], [[sodium]], [[chlorine]], and [[magnesium]].<ref name="Ashcroftbook">{{Cite book | url = https://books.google.co.uk/books?id=LaE-PSQJRwgC&printsec=frontcover&dq=channelopathy&hl=en&sa=X#v=onepage&q=channelopathy&f=true | title = Ion Channels and Disease | last = Ashcroft | first = Frances M. | date = 1999-10-20|publisher=Academic Press|isbn=9780080535210|language=en}}</ref> | ||
Cell membranes are normally impermeable to ions. [[Ion channel]]s, ion pumps, and ion transporters are cell membrane proteins that allow and control ion transport into and out of cells, or between different compartments within cells.<ref name="Ashcroftbook" /> | Cell membranes are normally impermeable to ions. [[Ion channel]]s, ion pumps, and ion transporters are cell membrane proteins that allow and control ion transport into and out of cells, or between different compartments within cells.<ref name="Ashcroftbook" /> | ||
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==ME/CFS== | ==ME/CFS== | ||
[[Klaus Wirth]] and [[Carmen Scheibenbogen]] hypothesize that high intracellular sodium levels may be the primary cause of the dysfunction in MECFS. This hypothesis states that high intracellular sodium caused by infection or [[exercise intolerance|exertion]] triggers calcium channels to reverse. This creates a positive feedback loop where even small amounts of exertion can cause severe intracellular ion imbalance (PEM). In particular, intracellular calcium is essential to [[mitochondria]]l function, causing the energy dysfunction seen in ME/CFS. This hypothesis also predicts low intracellular potassium following exertion in ME/CFS patients, causing a form of [[hypokalemic periodic paralysis]] seen in [[severe and very severe ME|severe patients]]. | [[Klaus Wirth]] and [[Carmen Scheibenbogen]] hypothesize that high intracellular sodium levels may be the primary cause of the dysfunction in MECFS. This hypothesis states that high intracellular sodium caused by infection or [[exercise intolerance|exertion]] triggers calcium channels to reverse. This creates a positive feedback loop where even small amounts of exertion can cause severe intracellular ion imbalance (PEM). In particular, intracellular calcium is essential to [[mitochondria]]l function, causing the energy dysfunction seen in ME/CFS. This hypothesis also predicts low intracellular potassium following exertion in ME/CFS patients, causing a form of [[hypokalemic periodic paralysis]] seen in [[severe and very severe ME|severe patients]]. | ||
An Australian research team led by [[Sonya Marshall-Gradisnik]] found that both [[ME/CFS]] and [[Long COVID]] patients had ion channel receptor dysfunction that affected the flow of [[calcium]] into and out of cells.<ref name="Cabanas2021"/> | |||
==Symptom Recognition== | ==Symptom Recognition== | ||
Symptoms resulting from ion transportation problems are part of the [[International Consensus Criteria]].<ref name="ICC2011primer">{{citation | Symptoms resulting from ion transportation problems are part of the [[International Consensus Criteria]].<ref name="ICC2011primer">{{citation | last = Carruthers | first1 = BM | authorlink1 = Bruce Carruthers | last2 = van de Sande | first2 = MI | authorlink2 = Marjorie van de Sande | last3 = De Meirleir | first3 = KL | authorlink3 = Kenny de Meirleir | last4 = Klimas | first4 = NG | authorlink4 = Nancy Klimas | last5 = Broderick | first5 = G | authorlink5 = Gordon Broderick | last6 = Mitchell | first6 = T | authorlink6 = Terry Mitchell | last7 = Staines | first7 = D | authorlink7 = Donald Staines | last8 = Powles | first8 = ACP | authorlink8 = A C Peter Powles | last9 = Speight | first9 = N | authorlink9 = Nigel Speight | last10 = Vallings | first10 = R | authorlink10 = Rosamund Vallings | last11 = Bateman | first11 = L | authorlink11 = Lucinda Bateman | last12 = Bell | first12 = DS | authorlink12 = David Bell | last13 = Carlo-Stella | first13 = N | authorlink13 = Nicoletta Carlo-Stella | last14 = Chia | first14 = J | authorlink14 = John Chia | last15 = Darragh | first15 = A | authorlink15 = Austin Darragh | last16 = Gerken | first16 = A | authorlink16 = Anne Gerken | last17 = Jo | first17 = D | authorlink17 = Daehyun Jo | last18 = Lewis | first18 = DP | authorlink18 = Donald Lewis | last19 = Light | first19 = AR | authorlink19 = Alan Light | last20 = Light | first20 = KC | authorlink20 = Kathleen Light | last21 = Marshall-Gradisnik | first21 = S | authorlink21 = Sonya Marshall-Gradisnik | last22 = McLaren-Howard | first22 = J | authorlink22 = John McLaren-Howard | last23 = Mena | first23 = I | authorlink23 = Ismael Mena | last24 = Miwa | first24 = K | authorlink24 = Kunihisa Miwa | last25 = Murovska | first25 = M | authorlink25= Modra Murovska | last26 = Stevens | first26 = SR | authorlink26 = Staci Stevens| title = Myalgic encephalomyelitis: Adult & Paediatric: International Consensus Primer for Medical Practitioners | date = 2012| isbn = 978-0-9739335-3-6 | url = http://www.investinme.org/Documents/Guidelines/Myalgic%20Encephalomyelitis%20International%20Consensus%20Primer%20-2012-11-26.pdf}}</ref> | ||
| | |||
| last24 = Miwa | first24= K | authorlink24= Kunihisa Miwa| last25 = Murovska | first25= M | authorlink25= Modra Murovska| last26 = Stevens | first26= SR | authorlink26= Staci Stevens| title = Myalgic encephalomyelitis: Adult & Paediatric: International Consensus Primer for Medical Practitioners | date = 2012| isbn = 978-0-9739335-3-6 | url = http://www.investinme.org/Documents/Guidelines/Myalgic%20Encephalomyelitis%20International%20Consensus%20Primer%20-2012-11-26.pdf}}</ref> | |||
==Notable studies== | ==Notable studies== | ||
*2021, Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment<ref name="Cabanas2021">{{Cite journal|title=Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment|date=2021|url=https://www.frontiersin.org/articles/10.3389/fimmu.2021.687806|journal=Frontiers in Immunology|volume=12|issue=|pages=687806|last=Cabanas|first=Helene| | *2021, Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment<ref name="Cabanas2021">{{Cite journal | title = Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment | date = 2021 | url=https://www.frontiersin.org/articles/10.3389/fimmu.2021.687806|journal=Frontiers in Immunology|volume=12|issue= | pages = 687806 | last = Cabanas | first = Helene | authorlink = Hélène Cabanas | last2 = Muraki | first2 = Katsuhiko | authorlink2 = | last3 = Eaton-Fitch | first3 = Natalie | authorlink3 = Natalie Eaton-Fitch | last4 = Staines | first4 = Donald Ross | authorlink4 = Donald Staines | last5 = Marshall-Gradisnik | first5 = Sonya | authorlink5 = Sonya Marshall-Gradisnik|doi=10.3389/fimmu.2021.687806|pmc=PMC8313851|pmid=34326841|access-date=|issn=1664-3224|quote=|via=}}</ref> - [https://www.frontiersin.org/articles/10.3389/fimmu.2021.687806/full (Full text)] | ||
== Possible Causes == | == Possible Causes == | ||
Latest revision as of 15:39, April 2, 2023
Ion transportation refers to the transport of ions into or out of cells or cell compartments.[1]
Function[edit | edit source]
Ion transportation plays key roles in the functioning of many different bodily systems, including the nervous system, the endocrine system, energy metabolism and the cardiovascular system. Important ions, sometimes called electrolytes, include calcium, potassium, sodium, chlorine, and magnesium.[1]
Cell membranes are normally impermeable to ions. Ion channels, ion pumps, and ion transporters are cell membrane proteins that allow and control ion transport into and out of cells, or between different compartments within cells.[1]
Ion channel diseases[edit | edit source]
Ion channel diseases are caused by mutations in ion channel genes.[1] Evidence of ion transportation dysfunction has been found in ME/CFS.[2]
Ion transportation dysfunction can result in an incorrect balance of different ions, which in extreme cases may cause death.
Sources[edit | edit source]
Ions are introduced to the body from food, drinks (including trace amounts in water), and can also be taken as supplements. Supplements can be injected or taken by mouth.
ME/CFS[edit | edit source]
Klaus Wirth and Carmen Scheibenbogen hypothesize that high intracellular sodium levels may be the primary cause of the dysfunction in MECFS. This hypothesis states that high intracellular sodium caused by infection or exertion triggers calcium channels to reverse. This creates a positive feedback loop where even small amounts of exertion can cause severe intracellular ion imbalance (PEM). In particular, intracellular calcium is essential to mitochondrial function, causing the energy dysfunction seen in ME/CFS. This hypothesis also predicts low intracellular potassium following exertion in ME/CFS patients, causing a form of hypokalemic periodic paralysis seen in severe patients.
An Australian research team led by Sonya Marshall-Gradisnik found that both ME/CFS and Long COVID patients had ion channel receptor dysfunction that affected the flow of calcium into and out of cells.[3]
Symptom Recognition[edit | edit source]
Symptoms resulting from ion transportation problems are part of the International Consensus Criteria.[2]
Notable studies[edit | edit source]
- 2021, Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment[3] - (Full text)
Possible Causes[edit | edit source]
Potential Treatments[edit | edit source]
Electrolytes are one of the suggestions for treating energy metabolism and ion iransportation problems in general.
See also[edit | edit source]
- Channelopathy
- Transient receptor potential melastatin 3 (TRPM3)
- Hypokalemic periodic paralysis
- Electrolytes
Learn more[edit | edit source]
- Channelopathies (review) - Kim June-Bum
References[edit | edit source]
- ↑ 1.0 1.1 1.2 1.3 Ashcroft, Frances M. (October 20, 1999). Ion Channels and Disease. Academic Press. ISBN 9780080535210.
- ↑ 2.0 2.1 Carruthers, BM; van de Sande, MI; De Meirleir, KL; Klimas, NG; Broderick, G; Mitchell, T; Staines, D; Powles, ACP; Speight, N; Vallings, R; Bateman, L; Bell, DS; Carlo-Stella, N; Chia, J; Darragh, A; Gerken, A; Jo, D; Lewis, DP; Light, AR; Light, KC; Marshall-Gradisnik, S; McLaren-Howard, J; Mena, I; Miwa, K; Murovska, M; Stevens, SR (2012), Myalgic encephalomyelitis: Adult & Paediatric: International Consensus Primer for Medical Practitioners (PDF), ISBN 978-0-9739335-3-6
- ↑ 3.0 3.1 Cabanas, Helene; Muraki, Katsuhiko; Eaton-Fitch, Natalie; Staines, Donald Ross; Marshall-Gradisnik, Sonya (2021). "Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment". Frontiers in Immunology. 12: 687806. doi:10.3389/fimmu.2021.687806. ISSN 1664-3224. PMC 8313851. PMID 34326841.
