Leevi
ALStuttu:n jäsen
K2-vitamiinista saattaa olla apua ALS:ssa.
http://www.sciencemag.org/content/336/6086/1241.summary
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1241-1242
DOI: 10.1126/science.1223812
Vitamin K2 Takes Charge
Sheetal Bhalarao, Thomas R. Clandinin
Mitochondria are dynamic organelles that play central roles in eukaryotic cellular energy metabolism. They harbor an electron transport chain (ETC) that couples electron transfer to the movement of protons across the mitochondrial inner membrane, forming an electrochemical gradient that captures chemical energy in the form of adenosine triphosphate (ATP). The biochemical and biophysical properties of the ETC have been studied in detail (1). On page 1306 of this issue, Vos et al. (2) report a new constituent of this chain. The authors show that vitamin K2 is an electron carrier, suggesting this small organic molecule as a possible treatment for mitochondrial pathologies such as Parkinson's disease and amyotrophic lateral sclerosis.
http://www.sciencemag.org/content/336/6086/1306.abstract
Published Online May 10 2012 Science 8 June 2012:
Vol. 336 no. 6086 pp. 1306-1310
DOI: 10.1126/science.1218632
Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
Melissa Vos, Giovanni Esposito, Janaka N. Edirisinghe, Sven Vilain, Dominik M. Haddad, Jan R. Slabbaert, Stefanie Van Meensel, Onno Schaap, Bart De Strooper, R. Meganathan, Vanessa A. Morais, Patrik Verstreken
Human UBIAD1 localizes to mitochondria and converts vitamin K1 to vitamin K2. Vitamin K2 is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K2 exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson’s disease that affects mitochondrial function. We found that vitamin K2 was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K2, and, similar to ubiquinone, vitamin K2 transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K2 that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.
http://neurosciencenews.com/als-parkinsons-pink1-2424/
New Potential Pathway for Treating ALS and Parkinson’s Diseases
Neuroscience News August 12, 2015
"Mutations in PINK1 and its partner molecule Parkin cause hereditary forms of Parkinson’s disease. Moreover, the inability to remove defective mitochondria from nerve cells has been linked to numerous neurodegenerative diseases, including the more common forms of Parkinson’s disease and amyotrophic lateral sclerosis (ALS)."
http://www.ncbi.nlm.nih.gov/pubmed/24128678
Altered expression of DJ-1 and PINK1 in sporadic ALS and in the SOD1(G93A) ALS mouse model.
Mitochondrial dysfunction is an important mechanism in the pathogenesis of neurodegenerative diseases such as Parkinson disease and amyotrophic lateral sclerosis (ALS). DJ-1 and PTEN-induced putative kinase 1 (PINK1) are important proteins for the maintenance of mitochondrial function and protection against cell death. Mutations in the genes coding for these proteins cause familial forms of Parkinson disease. Recent studies have postulated that changes in the expression of both proteins are also involved in pathologic mechanisms in ALS mouse models. Here, we studied the mRNA and protein expression of PINK1 and DJ-1 in postmortem brain and spinal cord tissue and muscle biopsy samples from ALS patients and controls and in brain, spinal cord, and gastrocnemius muscle of SOD1(G93A) ALS mice at different disease stages. We found significant decreases of PINK1 and DJ-1 mRNA levels in muscle tissue of SOD1(G93A) mice. Together with the significant decrease of PINK1 mRNA levels in human ALS muscle tissue, statistically nonsignificant reduction of DJ-1 mRNA levels, and reduced immunostaining for PINK1 in human ALS muscle, the results suggest potential pathophysiologic roles for these proteins in both mutant SOD1 transgenic mice and in sporadic ALS(G93A).
Wikipedia kertoo K2-valmisteista seuraavaa: https://fi.wikipedia.org/wiki/K2-vitamiinit#Ravintolis.C3.A4t
Ravintolisät
Vain harvoista elintarvikkeista löytyy runsaasti K2-vitamiinia. Sen takia on alettu valmistaa menakinonia sisältäviä ravintolisiä (B5). Markkinoilta löytyy sekä MK-4 että MK-7 -muodossa olevaa K2-vitamiinia. [5] Menakinoni-7 on niistä pitkävaikutteisempi ja sen imeytyminen tableteista on noin 78 % luokkaa. [7]
MK-7
Pakkauksissa suositeltu MK-7:n päiväannos on 45 µg .[5]Kuitenkin vasta noin 200 µg päiväannoksella K2-vitamiinista riippuvien Gla-proteiinien arvellaan pääsevän lähelle aktiivisuuden maksimitasoa.[12] Joillekin suuremmat annokset ovat aiheuttaneet sydämen tykytystä.[38] Annosmäärän optimointiin kaivataan lisätutkimuksia.[29] Ilmeisesti tarvittavaan K2-vitamiiniannoksen määrään vaikuttavat myös geneettiset tekijät, koska luunmurtumariski sekä verisuonten kalkkeutuminenkin riippuvat perimästä.[17]
...
MK-4
MK-4-muotoisen K2-vitamiinin vaikuttavat annoskoot liikkuvat 1,5 milligrammasta ylöspäin.[21] Sen lyhyestä bioaktiviteetista johtuen MK-4-ravintolisiä on käytettävä kolmasti päivässä.
http://www.sciencemag.org/content/336/6086/1241.summary
Science 8 June 2012:
Vol. 336 no. 6086 pp. 1241-1242
DOI: 10.1126/science.1223812
Vitamin K2 Takes Charge
Sheetal Bhalarao, Thomas R. Clandinin
Mitochondria are dynamic organelles that play central roles in eukaryotic cellular energy metabolism. They harbor an electron transport chain (ETC) that couples electron transfer to the movement of protons across the mitochondrial inner membrane, forming an electrochemical gradient that captures chemical energy in the form of adenosine triphosphate (ATP). The biochemical and biophysical properties of the ETC have been studied in detail (1). On page 1306 of this issue, Vos et al. (2) report a new constituent of this chain. The authors show that vitamin K2 is an electron carrier, suggesting this small organic molecule as a possible treatment for mitochondrial pathologies such as Parkinson's disease and amyotrophic lateral sclerosis.
http://www.sciencemag.org/content/336/6086/1306.abstract
Published Online May 10 2012 Science 8 June 2012:
Vol. 336 no. 6086 pp. 1306-1310
DOI: 10.1126/science.1218632
Vitamin K2 Is a Mitochondrial Electron Carrier That Rescues Pink1 Deficiency
Melissa Vos, Giovanni Esposito, Janaka N. Edirisinghe, Sven Vilain, Dominik M. Haddad, Jan R. Slabbaert, Stefanie Van Meensel, Onno Schaap, Bart De Strooper, R. Meganathan, Vanessa A. Morais, Patrik Verstreken
Human UBIAD1 localizes to mitochondria and converts vitamin K1 to vitamin K2. Vitamin K2 is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K2 exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson’s disease that affects mitochondrial function. We found that vitamin K2 was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K2, and, similar to ubiquinone, vitamin K2 transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K2 that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.
http://neurosciencenews.com/als-parkinsons-pink1-2424/
New Potential Pathway for Treating ALS and Parkinson’s Diseases
Neuroscience News August 12, 2015
"Mutations in PINK1 and its partner molecule Parkin cause hereditary forms of Parkinson’s disease. Moreover, the inability to remove defective mitochondria from nerve cells has been linked to numerous neurodegenerative diseases, including the more common forms of Parkinson’s disease and amyotrophic lateral sclerosis (ALS)."
http://www.ncbi.nlm.nih.gov/pubmed/24128678
Altered expression of DJ-1 and PINK1 in sporadic ALS and in the SOD1(G93A) ALS mouse model.
Mitochondrial dysfunction is an important mechanism in the pathogenesis of neurodegenerative diseases such as Parkinson disease and amyotrophic lateral sclerosis (ALS). DJ-1 and PTEN-induced putative kinase 1 (PINK1) are important proteins for the maintenance of mitochondrial function and protection against cell death. Mutations in the genes coding for these proteins cause familial forms of Parkinson disease. Recent studies have postulated that changes in the expression of both proteins are also involved in pathologic mechanisms in ALS mouse models. Here, we studied the mRNA and protein expression of PINK1 and DJ-1 in postmortem brain and spinal cord tissue and muscle biopsy samples from ALS patients and controls and in brain, spinal cord, and gastrocnemius muscle of SOD1(G93A) ALS mice at different disease stages. We found significant decreases of PINK1 and DJ-1 mRNA levels in muscle tissue of SOD1(G93A) mice. Together with the significant decrease of PINK1 mRNA levels in human ALS muscle tissue, statistically nonsignificant reduction of DJ-1 mRNA levels, and reduced immunostaining for PINK1 in human ALS muscle, the results suggest potential pathophysiologic roles for these proteins in both mutant SOD1 transgenic mice and in sporadic ALS(G93A).
Wikipedia kertoo K2-valmisteista seuraavaa: https://fi.wikipedia.org/wiki/K2-vitamiinit#Ravintolis.C3.A4t
Ravintolisät
Vain harvoista elintarvikkeista löytyy runsaasti K2-vitamiinia. Sen takia on alettu valmistaa menakinonia sisältäviä ravintolisiä (B5). Markkinoilta löytyy sekä MK-4 että MK-7 -muodossa olevaa K2-vitamiinia. [5] Menakinoni-7 on niistä pitkävaikutteisempi ja sen imeytyminen tableteista on noin 78 % luokkaa. [7]
MK-7
Pakkauksissa suositeltu MK-7:n päiväannos on 45 µg .[5]Kuitenkin vasta noin 200 µg päiväannoksella K2-vitamiinista riippuvien Gla-proteiinien arvellaan pääsevän lähelle aktiivisuuden maksimitasoa.[12] Joillekin suuremmat annokset ovat aiheuttaneet sydämen tykytystä.[38] Annosmäärän optimointiin kaivataan lisätutkimuksia.[29] Ilmeisesti tarvittavaan K2-vitamiiniannoksen määrään vaikuttavat myös geneettiset tekijät, koska luunmurtumariski sekä verisuonten kalkkeutuminenkin riippuvat perimästä.[17]
...
MK-4
MK-4-muotoisen K2-vitamiinin vaikuttavat annoskoot liikkuvat 1,5 milligrammasta ylöspäin.[21] Sen lyhyestä bioaktiviteetista johtuen MK-4-ravintolisiä on käytettävä kolmasti päivässä.