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Mitochondriopathy- Archaeal/Mitochondrial Digoxin and Na-K ATPase - Ravikumar Kurup - Bog

Mitochondriopathy- Archaeal/Mitochondrial Digoxin and Na-K ATPaseaf Ravikumar Kurup
Bag om Mitochondriopathy- Archaeal/Mitochondrial Digoxin and Na-K ATPase

Inhibition of Na+-K+ ATPase can bring about mitochondrial dysfunction in several ways. As mentioned above, it causes PT pore opening, which brings about collapse of the hydrogen gradient across the inner membrane and uncouples the respiratory chain. The decreased availability of magnesium consequent to increased calcium causes defective mitochondrial ATP generation of affecting ATP synthase. Mitochondrial dysfunction results in incomplete reduction of O2 and increased production of the free radical, the superoxide ion. The superoxide ion can open the PT pore, completing the cycle of mitochondrial destruction. Mitochondrial dysfunction has been implicated in the pathogenesis of neuronal degeneration such as Parkinson¿s disease and neuronal aging. Free radical damage has been implicated in oncogenesis, neuronal degeneration and aging.

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  • Sprog:
  • Engelsk
  • ISBN:
  • 9786206739371
  • Indbinding:
  • Paperback
  • Sideantal:
  • 436
  • Udgivet:
  • 12. juli 2023
  • Størrelse:
  • 150x27x220 mm.
  • Vægt:
  • 667 g.
  • 2-15 hverdage.
  • 10. december 2024
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Beskrivelse af Mitochondriopathy- Archaeal/Mitochondrial Digoxin and Na-K ATPase

Inhibition of Na+-K+ ATPase can bring about mitochondrial dysfunction in several ways. As mentioned above, it causes PT pore opening, which brings about collapse of the hydrogen gradient across the inner membrane and uncouples the respiratory chain. The decreased availability of magnesium consequent to increased calcium causes defective mitochondrial ATP generation of affecting ATP synthase. Mitochondrial dysfunction results in incomplete reduction of O2 and increased production of the free radical, the superoxide ion. The superoxide ion can open the PT pore, completing the cycle of mitochondrial destruction. Mitochondrial dysfunction has been implicated in the pathogenesis of neuronal degeneration such as Parkinson¿s disease and neuronal aging. Free radical damage has been implicated in oncogenesis, neuronal degeneration and aging.

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