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Glutathione and kidney disease

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Oxidative stress is considered a main player in kidney disease and associated mortality rates. This sustained production of free radicals is in part caused by the frequent and regular dialysis required to treat patients. Glutathione demand in these patients is therefore much higher in order to cope with the increased oxidative stress.

Low levels of glutathione are a hallmark in kidney disease and this is thought to be caused by diminished levels of an enzyme called GCL which is the first step in the production of cellular glutathione. This enzyme is responsible for the production of gamma-glutamylcysteine, the direct precursor to glutathione. Since cysteine is removed from the blood in dialysis patients, supplementing with cysteine has a positive effect on glutathione levels, however it only addresses a small part of the problem. The diminished levels of GCL are of much greater concern. To address this problematic enzyme in dialysis patients, supplementation with gamma-glutamylcysteine has been shown to bypass GCL altogether by providing cells with the first building block of glutathione.  Not only does gamma-glutamylcysteine readily enter cells, once inside it is quickly and easily converted to glutathione.[1]  [2, 3]

References

  1. Alhamdani, M.S., Impairment of glutathione biosynthetic pathway in uraemia and dialysis. Nephrol Dial Transplant, 2005. 20(1): p. 124-8.
  2. Santangelo, F., et al., Restoring glutathione as a therapeutic strategy in chronic kidney disease. Nephrology Dialysis Transplantation, 2004. 19(8): p. 1951-5.
  3. Ashworth, A. and S.T. Webb, Does the prophylactic administration of N-acetylcysteine prevent acute kidney injury following cardiac surgery? Interact CardioVasc Thorac Surg, 2010. 11(3): p. 303-308.

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