Mitochondrial nitric oxide synthase, mitochondrial brain dysfunction in aging, and mitochondria-targeted antioxidants☆

This paper reviews the current ideas on nitric oxide physiology in brain and other mammalian organs and on the subcellular distribution of nitric oxide synthases emphasizing on the evidence of a mitochondrial NOS isoform that exhibits a mean activity of 0.86 ± 0.09 nmol NO/min × mg protein in 13 mouse and rat organs

Ana Navarro; Alberto Boveris

2008

Scholarcy highlights

  • This paper reviews the current ideas on nitric oxide physiology in brain and other mammalian organs and on the subcellular distribution of nitric oxide synthases emphasizing on the evidence of a mitochondrial NOS isoform that exhibits a mean activity of 0.86 ± 0.09 nmol NO/min × mg protein in 13 mouse and rat organs
  • Mammalian brain aging is associated with mitochondrial dysfunction, determined as decreased electron transfer and enzymatic activities and as an increased content of phospholipid oxidation products and of protein oxidation/nitration products
  • Brain mitochondrial NOS isoform is the most decreased enzymatic activity upon aging; decreased levels of NO are interpreted as the cause of decreased mitochondrial biogenesis in aged brain
  • The beneficial effect of high doses of vitamin E on mice survival and neurological function are related to its effect as antioxidant in brain mitochondria and to the preservation of mtNOS activity
  • This review is part of the Advanced Drug Delivery Reviews theme issue on “Mitochondrial Medicine and Mitochondrion-Based Therapeutics”

Need more features? Save interactive summary cards to your Scholarcy Library.