Action of L-acetylcarnitine on different cerebral mitochondrial populations from hippocampus and striatum during aging.
ABSTRACT The maximum rates (Vmax) of some mitochondrial enzyme activities related to energy transduction (citrate synthase, malate dehydrogenase, NADH cytochrome c reductase, cytochrome oxidase) and amino acid metabolism (glutamate dehydrogenase) were evaluated in non-synaptic (free) and synaptic mitochondria from rat hippocampus and striatum. Three types of mitochondria were isolated from control rats aged 4, 8, 12, 16, 20 and 24 months and treated ones with L-acetylcarnitine (100 mg.kg-1, i.p., 60 min). Enzyme activities of non-synaptic and synaptic mitochondria are different in hippocampus and striatum, confirming that a different metabolic machinery exists in various types of brain mitochondria. During aging, enzyme activities behave quite similarly in both areas. In vivo administration of L-acetylcarnitine decreased the enzyme activities related to Krebs' cycle mainly of synaptic mitochondria, suggesting a specific subcellular trigger site of action. The drug increased cytochrome oxidase activity of synaptic and non-synaptic mitochondria, indicating the specificity of molecular interaction with this enzyme.
Article: Structural damage induced by peroxidation may account for functional impairment of heavy synaptic mitochondria.[show abstract] [hide abstract]
ABSTRACT: Coenzyme Q distribution, as well as respiratory chain features, in rat brain mitochondria depend on mitochondrial subpopulation, brain region and age. Heavy mitochondria (HM) usually display the lowest content of respiratory components and the lowest enzymatic activities and it has been suggested that they represent the oldest mitochondrial population. In this study, we confirmed that HM are considerably compromised in their structure. In fact, HM showed to have the highest hydroperoxide content and the most consistent modifications in their fatty acid pattern with wide loss of fatty acids (or part of them) in the phospholipid moiety. Such situation could explain the typical impairment of HM and could support the hypothesis that they represent an old mitochondrial population.Free Radical Research 05/2002; 36(4):479-84. · 2.88 Impact Factor