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The article presents abstracts of research papers related to glutathione metabolism in the central nervous system. They include "Pathways involved in peroxide detoxification by brain cells," "Cellular and subcellular localization of glutathione and glutathione precursors: high resolution immunogold analyses," and "Impairment of energy production in brain mitochondria by glutathione deprivation and nitric oxide production."

The article presents an abstract of the research paper "Mitochondrial Respiratory Chain Complex Deficiency in Human Epileptic Hippocampus." The research determines that selective changes in the activity of complex 1 of mitochondrial oxidative phosphorylation occur in epileptogenic human central nervous system tissue. The research shows that the local functional impairment of mitochondria in human hippocampus can be a novel pathomechanism in temporal lobe epilepsy.

The article presents an abstract of the research paper "Pathways Underlying the Disposal of H2O2 in the Mitochondria of the Central Nervous System." The findings indicate that isocitrate dehydrogenase, malic enzyme and nicotinamide nucleotide transhydrogenase contribute to the regeneration of mitochondrial NAPDH required for the reduction of oxidized glutathione, which in turn is produced during elimination of H2O2 by the glutathione system.

AbstractCytidine-5′-diphosphocholine (citicoline or CDP-choline), an intermediate in the biosynthesis of phosphatidylcholine (PtdCho), has shown beneficial effects in a number of CNS injury models and pathological conditions of the brain. Citicoline improved the outcome in several phase-III clinical trials of stroke, but provided inconclusive results in recent clinical trials. The therapeutic action of citicoline is thought to be caused by stimulation of PtdCho synthesis in the injured brain, although the experimental evidence for this is limited. This review attempts to shed some light on the properties of␣citicoline that are responsible for its effectiveness. Our studies in transient cerebral ischemia suggest that citicoline might enhance reconstruction (synthesis) of PtdCho and sphingomyelin, but could act by inhibiting the destructive processes (activation of phospholipases). Citicoline neuroprotection may␣include: (i) preserving cardiolipin (an exclusive inner mitochondrial membrane component) and sphingomyelin; (ii)␣preserving the arachidonic acid content of PtdCho and phosphatidylethanolamine; (iii) partially restoring PtdCho levels; (iv) stimulating glutathione synthesis and glutathione reductase activity; (v) attenuating lipid peroxidation; and (vi)␣restoring Na+ /K+ -ATPase activity. These observed effects␣of citicoline could be explained by the attenuation of␣phospholipase A2 activation. Based on these findings, a singular unifying␣mechanism has been hypothesized. Citicoline also provides choline for synthesis of neurotransmitter acetylcholine, stimulation of tyrosine hydroxylase activity and dopamine release. [ABSTRACT FROM AUTHOR]