Lori K. Klaidman

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An ultrasensitive HPLC method has been developed for measuring NADP+, NADPH, NAD+, and NADH. A simple, rapid reaction of the oxidized nucleotides with cyanide in basic solution leads to two stable fluorescent products and allows all four nucleotides to be separated and quantitated on one chromatogram. Furthermore, only one extraction is needed, rather than(More)
Pyridine nucleotides are critical during oxidative stress due to their roles in reductive reactions and energetics. The aim of the present study was to examine pyridine nucleotide changes in six brain regions of mice after an intracerebroventricular injection of the oxidative stress inducing agent, t-butyl hydroperoxide (t-BuOOH). A secondary aim was to(More)
MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines1–5. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and nore-pinephrine (NE), whereas MAOB preferentially oxidizes β-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in MAOA results in a clinical phenotype characterized by borderline(More)
MAOA and MAOB are key iso-enzymes that degrade biogenic and dietary amines. MAOA preferentially oxidizes serotonin (5-hydroxytryptamine, or 5-HT) and norepinephrine (NE), whereas MAOB preferentially oxidizes beta-phenylethylamine (PEA). Both forms can oxidize dopamine (DA). A mutation in MAOA results in a clinical phenotype characterized by borderline(More)
MPP+ has been reported to inhibit reduced nicotinamide adenine dinucleotide (NADH) dehydrogenase in mitochondria, which results in the formation of O2(.-). The current report demonstrates that H2O2 and HO. are also products of MPP+ interaction with NADH dehydrogenase. It is possible that MPP. formation precedes the formation of some of these active oxygen(More)
The vitamin nicotinamide can protect against oxidative stress-induced apoptosis in the brain when used as a precursor for nicotinamide adenine dinucleotide (NAD+). The intracerebroventricular administration of tertiary-butylhydroperoxide (t-buOOH) to mice was used to simulate physiologic oxidative stress and apoptosis which may occur in some(More)
Apoptosis is a characteristic form of cell death which has been implicated in neurodegeneration. In this study we document the induction of apoptosis and DNA fragmentation in vivo by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin. MPTP selectively damages dopaminergic neurons in the substantia nigra of the midbrain. It is a potent inducer(More)
The mechanism of acrolein-induced lipid peroxidation is unknown. This study found that acrolein and its glutathione adduct, glutathionylpropionaldehyde, induce oxygen radical formation. These oxygen radicals may be responsible for the induction of lipid peroxidation by acrolein. The enzymes xanthine oxidase and aldehyde dehydrogenase were found to interact(More)
BACKGROUND AND PURPOSE Nicotinamide protects against brain damage in ischemia-reperfusion. However, the dosage and time of treatment require clarification. It is also not clear if nicotinamide can protect against both necrosis and apoptosis. METHODS Dose-response and time-effect studies were designed. Transient focal cerebral ischemia was induced by(More)
A new mechanism of oxygen radical formation in dopaminergic neurons is proposed, based on the oxidative mechanism of tyrosine hydroxylase. The cofactor (6R,6S)-5,6,7,8-tetrahydrobiopterin can rearrange in solution which allows an autoxidation reaction producing O2.-, H2O2 and HO.. The combination of tyrosine hydroxylase and the cofactor produces more oxygen(More)