propionic acidemia/kalij

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Biochemical characterization of propionyl CoA carboxylase deficiency: heterogeneity within a single genetic complementation group.

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Liver tissues and fibroblasts from patients with propionic acidemia assigned to the pcc BC genetic complementation group have previously been shown to contain normal or near-normal quantities of structurally altered propionyl CoA carboxylases (PCC). Biochemical comparisons of PCCs from extracts of

Human propionyl CoA carboxylase: some properties of the partially purified enzyme in fibroblasts from controls and patients with propionic acidemia.

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We report some properties of propionyl CoA carboxylase (PCC) partially purified from cultured human fibroblasts obtained from controls and several patients with propionic acidemia. A series of steps (Triton X-100 treatment, high speed centrifugation, ammonium sulfate precipitation, and density

Possible mechanisms for sensorineural hearing loss and deafness in patients with propionic acidemia.

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Propionic acidemia is an inborn error of metabolism caused by deficiency of the mitochondrial enzyme propionyl-CoA carboxylase. Sensorineural deafness and severe hearing loss have been described as long-term complications of this disease, however, the mechanism has not yet been elucidated. We have

Mechanisms of acquired long QT syndrome in patients with propionic academia.

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Propionic acidemia (PROP) is a rare metabolic disorder caused by deficiency of propionyl-CoA carboxylase. PROP patients demonstrate QT prolongations associated with ventricular tachycardia and syncopes. Mechanisms responsible for this acquired long QT syndrome (acqLQTS) are unknown. The aim of the

High-performance liquid chromatographic separation of acylcarnitines following derivatization with 4'-bromophenacyl trifluoromethanesulfonate.

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A high-performance liquid chromatographic method for the separation of acylcarnitines after derivatization with 4'-bromophenacyl trifluoromethanesulfonate is presented. Derivatization of acylcarnitines was achieved at room temperature within 10 min. Separation of the acylcarnitine 4'-bromophenacyl

Effects of methylmalonic and propionic acids on glutamate uptake by synaptosomes and synaptic vesicles and on glutamate release by synaptosomes from cerebral cortex of rats.

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Neurological dysfunction is common in patients with methylmalonic and propionic acidemias. However, the mechanisms underlying the neuropathology of these disorders are far from understood. In the present study we investigated the in vitro effects of methylmalonic (MMA) and propionic (PA) acids at

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