ArticleVirchows Archiv. A, Pathological anatomy and histopathology1993
Morphometry of peroxisomes and immunolocalization of peroxisomal proteins in the liver of patients with generalised peroxisomal disorders.
Article in Virchows Archiv. A, Pathological anatomy and histopathology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Pex13 inactivation in the mouse disrupts peroxisome biogenesis and leads to a Zellweger syndrome phenotype.Molecular and cellular biology · 2003Article
- Oxidation of pristanic acid in fibroblasts and its application to the diagnosis of peroxisomal beta-oxidation defects.The Journal of clinical investigation · 1996Article
- Immunoblot analysis of peroxisomal proteins in liver and fibroblasts from patients.Journal of inherited metabolic disease · 1995Article
- Immunocytochemical localization of peroxisomal proteins in human liver and kidney.Journal of inherited metabolic disease · 1995Article
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Abstract
Hepatic peroxisomes were studied by morphometric and immunocytochemical techniques in control patients and in four Zellweger syndrome patients, two infantile Refsum's (IRD) patients, one neonatal adrenoleukodystrophy (NALD) patient, and three patients with peroxisomal disorders (PD) which do not fit any currently recognised classification, but have disorders involving a defect in peroxisomal biogenesis. Peroxisomes which were ultrastructurally abnormal and greatly reduced in size and/or number were found in two of the Zellweger syndrome patients, and the NALD and IRD patients. There was variation in their numerical density ranging from none at all in two of the Zellweger syndrome patients to normal numbers in the IRD patients. In most patients there was a decrease in the immunolabelling of catalase over the peroxisomes. In the Zellweger syndrome and NALD patients, the small, abnormal peroxisomes did not label for any of the beta-oxidation proteins. The IRD patients and the PD patients however, were heterogeneous with respect to beta-oxidation labelling. The ultrastructural heterogeneity of peroxisomes in these peroxisomal disorders patients indicates there may be genotypic differences between the major groups and also within each group. The common factor in all the patients in this study where peroxisomes were present was the presence in the hepatic peroxisomes of an electron dense centre which did not label immunocytochemically for catalase or the beta-oxidation enzymes. This electron dense centre may indicate a structural abnormality in the peroxisomes in these patients.
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