By Hugo W. Moser (auth.), Harry Harris, Kurt Hirschhorn (eds.)
The present quantity contains chapters on peroxisomal problems, genetic elements of melanoma, Gaucher ailment, and different topics.
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Extra resources for Advances in Human Genetics 21
1980), in the adrenal cortex by ACTH (Black and Russo, 1980), and by administration of thyroid hormone (Fringes and Reith, 1982). Peroxisome function thus is influenced by metabolic state, nutrition, and pharmaceutical agents in ways that have been studied only incompletely, but may prove relevant to the pathogenesis and treatment of peroxisomal disorders. Chapter 1: Peroxisomal Diseases 21 PEROXISOMAL DISORDERS Table I lists the genetically determined peroxisomal disorders that have been identified so far.
Induction of Peroxisome Proliferation Hess et al. (1965) were the first to show that hypolipemic agents such as clofibrate and industrial phthalate plasticizers resulted in proliferation of liver peroxisomes. This proliferation accounts for the striking liver enlargement produced by these agents in rodents. The administration of peroxisome proliferators has facilitated the study of peroxisome function: The initial demonstration that peroxisomes played a role in fatty acid ~-oxidation was conducted in clofibratetreated rats (Lazarow, 1978).
1964) and was assigned to the multiple congenital anomaly category. It represents the most severe prototype of a human peroxisome deficiency disorder, and affected children only rarely survive beyond the fourth month. Neonatal adrenoleukodystrophy (NALD) was TABLE I. Peroxisomal Disorders Disorders of peroxisome biogenesis Defects of single peroxisomal enzyme Multiple biochemical defects; peroxisome intact Zellweger syndrome Neonatal ALD Infantile Refsum disease Hyperpipecolic acidemia X-linked ALD Oxidase deficiency Bifunctional enzyme deficiency Thiolase deficiency Glutaryl CoA oxidase deficiency Acatalasemia Hyperoxaluria type 1 Rhizomelic chondrodysplasia punctata 22 Hugo W.