22.1 Introduction 22.2To live perilously 22.3 The damaging role of hemichromes, free haem and free iron 22.4 Pathophysiologic consequences of oxidative damage 22.5 G6PD deficiency 22.5.1. Structure of normal and mutant G6PD 22.5.2 Intracellular regulation of G6PD in normal and deficient red cells 22.5.3 Oxidant-induced haemolysis 22.5.4 The favic crisis 22.5.5 Toxic components of the Fava Beans and their haemolytic activity 22.5.6 Oxidative stress and calcium homeostasis 22.5.7 Predominantly extravascular haemolysis in oxidatively stressed G6PD-deficient red cells 22.6 red cell alterations in Diabetes mellitus 22.6.1 Glycation of proteins in diabetes 22.6.2 Functional effects of red cell protein glycation 22.6.3 Increased phagocytosis of diabetic red cells :possible mechanisms 22.6.4 Role of red cell alterations in diabetes complications 22.7 Concluding remarks
METABOLIC DISORDERS
ARESE, Paolo;KEILING, BRIGITTE EVELIN
2003-01-01
Abstract
22.1 Introduction 22.2To live perilously 22.3 The damaging role of hemichromes, free haem and free iron 22.4 Pathophysiologic consequences of oxidative damage 22.5 G6PD deficiency 22.5.1. Structure of normal and mutant G6PD 22.5.2 Intracellular regulation of G6PD in normal and deficient red cells 22.5.3 Oxidant-induced haemolysis 22.5.4 The favic crisis 22.5.5 Toxic components of the Fava Beans and their haemolytic activity 22.5.6 Oxidative stress and calcium homeostasis 22.5.7 Predominantly extravascular haemolysis in oxidatively stressed G6PD-deficient red cells 22.6 red cell alterations in Diabetes mellitus 22.6.1 Glycation of proteins in diabetes 22.6.2 Functional effects of red cell protein glycation 22.6.3 Increased phagocytosis of diabetic red cells :possible mechanisms 22.6.4 Role of red cell alterations in diabetes complications 22.7 Concluding remarks
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