Asthma and oxidant stress: nutritional, environmental, and genetic risk factors.
A considerable body of evidence suggests that oxidant stress results in inflammation and tissue damage in the respiratory system, and later in immune damage, and that individuals with lowered cellular reducing capacity are at increased risk to develop asthma. Reducing capacity in the erythrocyte is generated through the pentose phosphate pathway and this pathway also generates a major portion of the reducing capacity in all cells of the body. Therefore, dietary, environmental, and genetic factors which diminish cellular reducing capacity will increase tissue vulnerability to oxidant stress and are likely to increase asthma risk. Dietary selenium deficiency lowers red cell glutathione peroxidase activity and is associated with an increased risk for asthma, and low dietary intakes of vitamins C and E also appear to increase asthma risk. High body iron stores increase free radical production and may also elevate asthma risk. Environmental lead exposure depresses the activities of a several enzyme systems that influence cellular reducing capacity (glucose-6-phosphate dehydrogenase, NAD synthetase, glutathione peroxidase, superoxide dismutase, catalase) and consequently may increase asthma risk. Genetically-determined low activity of glucose-6-phosphate dehydrogenase lowers cellular reducing capacity and may also heighten asthma risk. Simple dietary and environmental interventions may significantly reduce oxidant stress and prevent or minimize the development of asthmatic symptoms and should prove to be a cost effective approach to asthma management in addition to current pharmacological strategies.
Greene
L S
LS
Department of Anthropology, University of Massachusetts/Boston 02125-3393, USA.
D001249:Asthma / Q000209:etiology* / Q000503:physiopathology; D001361:Avitaminosis / Q000150:complications; D004781:Environmental Exposure / Q000009:adverse effects; D005954:Glucosephosphate Dehydrogenase / Q000235:genetics* / Q000502:physiology; D005979:Glutathione Peroxidase / Q000032:analysis; D006801:Humans; D007501:Iron / Q000009:adverse effects; D007854:Lead / Q000009:adverse effects; D016877:Oxidants / Q000494:pharmacology*; D018384:Oxidative Stress / Q000502:physiology*; D012307:Risk Factors; D012643:Selenium / Q000172:deficiency / Q000502:physiology
D016877:Oxidants; D007854:Lead; D007501:Iron; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D012643:Selenium