We studied the involvement of oxidative stress in chronic idiopathic urticaria (CIU), assessing the activities of superoxide dismutase (SOD) and glutathione and the levels of malondialdeyde (MDA), a marker of lipid peroxidation, in samples taken from lesional skin (n = 16) and nonlesional skin (n = 11) of CIU patients. The activity of SOD and glutathione and the levels of MDA were markedly increased in lesional skin as compared with skin of healthy subjects, whereas no differences were detected between nonlesional skin of CIU patients and control samples. Immuno-dot blot assay revealed an up-regulation of Mn-SOD expression in lesional skin. These findings show that oxidative stress is crucially involved in CIU. The evidence of lipid peroxidation and compensatory increase of Mn-SOD and glutathione activities in lesional skin, in the absence of any alteration in uninvolved skin, suggests that oxidative stress is secondary to the development of inflammation.
The pathogenesis of the physical urticarias has not been completely defined. Indeed, different stimuli can induce similar clinical manifestations, some of which are capable of generating reactive oxygen species. In order to evaluate whether the generation of an oxidative stress response could be a common pathogenetic mechanism of the disease, we have determined the profile of a number of chemical and enzymatic antioxidants in blood samples from a group of patients with physical urticarias. Compared with controls, a systemic imbalance of the antioxidants was detected in the patient group with a decrease of both plasma vitamin E and cellular catalase and glutathione peroxidase activities along with an increase of superoxide dismutase activity. Moreover, an increase in the percentage of plasma polyunsaturated fatty acids, as a target for peroxidative damage, was also observed. These alterations may lead to an increased percentage of peroxidable compounds in skin and to the intracellular generation of reactive oxygen species and could therefore provide one possible explanation for the patients' urticarial response to stimuli. Even if the alteration of the antioxidant status is secondary to changes in cytokine or complement activation, our results suggest a common biochemical profile in patients with different forms of physical urticaria.
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