Erythrocyte superoxide dismutase activity and plasma malondialdehyde levels in children with Henoch Schönlein purpura

Abstract

Demircin G, Ö ner A, Ü nver Y, Bülbül M, Erdogan Ö . Erythrocyte superoxide dismutase and plasma malondialdehyde levels in children with Henoch Schönlein purpura. Acta Paediatr 1998; 87: 848-52. Stockholm. ISSN 0803-5253 Reactive oxygen molecules (ROM) have been suggested to contribute to many pathological conditions including vasculitides and renal diseases. In the present study we measured the activity of superoxide dismutase (SOD) as an antioxidant enzyme in red blood cells and the level of malondialdehyde (MDA), which is a product and an indicator of lipid peroxidation, in the plasma of 16 children (7M, 9F) with Henoch Schönlein purpura (HSP) at the onset of the disease (SOD 1 and MDA 1) and at the remission period (SOD 2 and MDA 2). The results were compared with the results of 17 healthy children studied as a control group. There was no significant difference for SOD activities between the patients in each period and the control group ( p Ͼ 0:05). There was a statistically significant difference between MDA 1 and MDA 2 levels ( p Ͻ 0:01), each of which were also significantly different from the MDA levels of control group ( p Ͻ 0:001 and p Ͻ 0:01, respectively). The effect of ROMs on different clinical conditions of HSP was also examined and lipid peroxidation was found to be increased more in patients with renal involvement. It is concluded that oxidant stress especially lipid peroxidation plays an important role in the pathogenesis of HSP and in development of renal injury. ٖ Henoch Schönlein purpura, malondialdehyde, oxidant injury, superoxide dismutase G Demircin,

Renal bcl-2/bax expression in childhood Henoch–Schönlein nephritis: prognostic importance?

“…Involvement of oxidative stress and reactive oxygen molecules (ROMs) in HSP is more indirect evidence for the role of apoptosis in HSN pathogenesis. Besides, ROM levels are under the control of the Bcl-2 gene product (20,21). The mainly tubular expression of bax and bcl-2 in our patients is in agreement with the literature (18,22).…”

Neutrophil activation, protein oxidation and ceruloplasmin levels in children with Henoch-Schönlein purpura

“…Despite the existence of various experimental studies concerning oxidant injury in vascular diseases [6,7], few clinical studies evaluated the role of oxidative injury in the pathogenesis of vasculitis [9,10]. In this study, we investigated the role of neutrophil activation and protein oxidation (thiol stress) in the pathogenesis of HSP by measuring serum enzyme activity of MPO as a marker of neutrophil activation and total free thiol groups as a marker of protein oxidation together with serum antioxidant enzyme ARYL activity, serum TOS, and CLP levels.…”

“…This mechanism has a crucial and probably causative role in the pathogenesis of various acute and chronic diseases, including inflammation, renal failure, and cardiovascular damage [3][4][5]. Experimental studies on oxidative injury have been carried out in glomerular diseases and vasculitis [6][7][8]; however, clinical investigations on oxidative stress in HSP are scarce [9][10][11].…”

Oxidative Stress in Children with Acute Glomerulonephritis

“…If the oxidative damage is excessive, SOD will also be expected to increase for the compensation and protection of tissue injury. [23] Thus, the lack of increase in acute stage SOD activity may be due to some depletion resulting from oxidative stress as detected by higher MDA levels. Sustained SOD activity in acute stage of AGN suggested that antioxidant defense mechanisms work well in these patients; antioxidant enzymes were not totally depleted and remained at a steady state as a compensation for protection from hazardous effects of increased ROS.…”