Serum paraoxonase 1 (PON1) activity and the oxidation of lipoproteins were investigated in 35 women with pre-eclampsia and in 35 healthy control women with normal pregnancies. Blood pressure, body mass index (BMI), serum levels of total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB) and lipoprotein (a) (Lp[a]), and PON1 activity were assessed. There were no significant between-group differences in subject age, gestational age at diagnosis of pre-eclampsia, BMI, serum total cholesterol, triglycerides, LDL and ApoB levels. Mean systolic and diastolic blood pressures and serum Lp(a) were significantly higher in subjects with pre-eclampsia than in controls. Mean serum HDL, ApoA1 and PON1 activity were significantly lower in subjects with pre-eclampsia compared with controls. In conclusion, lipids and oxidized lipoproteins may play important roles in the pathogenesis of pre-eclampsia.
The aim of this study was to assess the role of oxidative stress in the pathogenesis of Henoch-Schönlein purpura (HSP) vasculitis. The activities of catalase (CAT), arylesterase (ARYL), and paraoxonase (PON) as antioxidant enzymes and serum malondialdehyde (MDA) level as an indicator of lipid peroxidation, together with total antioxidant status (TAS), were measured in 29 children with HSP (mean age 9.3 +/- 2.7 years), both at the onset of the disease and at the remission period and in matched controls. Active-stage HSP had significantly higher MDA level (15.5 +/- 7.3 vs 7.8 +/- 3.9 nmol/l, respectively, P < 0.001) and lower TAS (524 +/- 122 vs 699 +/- 122 mumol Trolox Equiv/l, P < 0.001), PON (97 +/- 47 vs 136 +/- 95 U/l, P = 0.042), ARYL (158 +/- 39 vs 212 +/- 52 U/l, P < 0.001), and CAT (50 +/- 27 vs 69 +/- 20 U/l, P = 0.002) activities compared with the control subjects. Although CAT (P > 0.05) and PON (P > 0.05) activities were found to be similar between active and remission stages of HSP, the active stage of the disease had significantly lower ARYL (P = 0.011) and TAS (P = 0.006) and higher MDA (P < 0.001) values compared with remission period. Significant positive correlations were found between CAT and MDA (r = 0.433, P = 0.019) and between CAT and C-reactive protein (r = 0.386, P = 0.035) in the active stage of HSP. No significant differences were detected in oxidant/antioxidant parameters between patients with or without renal, gastrointestinal, or joint involvement (P > 0.05). Increased oxidative stress and lipid peroxidation may play important roles in the pathogenesis of HSP vasculitis. Antioxidant therapeutic interventions in long-lasting vasculitis and risk of atherosclerosis secondary to increased oxidant stress remain to be investigated.
We investigated the changes in the serum levels of tumor necrosis factor (TNF)-a and interleukin (IL)-6, the pro-inflammatory cytokines, and the possible effect of melatonin on the modulation of these inflammatory molecules after renal ischemia reperfusion (IR). The study was carried out in the laboratory of Department of Pharmacology. Forty-six male Wistar albino rats were divided into five groups as control (n ¼ 6), positive control (n ¼ 4), sham (n ¼ 12), renal IR (n ¼ 12), and renal IR melatonin (n ¼ 12). After 1 h renal pedicle occlusion, the blood samples were taken for the measurement of cytokine levels at second hour of the reperfusion. The rats were sacrificed after 24 h of reperfusion for histopathological evaluation. Melatonin or vehicle was administrated to IR rats. Lipopolysaccharide (LPS) was administered to the positive control group and the blood was taken at fourth hour. Serum TNF-a levels increased significantly in renal IR and LPS groups. Serum IL-6 levels were not different from control except the LPS group. There was no significant correlation between the serum TNF-a levels and the histopathological score after renal IR. Melatonin treatment reversed the increase of serum TNF-a levels and histopathological injury in renal tissue after renal IR. Melatonin may have a protective effect by reducing the serum level of TNF-a in renal IR.
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