Oxidative status and paraoxonase activity in children with asthma

Abstract

Objective: To compare paraoxonase activity and changes in oxidative status in asthmatic children and healthy children by determining serum paraoxonase activity and total oxidative status, total antioxidant capacity and lipid hydroperoxidation. Methods: Forty two asthmatic children were compared with 32 healthy children of similar age and sex. To evaluate the paraoxonase and oxidative status, total antioxidant capacity and lipid hydroperoxidation were examined. Serum paraoxonase activity was evaluated by measuring the rate of paraoxon hydrolosis. Oxidative status was evaluated by the method developed by Erel. Lipid hydroperoxide was measured by an iodometric method. Results: In comparison with the healthy control group, the paraoxonase activity of the asthmatic children was found to be low (163.7 ± 73.0 (U/L) and 349.2 ± 153.9 (U/L), P = 0.002) and total oxidant status (9.0 ± 3.5 µmol H2O2 Eq/L and 13.4 ± 7.0 µmol H2O2 Eq/L, P =0.002), total antioxidant capacity (5.5 ± 2.5 µmol Trolox Eq/L and 1.0 ± 0.6 µmol Trolox Eq/L, P < 0.001), and lipid hydroperoxidation values (9.9 ± 3.4 µmol H2O2 Eq/L and 4.4 ± 1.5 µmol H2O2 Eq/L, P < 0.001) were found to be high. The high density lipoprotein (HDL) concentration of the asthmatic children was lower than that in the control group (40.1 ± 9.2 mg/dl and 54.5 ± 15.9 mg/dl, P < 0.001) Conclusion: In asthmatic children, when total oxidant status, total antioxidant capacity and lipid hydroperoxidation levels increase, paraoxonase activity decreased.Coronary heart disease (CHD) is a major killer and the most common cause of mortality and morbidity in the world. 1 It usually involves middle and older age groups but, recently, the incidence of CHD in younger individuals has been increasing. 2 Atherosclerosis is a process that starts in childhood and has a long preclinical phase before leading to clinical manifestations which usually appear in middle age. 3 Changes in the peripheral vascular endothelium are the earliest signs of atherosclerosis and CHD. 4 This has been demonstrated in asymptomatic children and young adults who are healthy but carry risk factors for atherosclerosis (e.g., high cholesterol, smoking, diabetes). 5 HDL retards the accumulation of lipid peroxides on LDL cholesterol 6 apparently due to paraoxonase which is an enzyme located on HDL particles. 7 Paraoxonase has two functions. First, it contributes to detoxification of organophosphorous compounds, including the pesticide paraoxon. Secondly, it hydrolyzes lipid peroxides and prevents LDL oxidation. 8 In both asthma and atherosclerosis, leukotrienes, which are potential inflammation mediators, play a role. 9,10 Some studies have suggested that asthma itself could be a risk factor for stroke and heart ORIGINAL RESEARCH

In UteroExposure to Second-Hand Smoke Aggravates the Response to Ovalbumin in Adult Mice

“…B1-integrin (Itgb1, ♀: ↓1.60; ♂: ↓2.49), initially activated by P-selectin, has been reported to increase during early stages of asthma but to diminish in subjects with severe asthma (17). Pon1 (♀: ↓2.01; ♂: ↓2.10) is decreased in children with asthma versus children without asthma (18). The decreases in expression of Itgb1 and Pon1 found during asthma exacerbation suggest a protective role for these genes against asthma progression.…”

Next stop for HDL: the lung

“…Many of these have been cross-sectional or retrospective analyses and some are limited by virtue of having examined only total cholesterol, a value comprised by both HDL- and LDL- (as well as other apolipoprotein B-containing lipoproteins) cholesterol fractions. Collectively, a variety of relationships have been reported between cholesterol measures and asthma, including no association for either LDL- or HDL-cholesterol [9, 13], a positive association for total cholesterol [8], positive for HDL-cholesterol and inverse for total cholesterol [10], positive for HDL-cholesterol [11], negative for HDL-cholesterol [14], and no association for HDL-cholesterol but a negative association for total- and non-HDL-cholesterol [12]. …”

Regulation of leukotriene and 5oxoETE synthesis and the effect of 5-lipoxygenase inhibitors: a mathematical modeling approach

“…To predict system responses to redox and non-redox inhibitors and to identify possible differences between them at different levels of LOOH we simulated the dependence of steady state LTA4 and oxoETE on PF and zileuton concentration. Several LOOH concentrations were chosen for this study: 0 µM (no oxidative stress), 5 µM (normal level according to available literature data [41]), 10 µM (asthmatic patients [41]) and 100 µM (extremely high oxidative stress). For all simulations the system was run to steady-state conditions with subsequent addition of inhibitor and the effect at the new steady-state noted.…”