association of TGF-beta1, angiotensin II and oxidative stress with diabetic nephropathy in type 2 diabetic patients

Diabetic nephropathy [DN] is a severe complication of diabetes which may progress to end-stage renal disease [ESRD]. Chronic hyperglycemia is considered as the major initiator of DN, either by creation of oxidative stress or by induction of growth factors and cytokines. Moreover, dyslipidemia plays a role in DN progression. The aim of our study was to examine the changes in lipid profile, malondialdehyde [MDA], transforming growth factor- beta1 [TGF-beta1] and angiotensin II [Ang II] levels in type 2 diabetic patients associated with kidney disease. Diabetic microalbuminuric [n=25] and macroalbuminuric [n=15] patients showed significantly higher levels of blood glucose, glycated hemoglobin [HbA1c], triglycerides [TG], total cholesterol [TC], MDA, TGF- beta1 and Ang II than either diabetic normoalbuminuric [n=14] or control [n=16] subjects. In the microalbuminuric and macroalbuminuric diabetic groups, albumin excretion rate [AER] was positively correlated with MDA [r=0.448, p < 0.01], TGF- beta1 [r=0.81, p < 0.01] and Ang II [r=0.772, p < 0.01]. Additionally, MDA correlated with TGF- beta1 [r=0.625, p < 0.01] and Ang II [r=0.428, p < 0.01]. In conclusion, dyslipidemia, oxidative stress, and increased TGF- beta1 and Ang II are associated with DN in type 2 diabetic patients

Role of nitric oxide, superoxide dismutase and cytokines as markers in childhood secretory otitis media

The aim of this study was to investigate the role of nitric oxide [NO], antioxidant enzyme activity [superoxide dismutase [SOD]] and cytokines [interleukin- 1 beta [IL- 1 beta], interleukin-6 [IL-6], interleukin-8 [IL-8], and tumor necrosis factor- alpha [TNF-alpha]] in pathogenesis of otitis media with effusion [OME] in children. Subjects and NO metabolites, SOD activity and cytokines concentration were measured in blood plasma and middle ear effusion [MEE] of 27 patients [46 ears] with secretary otitis media [SOM] [aged 1 -4 years] and in blood plasma of 10 healthy children of the same age, as a control group. MEE was classified macroscopically to, serous in 10 samples [21.73%], mucoid in 29 samples [63.04%] and purulent in 7 samples [15.21%]. The hearing loss with air-bone gap of 20-40 dB present in 66.6% of the patients. NO, SOD, IL-1 beta, IL-6, IL-8 and TNF-alpha were found in 89.1%, 82.6%, 86.9%, 84.7%, 80.4% and 52.2% of MEE, respectively. NO, SOD and cytokines were significantly higher in blood plasma and MEE samples of patients than in control group. This study showed that in serous fluid group, the concentration of IL-6 and IL-8 was remarkably higher than in both mucoid and purulent groups, but the concentration of NO, SOD and TNF-alpha was significantly lower than in both mucoid and purulent groups. IL-1 beta showed no significant difference between the previous three groups. The shorter the course of MEE, the higher the concentration of IL-6 and IL-8, and the longer the course of MEE, the higher the concentration of NO, SOD and TNF-alpha. Highly elevated levels of NO, SOD, IL-1 beta, IL-6, IL-8 and TNF-alpha in MEE indicate ongoing cytokines activation. IL-6 and IL-8 might participate in the defensive reaction of organism during the early stage of SOM, and play a role in serous effusion secretion. Finally, NO, SOD and some proinflammatory cytokines in the MEE could be important mediators in MEE of SOM in children and used to monitor the inflammatory process of otitis media

8-Isoprostane and endothelin-1 as markers of oxidative stress in smokers

The aim of this study was to quantify oxidative stress in 40 smokers with chronic obstructive pulmonary disease [COPD], 25 healthy smokers and 20 healthy nonsmokers, as reflected by 8-isoprostane [8-IP] as a marker of lipid peroxidation, protein carbonyl as an index of protein oxidation and endothelin-1 [ET-1] concentrations. This study was also undertaken to determine whether plasma 8-IP, protein carbonyl and ET- 1 status correlated with lung function as assessed by forced expiratory volume in one second [FEV1] and forced vital capacity [FVC] in smokers and in smokers with COPD. Plasma levels of 8-IP and ET-1 were measured by ELISA technique and protein carbonyl was determined by colorimetric method. Antioxidant status, assessed by measuring the glutathione [GSH] and vitamin C levels. Plasma 8-IP, ET-1 and protein oxidation levels were significantly increased in smokers with COPD [45.2 +/- 3.2 pg/ml, 159.6 +/- 9.8 pg/mg protein and 0.55 +/- 0.09 nmol/mg protein respectively] and in healthy smokers [30.6 +/- 2.1 pg/ml, 142 +/- 7.7 pg/mg protein and 0.37 +/- 0.04, nmol/mg protein, respectively] compared with healthy nonsmokers [13.2 +/- 0.92 pg/ml, 72.5 +/- 5.2 pg/mg protein and 0.22 +/- 0.01 nmol/mg protein respectively]. The mean differences of plasma antioxidants, GSH [24.3 +/- 1.61, 28.1 +/- 2.2 and 36.3 +/- 1.93 nmol/mg protein] and vitamin C [1.92 +/- 0.03, 3.17 +/- 0.1 and 5.26 +/- 0.17 mg/L] were significantly decreased in smokers with COPD and healthy smokers compared with healthy nonsmokers, respectively. Significant negative correlations were found between Spirometric data measured as FEV 1% predicted and the plasma levels of 8-IP, ET- 1 and protein oxidation in smokers with COPD, healthy smokers, or healthy nonsmokers. On the other hand, there were significant positive correlations between FEV1% predicted and the levels of plasma vitamin C and GSH in the three studied groups. Conclusions: These data confirm decreased antioxidant capacity [GSH and vitamin C] and increased oxidative stress markers [8-IP, ET- I and protein oxidation] in healthy smokers and smokers with COPD, indicating the presence of systemic oxidative stress. However, relationship was found between plasma oxidant/antioxidant levels and measurements of airflow limitation in either healthy smokers or in smokers with COPD

Serum trace elements, related antioxidant enzymes and inflammatory markers in bronchial asthma and chronic obstructive pulmonary diseases: a comparative study

To evaluate the possible abnormalities in serum trace elements [zinc [Zn], copper [Cu] and selenium [Se]] and related antioxidant enzymes [glutathione peroxidase [GSH-Px] and superoxide dismutase [SOD]] in asthmatic and chronic obstructive pulmonary disease [COPD]. In addition, to study the hypothesis that eosinophilic and neutrophilic airway inflammation are common in asthma and patients with COPD respectively, by measuring the total and differential cell counts and assaying the inflammatory enzyme markers [eosinophil peroxidase [EPO] and myeloperoxidase [MPO]]. Design: The studied cases were divided into three groups: Twenty healthy volunteers [group I], twenty five patients with bronchial asthma [group H] and twenty five patients with COPD [group III]. Serum Cu, Zn, Se, EPO and MPO and blood GSH-Px and SOD activities were measured in all subjects. In addition, differential leucocytic counts, blood gases and pulmonary function tests [forced expiratory volume in first second [FEV 1], forced vital capacity [FVC] and forced expiratory flow at 25-75% [FEF25-75%]] were also determined. Serum Se and Zn levels and related antioxidant enzymes, GSH-Px and SOD activities were significantly decreased but Cu was markedly increased in asthmatic and COPD patients compared with healthy control group. In addition Cu/Zn ratio showed reasonable higher value in patient groups. Inflammatory MPO and allergic EPO enzymatic markers were significantly increased in COPD and asthmatic patients respectively compared with control groups. FVC and FEV1 were significantly decreased in the asthma and COPD compared with control. Blood gases were significantly changed only in COPD group compared with both asthmatic and healthy control groups. Abnormalities in serum trace elements and related antioxidant enzymes revealed that, free oxygen radicals generation are more evident in asthmatic and COPD patients. In addition, increased in blood eosinophils and EPO are characteristic of asthmatic patients, while an increased in neutrophils counts and MPO concentrations are found in COPD. These changes lead to further increase in inflammation, hyperreactivity and oxidative stress in the lungs