Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.

No abstract

Increased activity of urinary N-acetyl-beta-D-glucosaminidase (NAG) can be used as an early indicator of damage to the tubular epithelium. Systemic lupus erythematosus (SLE) is a multisystem autoimmune rheumatic disease. Nephritis is known as the most serious complication of SLE and the strongest predictor of poor outcome. In this study urinary NAG excretion was investigated in 24 SLE patients with normal renal function (serum creatinine < or =1.2 mg/dL) and the results were compared with those from 26 untreated patients with rheumatoid arthritis (RA) and 27 healthy controls. The SLE patients were divided into two groups according to their urinary total protein levels: group A consisted of 16 patients with < or =3.5 g/day proteinuria, and group B consisted of eight patients with nephrotic-range proteinuria (>3.5 g/day). Serum and urinary creatinine, total urinary protein levels, and urinary NAG excretion were measured in patients with SLE and RA. In addition, serum C3 and C4 levels were determined in the SLE patients. Renal biopsies were performed in all of the SLE patients. Glomerular lesions were classified according to WHO criteria for lupus nephritis (LN) I-V. The Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) was used to assess disease activity. Urinary NAG excretion was significantly higher in the SLE groups than in the healthy controls (P<0.001). In urinary NAG excretion there was also significant difference between SLE groups and RA patients (P<0.001). However, there was no significant difference in NAG excretion between the RA and control groups (P=0.062). Urinary NAG excretion was significantly higher (P<0.05) in group B compared to group A. There were no differences in SLEDAI scores, ages, and serum creatinine levels between study groups (P=0.601, P=0.285, P=0.669, respectively). Elevated SLEDAI values and hypocomplementemia were detected more often in younger patients (P<0.010, r=-0.529 and P<0.010, r=-0.569, respectively). There was a strong positive correlation between proteinuria and urinary NAG activity (P<0.001, r=0.759). These results suggest that the determination of urinary NAG activity may be a useful supplement to the routine biochemical analysis performed on the urine in cases of SLE.

Hypoxia/reoxygenation (H/R)-induced intestinal injury plays a significant role in the development of necrotizing enterocolitis (NEC). We experimentally explored the effect of pentoxifylline (PTX) on an NEC model. Twenty-one newborn rabbits were divided into three groups: group 1 (control), group 2 (H/R) and group 3 (H/R + PTX). Five minutes of reoxygenation following 5 min of hypoxia was performed three times a day during 3 days. Before each H/R procedure in the H/R + PTX group, the rabbits were treated with PTX 25 mg/kg intraperitoneally. Animals were sacrificed on the third day and ileum samples were taken for histopathological examination and biochemical enzyme studies [superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST)]. There was a significant difference in the grade and number of the intestinal lesions between controls and the H/R and H/R + PTX groups (p < 0.001), but no significant difference was found between the H/R and the H/R + PTX groups (p > 0.05). Intestinal SOD, GR and GST activities in the H/R and H/R + PTX groups were significantly higher than in the control group (p < 0.05); however, there was no significant difference between the H/R and H/R + PTX groups (p > 0.05). Significantly reduced GPx activity was found in the H/R and H/R + PTX groups compared with the controls (p < 0.05). No significant difference in GPx activity existed between the H/R group and the H/R + PTX group (p > 0.05). Ischemia/reperfusion injury was responsible for mediating hypoxia-induced intestinal necrosis in NEC and PTX pretreatment did not have a protective effect on NEC.

Oxidative modification of low-density lipoprotein in the artery wall plays a crucial role in the development of atherosclerosis. This physiopathological mechanism is clearly inhibited by high-density lipoprotein possibly via paraoxonase enzyme activity, present in high-density lipoprotein. In this study, we determined the in vitro susceptibility of low-density lipoprotein to oxidation and the effect of various factors, such as paraoxonase phenotypes, on this process. Low-density lipoprotein from healthy volunteers (n=66) was isolated using the precipitant reagent and the oxidation was evaluated by measuring the malonyl dialdehyde and diene levels. Low-density lipoprotein cholesterol and phospholipid, vitamin E, serum cholesterol, high-density lipoprotein and low-density lipoprotein cholesterol levels, and erythrocyte antioxidant enzymes were also determined. There was no difference among the parameters with regard to gender. Low-density lipoprotein samples obtained from subjects with the AA allele were more prone to oxidation, as observed by their higher stimulated conjugated diene (P=0.041) and thiobarbituric acid-related substance (P=0.042) levels, than samples from subjects with AB or BB alleles. The subjects with the BB allele had higher superoxide dismutase (P=0.021) and catalase (insignificant increase) activities, while their conjugated diene (P=0.000) levels were lower. In conclusion, our results revealed that the high low-density lipoprotein oxidation is related to the high low-density lipoprotein cholesterol content and low phospholipid content. The present study demonstrated an increase in superoxide dismutase and catalase activities, as well as PON1 activities, in subjects with the BB allele. Since these enzymes all show activity against low-density lipoprotein oxidation, we propose that future investigations on atherosclerotic processes should address PON1 polymorphism as well as PON1 and other antioxidant enzymes.

Background: Renal involvement in Takayasu’s arteritis (TA) effects the disease outcome and endovascular treatment is an effective treatment of choice. We investigated nitric oxide (NO) levels and the effect of endovascular treatment in renovascular hypertensive TA patients. Methods: In five hypertensive patients with renal artery stenosis due to TA, serum creatinine, nitrite, nitrate; urinary microalbumin, nitrite, nitrate measurements and blood pressures were recorded at entry and after 24 h and 6 weeks of endovascular treatment. Results: Serum NO levels were higher in patients than controls (p = 0.008). Serum and urine NO levels increased 24 h after the treatment and decreased after 6 weeks (p = 0.015; p = 0.01, respectively). After the treatment blood pressures decreased. Urinary microalbumin excretions increased after the intervention (p = 0.02) and returned to normal in patients 1 and 4, and decreased in the others. There were no significant differences in estimated glomerular filtration rate (EGFR), serum creatinine, urinary sodium and potassium levels. Conclusion: Increased NO secretion in these patients may contribute to improve the prognosis of renal function through its vasodilator and antiproliferative activities possibly by counterbalancing the excessive vasoconstrictor actions. Endovascular treatment causes a dilatation-induced shear stress that may be responsible for the increased NO release, which in turn leads to the rapid hypotensive response.