Determination of diagnostic and prognostic values of urinary interleukin-8, tumor necrosis factor-alpha, and leukocyte arylsulfatase-A activity in patients with bladder cancer

Objectives: This study was planned to evaluate the feasibility of the assay of leukocyte arylsulfatase-A (AS-A) activity, and some urinary cytokine levels (tumor necrosis factor-alpha [TNF-alpha] and interleukin-8 [IL-8]), as noninvasive diagnostic tools in different stages of bladder cancer patients

Evaluation of the effect of low-dose oral theophylline therapy on some bone turnover markers and serum prolidase I activity in mild asthmatics

Hypercalcemia and hypercalciuria observed both in humans and in animals who were on long-term theophylline therapy, prompted us to investigate whether oral theophylline treatment at optimal doses causes any adverse side effects on bone metabolism in mild asthmatics. Therefore, serum osteocalcin (BGP) and total alkaline phosphatase (TALP, EC 3.1.3.1) as bone formation markers, serum prolidase I(EC 3.4.13.9) activity as a marker for collagen metabolism, urinary deoxypyridinoline (Dpd), hydroxyproline (Hyp) and fasting urinary calcium as bone resorption markers, were measured in 18 mild asthmatics who had been treated with theophylline over 1-10 years. Among measured bone turnover markers, BGP, TALP, and Hyp levels were found to be increased in mild asthmatics; and BGP showed the greatest percent mean increase (98%) over the healthy subjects. However, these increments did not exceed the upper reference limits. Serum prolidase I activity was also increased in mild asthmatics receiving theophylline. Our results indicate that theophylline therapy at optimal doses may not exert adverse side effects on bone homeostasis, but patients receiving supratherapeutic doses of theophylline should be under close examination in order to predict future bone mass status. (C) 1999 Academic Press

Acute effects of estradiol and of diethylstilbestrol: Pro- or antioxidant potential?

This study was aimed to examine the effects of a single high dose of natural and synthetic estrogens on the antioxidant defense enzymes in liver and blood. Female Wistar albino rats, four to six months old, were divided into three groups, and received either i.p. injections of diethylstilbestrol (DES; 150 mg kg(-1) b.w.) or s.c. injections of estradiol (E-2; 25 mg kg(-1) b.w.), and the third group (control) was injected the solvent. Animals were killed under light ether anesthesia three hours after injection. Cu-Zn superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (Cat) enzyme activities and fluorometric malondialdehyde (MDA) determination were performed in liver tissue homogenates and in blood. Acute estradiol injection caused a significant increase in both MDA levels and GPx activity in liver tissue when compared to the controls, (p < 0.05 and p < 0.02; respectively). Changes in both enzyme activities and MDA concentration were unremarkable following acute DES injection. In blood, only Cu-Zn SOD activity was significantly altered in blood following E-2 injection. Although the significance of alteration in GPx activity remains unclear, it is most likely related to enhanced generation of lipoperoxides. A significant increase in MDA concentrations in liver tissue is indicative of pro-oxidative damage rather than an antioxidant action by E-2

The effect of melatonin administration on ethanol-induced lipid peroxidation in rats

This study was carried out in order to determine the role of melatonin in preventing lipid peroxidation due to acute ethanol intoxication. Male Wistar Albino rats, 2.5-3 months old, were divided into two groups. Melatonin (in 1% ethanol, 2 mg kg(-1) body weight) was given intraperitoneally (i.p.) for 21 days to experimental rats whereas controls received 1% ethanol only. On day 21, 6 g kg(-1) body weight ethanol was injected to half of the animals in each group and the remainder were kept as corresponding controls. Animals were killed 5 h after ethanol injection. Malondialdehyde (MDA), reduced glutathione (GSH) and the antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and catalase) were determined in liver tissue homogenates. MDA levels were increased whereas GSH levels tend to decrease following alcohol injection. Melatonin administration prior to ethanol did not alter MDA and GSH levels of tissue and among antioxidant defence enzymes studied, only CuZn-SOD was found to be increased in animals that received melatonin + ethanol. According to the findings of this study, melatonin did not appear to have any direct effect on alcohol-induced lipid peroxidation. (C) 1998 The Italian Pharmacological Society

Advanced oxidation protein products in obese women: its relation to insulin resistance and resistin

Obesity is a major risk factor for insulin resistance and type 2 diabetes mellitus (TZDM). Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. Attempts were also made to see whether resistin levels are related to the degree of oxidative stress, as determined by the measurement of advanced oxidation protein products (AOPPs). The study groups consisted of obese diabetic (BMI: 30-42 kg/m(2), n=28) and prediabetic (BMI: 29-41 kg/m(2), n=23) women. Fourteen healthy women, with BMI in the range 21.5-25.5 kg/m2, were taken as controls. Serum levels of TNF-alpha, IL-6, resistin, glucose, insulin and AOPPs were measured. Insulin resistance was calculated by the homeostasis model assessment (HOMA-IR). Diabetic and prediabetic obese patients had increases in serum resistin and TNF-a levels (P < 0.01 and P < 0.001, respectively). IL-6 levels in diabetic patients were significantly higher than in prediabetics (P < 0.05). AOPP levels were also significantly higher in diabetics than prediabetics and controls (P < 0.05 and P < 0.001, respectively); and positively correlated with blood glucose. Insulin was significantly associated with circulating resistin and TNF-a. The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. Determination of AOPPs may be helpful for monitoring the impaired glucose metabolism in obesity

The relation between serum MDA and cystatin C levels in chronic spinal cord injury patients

Objectives: The assessment of renal function is particularly important in patients with spinal cord injury (SCI). Creatinine (Cr) is known to be unsuitable as a marker of renal function in SCI because of muscle wasting. Although cystatin C (cys-C) is more reliable than Cr, its expression may be affected by oxidative stress accompanying SCI. The aim of the study was to estimate the cys-C levels in SCI patients with normal functioning kidneys. The prooxidant/antioxidant state in plasma of the patients and controls was measured, and any correlations between these parameters and cys-C were determined

Urine 8-isoprostane F-2 alpha concentrations in patients with neurogenic bladder due to spinal cord injury

Background: Isoprostanes are prostaglandin-like end products of arachidonic acid peroxidation that are produced by a free radical-catalyzed mechanism. Considering its free radical-dependent formation and potent contractor effect, it is postulated that isoprostane 8-iso PGF(2alpha) may play an important role in oxidative stress-related smooth muscle dysfunction. These substances may also influence bladder activity directly by effects on the smooth muscle. The present study was designed to measure traditional biochemical parameters (MDA, TAS, vitamin E) in plasma and 8-iso PGF(2alpha) concentrations in urine of patients with spinal cord injury and to evaluate the relation of urinary isoprostane concentrations to the bladder function. Methods: All spinal cord patients underwent urodynamic evaluations. The biochemical tests were performed in both hyperreflexic bladder group (n = 23) and areflexic bladder group (n = 10), and the findings were compared to those of the patients with normally functioning bladder (controls, n = 19). Results: Urine 8-iso PGF(2alpha) concentrations were significantly increased in hyperreflexic group (median value 0.89 pg/mg creatinine) compared to both control (0.52 pg/mg creatinine) and areflexic groups (p < 0.001). The lowest concentrations of urinary 8-iso PGF(2alpha) were observed in the areflexic group (0.22 pg/mg creatinine), and these were positively correlated to the plasma MDA concentrations in areflexic patients (p = 0.05; r = 0.684). Conclusion: Isoprostanes may be involved in the pathogenesis of neurogenic bladder dysfunction. It may be of value to determine the urinary concentrations of 8-iso PGF(2alpha) in order to distinguish areflexic bladders from the hyperreflectics. (C) 2003 Elsevier B.V. All rights reserved

Evaluation of leukocyte arylsulphatase A, serum interleukin-6 and urinary heparan sulphate following tamoxifen therapy in breast cancer

Leukocyte arylsulphatase A (AS-A) was shown to be significantly high in newly-diagnosed breast cancer patients. Previous reports imply a connection between serum interleukin-6 (IL-6) and breast cancer, possibly through a modulation of enzymes involved in estrogen synthesis. Abnormal distribution of heparan sulphate proteoglycans (HSPGs) in malignant breast epithelial cells suggests that they play a key role in the regulation of cell growth. Estradiol is believed to be effective in modulating glycosaminoglycans (GAGs) and their depolymerizing enzymes. Therefore, in this study, attempts were made to evaluate the activity of leukocyte arylsulphatase A, serum interleukin-6, urinary GAGs and heparan sulphate (HS) in response to tamoxifen (TAM) therapy in mastectomised breast cancer patients. Thirty-four patients (aged 30-82 years) were administered TAM (20 mg twice daily). Blood and urine samples of each patient were collected three times (at the beginning, and in third and sixth month of TAM therapy), and biochemical parameters were measured. There was no difference between baseline leukocyte AS-A activity and that measured after three months. At the end of six months, enzyme activity was significantly higher than the former values (p = 0.022), but within the reference intervals reported in the literature. Although this increase might imply a normalization, the duration of TAM therapy is not long enough to make a decision about either regression or aggravation of the disease. TAM did not have any effect on serum IL-6, urinary HS and GAG levels which may be due to insensitivity of these variables to TAM during the short period of therapy. Both urinary GAG and HS levels measured at sixth month exhibited a positive correlation with the baseline level of leukocyte AS-A (P = 0.005 and 0.009, respectively), suggesting that positive responses to the drug might be seen in patients with low AS-A activity. (c) 2005 Elsevier Ltd. All rights reserved

Early and late effects of hyperbaric oxygen treatment on oxidative stress parameters in diabetic patients

Exposure to hyperbaric oxygen leads to increased amount of reactive oxygen species (ROS) that are derived from various sources. After the discovery that ROS can function as signaling molecules, the idea of ROS being hazardous to biological tissues has been challenged. The aim of this study was to examine the changes in oxidative stress parameters in diabetics undergoing hyperbaric oxygen therapy (HBOT) due to foot ulcers. Twenty patients, who received HBOT for diabetic foot ulcers, were included in the study. Blood samples were taken before HBOT and 30 min after exit from the chamber, on the day of the first and the 15th HBOT sessions. They were used for the determinations of malondialdehyde (MDA), 8-isoprostane and advanced oxidation protein products (AOPPs). 8-Isoprostane and AOPP levels were not altered significantly after the first HBOT session, while both were increased on the fifteenth day (p<0.05). MDA was significantly increased only after the first HBOT session, and remained unchanged on the fifteenth day (within-day variations). Plasma AOPP levels were lowered significantly after fifteen consecutive HBOT sessions (between-day variations). Decreased AOPP levels suggest that increased oxygenation of tissues due to HBO therapy may activate some endogenous factors that prevent hazardous effects of the disease itself