Pernur Öner

The effects of acute melatonin and ethanol treatment on antioxidant enzyme activities in rat testes

The pineal hormone melatonin (N -acetyl, 5-methoxytryptamine) was recently accepted to act as an antioxidant under both in vivo and in vitro conditions. In this study, we examined the possible preventive effect of melatonin on ethanol-induced lipid peroxidation in rat testes. Thirty-seven male Wistar albino rats, 5.5--6 months old, were randomly divided into four groups (9--10 animals in each). The first group (control animals) received 4% ethanol at similar intervals to the experimental groups to equalize the stress effect. The second group received only melatonin i.p. 7 mg kg(-1)bw three times over 1.5 h intervals. The third group received only 30% alcohol 3 g kg(-1)bw twice daily. The fourth group were treated with melatonin and ethanol according to the above protocol, melatonin injections preceding ethanol treatments. The product of lipid peroxidation, malondialdehyde (MDA) and antioxidant enzymes, superoxide dismutase (Cu--Zn SOD), glutathione peroxidase (GPx) and catalase (CAT) were measured in the post-mitochondrial fraction of the testes. MDA levels were significantly increased due to acute ethanol intoxication. GPx activity was higher in the three experimental groups than the control levels. The activity of CAT was increased significantly in the melatonin plus ethanol-treated group but the other groups appeared not to be influenced by acute ethanol treatment. Cu--Zn SOD activity remained unaltered. These results suggest that antioxidants may be a protective agent for the testicular injury caused by ethanol consumption.

Appetite-regulating Hormones in Chronic Kidney Disease Patients

OBJECTIVE Inflammation and loss of appetite is the most common problem in patients with chronic kidney disease (CKD). This comparative cross-sectional study aimed to characterize the changes in circulating levels of ghrelin, obestatin, leptin, all of which have an effect on food intake, and proinflammatory cytokines interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) in patients with CKD who were undergoing different treatments. DESIGN AND SETTING Study participants included 36 patients who had undergone hemodialysis (body mass index [BMI]: 22.3 ± 4.17 kg/m(2)); 41 who had undergone peritoneal dialysis (BMI: 23.5 ± 3.10 kg/m(2)), 30 with early stage CKD (BMI: 24.4 ± 3.32 kg/m(2)), and 31 healthy subjects (24.3 ± 2.14 kg/m(2)). The patients with CKD were kept under a standard diet with restricted salt, potassium, and protein intake. INTERVENTION Levels of leptin, acylated ghrelin, obestatin, TNF-α, and IL-6 were measured by commercially available enzyme-linked immunosorbent assay kits. Total nitrite/nitrate was analyzed using colorimetric assay kit. RESULTS Significantly high leptin levels, accompanied by low acylated ghrelin levels, were observed in patients with CKD. Maintenance dialysis did not affect these levels. TNF-α and IL-6 levels were significantly higher in CKD patients than in healthy subjects, the highest being in dialysis patients. Obestatin levels were relatively low in patients who had undergone hemodialysis. CONCLUSION Low acyl-ghrelin levels, accompanied with high levels of TNF-α and IL-6 may be involved in the loss of appetite and poor nutritional status in CKD patients.

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 (T2DM). 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-α) 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/m2, n=28) and prediabetic (BMI: 29–41 kg/m2, 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-a, 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-α 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-α. 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.

Dimethylarginines and inflammation markers in patients with chronic kidney disease undergoing dialysis

The aim of this study was to investigate the pro-oxidant and proinflammatory biomarkers and their relationship with dimethylarginines (DMAs) in patients at various stages of chronic kidney disease (CKD). We studied 114 CKD patients, 36 were hemodialyzed, 41 peritoneal dialyzed and 37 nondialyzed (early stage) CKD patients. The control group consisted of 31 healthy subjects. Plasma levels of asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), l-arginine, nitric oxide (NO) and proinflammatory cytokines (TNF-alpha and IL-6) were determined, and their relationships with the degree of disease were evaluated. Both DMAs were at high levels in all CKD patients, whereas arginine concentrations were low in patients undergoing dialysis. Elevated TNF-α and IL-6 in CKD patients were indicative of ongoing chronic inflammatory state. A significant positive correlation between SDMA and creatinine suggests that plasma SDMA level may be an index for renal function.

Comparison of the Activities of Na+,K+-ATPase in Brains of Rats at Different Ages

Background: Na+,K+-ATPase is known to be responsible for the ionic homeostasis in excitable tissues. The energy cost of Na+,K+-ATPase activity is increased in the active brain, so it would be important to ascertain whether defects in brain metabolism in aging are associated with changes in the properties of Na+,K+-ATPase. Objective: The aim of this study was to investigate the influence of age on the Na+,K+-ATPase activity in developing rat brains from the age of 1 day to 24–28 months. Methods: Crude microsomal preparations were obtained from the brains of newborn (n = 8), 18-day-old (n = 8), 4- to 5-month-old (n = 12), and 24- to 28-month-old (n = 14) rats. Then the ATPase activity was measured and expressed as micromoles of inorganic phosphorus released per milligram of protein per hour. Results: The increased tendency in brain Na+,K+-ATPase activity from newborn to 18 days of age suggested that the Na pump is mature soon after birth. No significant differences could be detected in the enzyme activity between newborn and adult rats. In contrast, the Na+,K+-ATPase activity in aged rat brains was found to be significantly lower than in the other age groups of rats tested (p < 0.001). Conclusion: Our results suggest that aging-induced inhibitions in the brain Na+,K+-ATPase activity may be implicated in the depression of neuronal excitability and in the age-related impairments of cognitive functions.

Serum asymmetric dimethylarginine and nitric oxide levels in obese postmenopausal women

Background: It has been reported that estrogen deficiency after menopause might cause a decrement in nitric oxide (NO) bioavailability by increasing the level of asymmetric dimethylarginine (ADMA), a major endogenous nitric oxide synthase inhibitor, thus leading to abnormalities in endothelial function. Because NO plays an important role on feeding behavior, ADMA may be involved in the pathogenesis of obesity, too. This cross‐sectional study aimed to evaluate the relations of ADMA and NO with the obesity‐linked peptides, such as ghrelin, leptin, and adiponectin in postmenopausal women free of hormone replacement therapy. Methods: Adiponectin, ghrelin, leptin, ADMA, and NOx (total nitrite/nitrate) were measured in 22 obese (BMI: 30–47 kg/m2) and 19 normal weight (BMI: 21.5–26 kg/m2) postmenopausal women.Anthropometric measurements (height, weight, BMI, waist, and hip circumferences) were recorded. Statistics were made by the Mann–Whitney U‐test. Results: Ghrelin and adiponectin levels were significantly lower (P<0.001), whereas ADMA and leptin levels were higher in obese women than in normal weight controls (P<0.01 and 0.001, respectively). BMI was correlated negatively with adiponectin and ghrelin and positively with ADMA and leptin levels. No correlation existed between ADMA and NO. Conclusion: Estrogen deficiency alone may not cause an increase in ADMA levels unless the women are prone to disturbances in energy homeostasis. In spite of the high ADMA levels, the unaltered NO levels in plasma may be owing to ongoing inflammatory conditions. J. Clin. Lab. Anal. 25:174–178, 2011.

Evaluation of leukocyte arylsulfatase-A activity in patients with breast cancer and benign breast disease

This study was planned to evaluate the feasibility of using the assay of leukocyte arylsulfatase-A (AS-A) activity as a non-invasive diagnostic tool in patients with benign and malignant breast disease. The leukocyte AS-A activity of a total of 81 women was analyzed, including 28 healthy women, 29 women with benign breast disease (BBD) and 24 patients with primary breast cancer (BC). The mean leukocyte AS-A activity in patients with BBD was slightly higher (14.3%) that observed in the healthy subjects, but the difference was not statistically significant. In patients with BC the enzyme activity was significantly higher than in the healthy subjects (60.3%, P<0.05) and in the benign group (40.2%, P<0.05). In addition, since no significant differences have been observed between premenopausal patients and their controls, it is suggested that the measurement of leukocyte AS-A activity may not be a reliable test for differential diagnosis of benign and malignant proliferation in mammary glands due to the possible interfering effect of gonadal hormones on AS-A activity. In contrast, since peri- and postmenopausal BC patients have negligible or no gonadal activity function, the elevation in the activity of leukocyte AS-A in these age groups of patients may only be expected to originate from malignant proliferation. Based on our results, it is concluded that in patients in whom high leukocyte AS-A activities were observed the possibility of the presence of malignancy might also be high. Therefore, this test might be valuable as a non-invasive biochemical technique in combination with other established markers for the identification of masses in the breast.

Sex-dependent changes in blood-brain barrier permeability and brain NA+,K+ATPase activity in rats following acute water intoxication

To understand the increased susceptibility of the development of serious complications to hypoosmotic hyponatremia in young females, we examined the resistance of blood brain barrier (BBB) permeability to water along with the synaptosomal Na+,K+ATPase activity in both sexes of rats during acute water intoxication. Four groups of rats were used: Group I and II were normal female and male rats injected with only Evans‐blue. Group III and IV were water intoxicated female and male rats respectively. BBB permeability in female rats was found to be increased following acute water intoxication. In contrast, synaptosomal Na+,K+ATPase activities in both water intoxicated male and female rats were found significantly lower than those in control rats. But inhibition in enzyme activity in synaptosomes from water intoxicated female rats was more pronounced than those of corresponding male rats. Our results concuded that female sex steroids may be responsible for the highly significant decrease in synaptosomal Na+,K+ATPase activity and increased BBB permeability in female rats following water intoxication. J. Neurosci. Res. 62:750–753, 2000.

Serum prolidase I activity and some bone metabolic markers in patients with breast cancer: in relation to menopausal status

OBJECTIVES The purpose of this study was to investigate the diagnostic value of some osteoblastic/osteoclastic biochemical markers and serum prolidase I activity in breast cancer (BC). DESIGN AND METHODS Serum bone gla protein (BGP), prolidase I activity, urinary deoxypyridinoline (Dpy) and calcium excretions were measured, in metastatic and nonmetastatic BC patients, and in 52 healthy women. RESULTS In patients with metastases, bone turnover markers were found to be significantly higher than those in the control group and in patients without metastases. Serum prolidase activity in patients with and without metastases was also significantly higher than those in the control group, but there was no difference between the two patient groups. CONCLUSIONS Bone turnover has been suggested to be accelerated in BC patients with the more pronounced osteolytic activation, especially in metastatic state. Serum prolidase in premenopausal period appears to be valuable in discriminating cancer patients from controls. BGP and to a lesser degree of Dpy, may be useful markers for predicting the metastatic bone involvement, as well as for the more cost effective management of BC patients and monitoring the effects of antiresorptive therapy of malignant osteolysis before any metastasis could be detected by other invasive techniques.

Effect of exogenous melatonin on ethanol-induced changes in Na+, K+- and Ca2+-ATPase activities in rat synaptosomes

In the present study, the effects of acute ethanol (EtOH) toxicity and of exogenous melatonin (MLT) on this toxicity were examined by measuring membrane-bound ATPases and acetylcholinesterase activities in rat synaptosomal membranes. The concentrations of plasma α-tocopherol and adrenal ascorbic acid (AA) were also measured. Synaptosomal Na+,K+-ATPase and Ca2+-ATPase activities were significantly depressed in acute EtOH-intoxicated rats compared with controls, while acetylcholinesterase activity remained unaltered. Pretreatment with MLT (10 mg/kg) prior to acute EtOH administration prevented EtOH-induced inhibition of ATPases. Adrenal AA and plasma α-tocopherol levels were also depressed regardless of MLT pretreatment. MLT treatment alone affected neither membrane-bound enzyme activities nor tissue and blood levels of vitamins C and E. It is concluded that acute EtOH intoxication disturbs neural transport functions through the membrane-bound ATPase activity depression. Reduced AA and α-tocopherol levels may contribute to the neurodegenerative effects of EtOH. However, pretreatment with a high dose of MLT before EtOH administration may be beneficial to prevent EtOH-induced toxicity on ATPase-mediated neural transport functions.