Ali Rıza Ocak

Effect of Mobile Phone Exposure on Apoptotic Glial Cells and Status of Oxidative Stress in Rat Brain

The aim of this study was to investigate the effects of mobile phone exposure on glial cells in brain. The study carried out on 31 Wistar Albino adult male rats. The rat heads in a carousel exposed to 900 MHz microwave. For the study group (n:14), rats exposed to the radiation 2h per day (7 days in a week) for 10 months. For the sham group (n:7), rats were placed into the carousel and the same procedure was applied except that the generator was turned off. For the cage control (n:10), nothing applied to rats in this group. In this study, rats were euthanized after 10 months of exposure periods and brains were removed. Brain tissues were immunohistochemically stained for the active (cleaved) caspase-3, which is a well-known apoptosis marker, and p53. The expression of the proteins was evaluated by a semi-quantitative scoring system. However, total antioxidative capacity (TAC), catalase, total oxidant status (TOS), and oxidative stress index were measured in rat brain. Final score for apoptosis in the exposed group was significantly lower than the sham (p < 0.001) and the cage control groups (p < 0.01). p53 was not significantly changed by the exposure (p > 0.05). The total antioxidant capacity and catalase in the experimental group was found higher than that in the sham group (p < 0.001, p < 0.05). In terms of the TOS and oxidative stress index, there was no statistically significant difference between exposure and sham groups (p > 0.05). In conclusion, the final score for apoptosis, total antioxidant capacity and catalase in rat brain might be altered by 900 MHz radiation produced by a generator to represent exposure of global systems for mobile communication (GSM) cellular phones.

The association of serum prolidase activity with the presence and severity of coronary artery disease.

ObjectivesProlidase is a cytosolic exopeptidase that cleaves iminodipeptides with carboxy-terminal proline or hydroxyproline and plays major role in collagen turnover. Collagen is the essential content in atherosclerotic plaque playing a key role in the stability/instability of and progression of coronary artery disease (CAD). Consequently, in this study we sought to determine serum prolidase activity and markers of oxidative stress such as lipid hydroperoxide and total free sulfhydryl in CAD. Design and methodsWe have evaluated 199 patients with CAD and 122 control cases with clinical, electrocardiographic, and laboratory investigation. We have measured serum prolidase activity and serum total free sulfhydryl levels spectrophotometrically. Serum lipid hydroperoxide levels were determined with ferrous ion oxidation-xylenol orange method. We assessed the association of serum prolidase activity with the presence and severity of CAD and clinical characteristics, and laboratory parameters. ResultsSerum prolidase activity (52.5±5.6 vs. 46.7±5.1 U/l, respectively, P<0.001) and serum lipid hydroperoxide levels were significantly increased in patients with CAD compared with control cases whereas, serum total free sulfhydryl levels were significantly decreased in patients with CAD compared with control cases. Serum prolidase activity and total free sulfhydryl levels were independent predictors of the presence of CAD [(χ2=75.532, ß=0.212, P=0.003) and (χ2=25.969, ß=−30.486, P=0.019), respectively] and Gensini score [(&bgr;=0.276, P<0.001) and (&bgr;=−0.274, P<0.001), respectively]. Independent predictors of serum prolidase activity were serum high-density lipoprotein cholesterol (&bgr;=−0.138, P=0.023) and urea levels (&bgr;=0.146, P=0.036), and Gensini score (&bgr;=0.317, P<0.001). ConclusionFindings of this study have shown that serum prolidase activity is significantly associated with the presence and severity of CAD, and elevated serum prolidase activity might be an independent predictor of coronary atherosclerosis.

Non-diabetic metabolic syndrome and obesity do not affect serum paraoxonase and arylesterase activities but do affect oxidative stress and inflammation

OBJECTIVE Paraoxonase-1 (PON-1), which has PON and arylesterase activities, is a high-density lipoprotein (HDL)-bound antioxidant enzyme that inhibits atherosclerosis. Diabetes has been shown to have an impact on oxidative stress. The effect of metabolic syndrome (MetS) on oxidative stress and PON-1 has been shown before, and PON-1 has been found to be related with accelerated atherogenesis. This study aimed to determine the oxidative state and PON and arylesterase activities in non-diabetic MetS and non-MetS obese patients. DESIGN Thirty obese patients (3 M and 27 F) without MetS, 40 non-diabetic obese patients (3 M and 37 F) with MetS, and 30 controls (2 M and 28 F) were enrolled. METHODS A 75 g glucose tolerance test was performed. PON-1, PON, arylesterase, total antioxidant status (TAS), high-sensitive C-reactive protein (hsCRP), and metabolic parameters were analyzed. RESULTS PON and arylesterase activities were similar between the groups, while TAS was low in both MetS and obese groups compared to controls (P<0.01 and P<0.05 respectively). CRP was higher in the MetS group compared with the obese and control groups (P<0.01 and P<0.001 respectively). In both the obese and MetS groups, CRP showed a positive correlation with body mass index (BMI). TAS was negatively correlated with BMI, waist circumference, triglyceride levels, and systolic and diastolic blood pressures (P<0.001). CONCLUSIONS Oxidative stress is altered in non-diabetic MetS and non-MetS obese patients, but PON and arylesterase activities seem not to be affected. This result may be due to the absence of diabetes, the most severe form of altered carbohydrate metabolism.

Evaluation of oxidant and antioxidant status in infants with hyperbilirubinemia and kernicterus

Objective: The objective of the present study was to determine oxidant and antioxidant status in infants with hyperbilirubinemia and/or kernicterus and to find whether there is a relationship between bilirubin level and oxidant/antioxidant status. Patients: The study includes 69 full-term newborns (neonates with hyperbilirubinemia needing phototherapy [Group 1, n = 36] and neonates with kernicterus [Group 2, n = 33]) and 25 age-matched healthy newborn. Results: Plasma total antioxidant capacity (TAC) and serum total oxidant status (TOS) were significantly higher in Groups 1 and 2 than the control group. There was a significant difference between Group 1 and control cases for malondialdehyde (MDA; p < 0.001). Total free sulfhydryl group (TTHI) values were significantly elevated in Group 1 compared to Group 2 and control cases. Correlation analysis showed that the correlation between total bilirubin (TB) and TAC, TOS, MDA and oxidative stress index may be expressed by a quadratic curve. After phototherapy, a statistically significant increase in nitrite level was observed. Conclusion: We demonstrated that the relationship between serum TB and antioxidants and oxidative stress could be expressed by a quadratic correlation curve.

Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats

This study examined the effects of Y‐27632, a selective Rho‐kinase inhibitor, on organophosphate‐induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30 mg kg−1 i.p.), 1 and 10 mg kg−1 Y‐27632 + dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper‐secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y‐27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y‐27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y‐27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y‐27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho‐kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats. Copyright

Effect of lycopene on caspase-3 enzyme activation in liver of methanol-intoxicated rats: comparison with fomepizole.

Lycopene is one of the major carotenoids and is found almost exclusively in tomatoes and tomato products. This study was performed to evaluate the effect of lycopene on methanol-induced liver injury and to compare the results with those after fomepizole, which is used in treatment of methanol intoxication. Experiments were carried out with 30 female Wistar rats weighting 180-200 g. Rats were injected with a intraperitoneally dose of 3 g/kg methanol as a 50% solution in isotonic saline once for intoxication. Rats were pretreated with fomepizole (50 mg/kg) and/or lycopene (10 mg/kg) before methanol. After 24 hours all the drug-treated and intoxicated rats were sacrificed under anesthesia. Malondialdehyde (MDA) levels were determined in order to assess lipid peroxidation, and caspase-3 activity was determined by immunostaining of liver tissues to evaluate apoptosis. Methanol administration significantly increased the MDA level and caspase-3 activity in liver. Pretreatment with lycopene and/or fomepizole decreased the MDA levels significantly. Similarly, lycopene and fomepizole decreased methanol-induced caspase-3 activity. The findings of the present study demonstrate that methanol intoxication causes hepatic toxicity in rats and that this is likely a result of reactive oxygen species and apoptosis induction. Lycopene has protective effects against methanol-induced hepatic injury similar to fomepizole. It was demonstrated for the first time that both lycopene and fomepizole prevent methanol-induced hepatic injury by reducing the increase of lipid oxidation and caspase-3 activation.