Semsettin Sahin

Lipid peroxidation and antioxidant status in lichen planus

Background.  Lichen planus (LP) is an inflammatory skin disease of unknown aetiology. Recently, increased oxidative stress has been implicated in the pathogenesis of various skin diseases such as atopic dermatitis, psoriasis vulgaris and vitiligo.

Serum homocysteine, vitamin B 12 and folic acid levels in different types of glaucoma

BackgroundThis study was performed to compare levels of serum homocysteine (Hcy), vitamin B12 and folic acid in patients with primary open-angle glaucoma (POAG), pseudoexfoliative glaucoma (PEXG), normotensive glaucoma (NTG) and healthy controls.MethodsTwentyfive patients with POAG, 24 with PEXG, and 18 with NTG, along with 19 control healthy subjects were included this prospective study. Levels of serum Hcy were measured using immunoassay, and those of serum vitamin B12 and folic acid were measured using competitive chemiluminescent enzyme immunoassay.ResultsThe mean Hcy concentration in the PEXG group was significantly higher (P < 0.001) as compared to the other groups. There were no significant differences with respect to the mean Hcy concentrations among other groups (P > 0.05). There were no statistical differences in serum vitamin B12 levels among POAG, PEXG, NTG and control subjects (P > 0.05).The mean serum folic acid level was significantly lower in the subjects with PEXG (P < 0.009). However, the mean folic acid concentrations among the other groups did not differ significantly (P > 0.05).ConclusionElevated levels of Hcy in PEXG may explain the role of endothelial dysfunction among patients with PEXG.

The activities of liver adenosine deaminase, xanthine oxidase, catalase, superoxide dismutase enzymes and the levels of malondialdehyde and nitric oxide after cisplatin toxicity in rats: protective effect of caffeic acid phenethyl ester.

The aim of this experimental study was to investigate the effects of caffeic acid phenethyl ester (CAPE), an antioxidant agent, on cisplatin-induced hepatotoxicity through adenosine deaminase (AD), xanthine oxidase (XO), catalase (CAT), superoxide dismutase (SOD) activities and malondialdehyde (MDA) and nitric oxide (NO) levels in liver tissue of rats. Wistar albino rats were divided into three groups: control group (n-6), cisplatin group (n-9) and CAPE+cisplatin group (n-8). All the chemicals used were applied intraperitoneally. Spectrophotometric methods were used to determine the activities of the above-mentioned enzymes in the liver tissue. NO level and XO activity were found to be increased in the cisplatin group compared to the control group. NO level was found to be decreased in the cisplatin+CAPE group in comparison with the cisplatin group. There was no significant change in the activity of XO between the cisplatin and cisplatin+CAPE groups. The activity of SOD was lower in the cisplatin group than both the control and cisplatin+CAPE groups. There was no significant change in the activity of CAT between the control and cisplatin groups. CAT activity was increased in the cisplatin+CAPE group compared to the cisplatin group. The AD activity and MDA level remained unchanged in all groups. The results obtained suggested that CAPE significantly attenuated the hepatotoxicity as an indirect target of cisplatin in an animal model of cisplatin-induced nephrotoxicity.

Protective effects of caffeic acid phenethyl ester on skeletal muscle ischemia-reperfusion injury in rats

There is a great evidence that reactive oxygen species (ROS) play an important role in the pathophysiology of ischemia −reperfusion(I/R)injury in skeletal muscle.Caffeic acid phenethyl ester(CAPE)is a component of honeybeep ropolis.It has antioxidant, anti−inflammatory and free radical scavenger properties.The aim of this study is to determine the protective effects of CAPE against I/R injury in respect of protein oxidation, neutrophil in filtration, and the activities of xanthine oxidase(XO)and adenosine deaminase(AD)onan<invivomodel of skeletal muscle I/R injury.Rats were divided into three equal groups each consisting of sixrats:Sham operation, I/R, and I/R plus CAPE(I/R+CAPE)groups.CAPE was administered intraperitoneally 60 min before the beginning of the reperfusion.At the end of experimental procedure, blood and gastrocnemius muscle tissues were used for biochemical analyses.Tissue protein carbonyl(PC)levels and the activities of XO, myeloperoxidase(MPO) and AD in I/R group were significantly higher than that of control(p0.01, p0.05, p0.01, p0.005, respectively).Administration of CAPE significantly decreased tissue PC levels, MPO and XO activities in skeletal muscle compared to I/R group(p0.01, p0.05, p0.05, respectively).In addition, plasma creatine phosphokinase(CPK), XO and ADactivities were decreased in I/R+CAPE group compared to I/R group(p0.05, p0.05, p0.001). The results of this study revealed that free radical attacks may play an important role in the pathogenesis of skeletal muscle I/R injury. Also, the potent free radical scavenger compound, CAPE, may have protective potential in this process. Therefore, it can be speculated that CAPE or other antioxidant agents may be useful in the treatment of I/R injury as well as diffused traumatic injury of skeletal muscle.

Antioxidant enzyme activities and lipid peroxidation products in heart tissue of subacute and subchronic formaldehyde-exposed rats: a preliminary study.

Objective: The aim of this experimental study was to evaluate the oxidant/antioxidant status and lipid peroxidation in the heart of rats exposed to formaldehyde (FA) inhalation for four weeks (subacute) or 13 weeks (subchronic) continuously. Methods and results: Sixty Wistar albino rats were divided into six groups randomly (ten in each group). The first and second groups were used as subacute and subchronic control groups. FA gas was generated from paraformaldehyde and pumped to a closed glass chamber. Rats were exposed to atmosphere containing 10 and 20 ppm FA (8 h/day, five days per week) during a four and 13 weeks period. After heart tissues were obtained and homogenized, thiobarbituric acid-reactant substances (TBARS) and nitric oxide (NO) levels, as well as superoxide dismutase (SOD) and catalase (CAT) activities, were measured. There were statistically significant findings in SOD and CAT activities in the study groups compared to the control group. Heart tissue SOD level was increased in the group exposed to subacute 10 and 20 ppm FA inhalation compared to the control group (P≤0.011 and ≤0.0001). In addition, heart tissue SOD level was increased in the group exposed to subchronic 10 and 20 ppm FA inhalation compared to the corresponding control group (P≤0.001). On the other hand, there were statistically significant decreases in CAT activity in subacute 10 and 20 ppm groups compared to the corresponding control group (P≤0.012 and ≤0.039, respectively). Although not significant, TBARS levels were increased in both subacute 10 ppm (P=0.100) and subchronic 20 ppm (P=0.053) groups compared to their corresponding control groups. Tissue NO levels were unchanged upon FA inhalation. In the correlation analyses, a meaningful relationship between SOD and CAT activities in subchronic 10 ppm group (r=-0.685, P≤0.029); SOD activity and TBARS level in subchronic 20 ppm group (r=-0.675, P≤0.032); and CAT activity and NO level in subchronic 20 ppm group (r=-0.810, P≤0.005) were found. Conclusion: From the findings of our study, it can be interpreted that subacute and subchronic FA inhalation may stimulate oxidative stress and thus, some secondary toxic effects in cardiac cells and tissue. This increase in the oxidative stress could not induce lipid peroxidation in the membranous structure of cardiac cells. An increased SOD enzyme activity was thought to be secondary to decreased CAT activity, as a compensation mechanism, preventing heart tissue from destruction induced by FA.

Oxidative Stress Levels in Exhaled Breath Condensate Associated With COPD and Smoking

BACKGROUND: COPD is characterized by chronic air-flow limitation. Smoking is the most important factor in the pathogenesis of COPD. Smoking is associated with increased oxidative stress in the lungs. In this study our aim was to evaluate the differences in the burden of oxidative stress in patients with COPD, smokers, and non-smokers by measuring hydrogen peroxide (H2O2), malondialdehyde (MDA), and 8-isoprostane levels in the exhaled breath condensate (EBC) samples. METHODS: Eighty subjects were included in the study. Group I (no. = 25) had COPD, Group II (no. = 26) was smokers, and Group III (no. = 29) was nonsmokers. The severity of the COPD and dyspnea was assessed according to the results of pulmonary function tests (PFTs) and Medical Research Council (MRC) scale. RESULTS: The mean age of the subjects was 58 ± 8.9 years. While 8-isoprostane and H2O2 levels were significantly higher in subjects with COPD (44.8 ± 40.2 pg/mL and 1.9 ± 0.8 μmol/L) and smokers (41.3 ± 26 pg/mL and 1.7 ± 0.7 μmol/L) than non-smokers (15.8 ± 6.9 pg/mL and 0.8 ± 0.4 μmol/L), levels were similar between smokers and COPD subjects. MDA levels were similar between the 3 groups (P = .31). There was no correlation between 8-isoprostane and H2O2 levels and PFT parameters. There was a significant positive correlation between dyspnea grade on the MRC scale and 8-isoprostane levels (r = 0.805, P < .001). CONCLUSIONS: Even if respiratory function tests are within normal limits, oxidant burden in lungs of smokers is equivalent to that in COPD patients. 8-isoprostane could be useful in assessing symptom severity and health status of COPD patients.

Protective effects of erdosteine on rotenone-induced oxidant injury in liver tissue

Rotenone, an insecticide of botanical origin, causes toxicity through inhibition of complex I of the respiratory chain in mitochondria. This study was undertaken to determine whether rotenone-induced liver oxidant injury is prevented by erdosteine, a mucolytic agent showing antioxidant properties. There were four groups of Male Wistar Albino rats: group one was untreated as control; the other groups were treated with erdosteine (50 mg/kg per day, orally), rotenone (2.5 mg/mL once and 1 mL/kg per day for 60 days, i.p.) or rotenone plus erdosteine, respectively. Rotenone treatment without erdosteine increased xanthine oxidase (XO) enzyme activity and also increased lipid peroxidation in liver tissue P < 0.05). The rats treated with rotenone plus erdosteine produced a significant decrease in lipid peroxidation and XO activities in comparison with rotenone group PB / 0.05). Erdosteine treatment with rotenone led to an increase in catalase (CAT) and superoxide dismutase (SOD) activities in comparison with the rotenone group PB / 0.05). There was no significant difference in nitric oxide (NO) level between groups. There were negative correlations between CAT activity and malondialdehyde (MDA) level (r= -0.934, P <0.05) with between CAT and SOD activities (r= -0.714, P <0.05), and a positive correlation between SOD activity and MDA level (r= 0.828, P <0.05) in rotenone group. In the rotenone plus erdosteine group, there was a negative correlation between XO activity and NO level in liver tissue (r= -0.833, P -0.05). In the light of these findings, erdosteine may be a protective agent for rotenone-induced liver oxidative injury in rats.

Inhibition of carbon tetrachloride-mediated apoptosis and oxidative stress by melatonin in experimental liver fibrosis

Melatonin, the principal secretory product of the pineal gland, functions as a potent antioxidant and free radical scavenger. Additionally, the antiapoptotic effect of melatonin has been observed both in vivo and in vitro. The aim of this experimental study was to investigate the protective effects of melatonin against carbon tetrachloride (CCl4)–induced apoptosis and oxidative stress in rat liver. Twenty-four male Wistar rats were divided in three equal groups. Group I was used as control. Rats in group II were injected every other day with CCl4 (0.5 mL/kg BW) for a month, whereas rats in group III were treated every other day with the same dose of CCl4 plus melatonin (25 mg/kg BW). At the end of the experiment, all animals were killed by decapitation and the livers were rapidly removed. Some of the liver tissue specimens were used for determination of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels. The remaining tissue specimens were processed for immunohistochemical assessment, and the percentage rates of apoptotic liver cells stained with immunoreactive Bax were determined. Chronic administration of CCl4 significantly increased liver MDA contents, as an end product of lipid peroxidation, and also significantly decreased SOD and GSH-Px activities, emphasizing the generation of increased oxidative stress. Moreover, it caused an evident increase in apoptotic cells. Melatonin treatment significantly reduced MDA levels and elevated SOD and GSH-Px activities in rats received CCl4 plus melatonin. Furthermore, apoptotic changes caused by CCl4 were considerably decreased in these animals. The results of the present study indicate that melatonin treatment substantially prevents CCl4-induced apoptosis and oxidative damage in the liver. Thus, melatonin may serve as a drug for treating many clinical conditions that arise from inappropriate apoptosis.

Familial Mediterranean fever gene mutations in the inner northern region of Turkey and genotype-phenotype correlation in children.

Aim:  Familial Mediterranean fever (FMF) is an autosomal recessive disorder characterised by recurrent episodes of fever, polyserositis and rash. The aim of this study was to determine the most common mutations and clinical features, and their relationships.

Cardiotrophin-1 plasma levels are increased in patients with diastolic heart failure

Summary Background Cardiotrophin-1 (CT-1) is a member of the interleukin (IL-6) family of cytokines and is increased in various cardiovascular diseases, including chronic heart failure. The aim of the study was to determine if plasma CT-1 is associated with diastolic heart failure (DHF) and to investigate the relationship between CT-1 and echocardiographic parameters. Material/Methods Fifty-seven consecutive patients (mean age 57±8 years, 24 males) diagnosed with DHF in our clinic and 33 controls (mean age 55±7 years, 12 males) were included in the study. All study participants underwent echocardiographic evaluation and blood samples were obtained. Results CT-1 and NT-proBNP values were significantly higher in DHF subjects than in controls (11.30 [8.09–16.51] vs. 17.5 [8.95–28.74] fmol/mL, P=0.017 and 64 [27.5–95] vs. 82 [55.5–241] pg/mL, P=0.009, respectively). The mitral peak velocity of early diastolic filling (E), mean ratio of E to early diastolic mitral annular velocity (E/Em), and the pulmonary capillary wedge pressure (PCWP) estimated from E/Em measurements were all significantly higher in the patient group (62.27±14.69 vs. 75.67±18.85 cm/sec, 6.40±1.48 vs. 10.30±3.48, and 10 [9–11]vs. 14[12–16] mmHg, P≤0.001 for all). Lateral and septal Em were significantly lower in the patient group (10.69±1.87 vs. 8.69±2.00 cm/sec and 8.91±1.22 vs. 6.65±1.58 cm/sec, P<0.001 for both). CT-1 positively correlated with NT-proBNP (P=0.001, r=0.349), mean E/Em (P=0.003, r=0.307), and estimated mean PCWP (P=0.001, r=0.308). Conclusions CT-1 is elevated in patients with DHF and is associated with NT-proBNP and estimated left ventricular filling pressures.