Propofol and erythropoietin antioxidant properties in rat brain injured tissue.

So far, several treatment modalities have been attempted to brain protection in cases such as brain trauma, stroke or brain hemorrhage. However, a treatment method that the effect begins immediately and definitely helpful has not been discovered yet. In this study, we aimed to compare the effects of propofol and erythropoietin (Epo) on brain injury caused by oxidative stress and antioxidant properties of these agents after closed head injury (CHI) in rats. For this study, female Wistar Albino rats were divided into five groups: non-traumatic control group, trauma performed group CHI, trauma with propofol (100 mg/kg) intraperitoneally (i.p.), trauma with Epo (5000 U/kg) i.p. and trauma with propofol and Epo performed study groups. Twenty-four hours after CHI, rats were sacrificed and the brains were removed. Superoxide dismutase (SOD), catalase (CAT), xanthine oxidase (XO), nitric oxide (NO), and malondialdehyde (MDA) levels were measured in brain tissue. MDA and NO levels were decreased significantly in Groups Epo, Propofol and Epo+Propofol than Group CHI (p<0.01). XO activity was significantly lower in Group Epo than Group CHI (p<0.05). Epo and propofol decreased oxidative stress by decreasing MDA and NO level in brain tissue after CHI. However, combination of Epo and propofol has no significant beneficial advantage than Epo or propofol alone.

Vitamin E protects against oxidative damage caused by formaldehyde in the liver and plasma of rats.

It is well known that formaldehyde (FA) and reactive oxygen species (ROS) are cytotoxic and potentially carcinogenic. Although the individual effects of these reactants on cells have been investigated, the cytotoxicity exerted by the coexistence of FA and ROS is poorly understood. The present study was carried out to evaluate oxidant/antioxidant status and biochemical changes occurring after chronic formaldehyde toxicity in liver tissue and plasma of rats and protective effect of vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control rats, (2) rats treated with FA (FAt), and (3) rats treated with FA plus vit E (FAt + vit E) groups. After the treatment, the animals were sacrificed and liver tissues were removed for biochemical investigations. As a result, FA treatment significantly increased the levels of tissue malondialdehyde (MDA), protein carbonyl (PC), nitric oxide (NO) and the activity of xanthine oxidase enzyme (XO). On the other hand, FA exposure led to decrease in superoxide dismutase (SOD) and catalase (CAT) activities in liver tissues compared to control. FA caused significant decreases in total protein (TP) and albumin (ALB) whereas increases in aspartate transaminase (AST), alanine aminotransferase (AST), alkaline phosphatase (ALP) and interleukine-2 (IL-2) levels in plasma. Vit E treatment abolished these changes at a level similar to the control group. It was concluded that vit E treatment might be beneficial in preventing FA-induced liver tissue damage, and therefore have potential for clinical use.

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.

The effects of ginkgo biloba extract on tissue adenosine deaminase, xanthine oxidase, myeloperoxidase, malondialdehyde, and nitric oxide in cisplatin-induced nephrotoxicity.

This study was carried out to determine if Ginkgo Biloba Extract (GBE or Egb 761) exerts a beneficial effect against cisplatin-induced renal failure in rats. Sprague Dawley rats were divided into four groups. The first group (control) received orally 1 mL/kg/day of 0.9% saline by an oral carrier vehicle on days 1 to 10. The second group was injected with 7 mg/kg cisplatin intraperitoneally (i.p.) on the fourth day, once only. The third group (vit E+cisplatin) was administered 10 mg/kg/day i.p. vit E on 1 to 10 days with one dose of i.p. cisplatin (7 mg/kg) injection on the fourth day. The fourth group (GBE+cisplatin) was given GBE orally at 100 mg/mL/kg started on the first day up to the tenth day with one dose of cisplatin (7 mg/kg) injection on the fourth day. Cisplatin was found to lead a statistically significant increase in plasma BUN and creatinine levels, as well as urine micro total protein (MTP) levels, leading to acute renal failure (ARF) in rats. Renal xanthine oxidase (XO) activities increased in all groups (statistically significant in cisplatin + GBE-treated rats; P < 0.001). Adenosine deaminase (AD) activities were increased in cisplatin-treated rats, and decreased in cisplatin+GBE-treated (P < 0.041) and cisplatin+vit E-treated (P < 0.005) rats, compared to controls. Malondialdehyde (MDA), nitric oxide (NO) levels and myeloperoxidase (MPO) activities were increased in the kidney tissue of cisplatin-treated rats. Vit E improved plasma creatinine and urine MTP levels, together with tissue MDA, NO levels, and MPO activities. But GBE had no statistically significant effect on those parameters. These results indicate that increased XO, AD and MPO activities, as well as MDA and NO levels play a critical role in cisplatin nephrotoxicity. GBE has been shown to protect against cisplatin-induced nephrotoxicity.

The effect of caffeic acid phenethyl ester on short-term acute myocardial ischemia.

BACKGROUND: We previously showed that caffeic acid phenethyl ester (CAPE) attenuated NO production, reduced apoptosis, diminished serum CK and AST activities, and is cardio-protective in rat heart subjected to ischemia/reperfusion (I/R). We now studied the short-term cardio-protective effect of CAPE in an I/R rat heart model. MATERIAL/METHODS: Wistar rats were divided into four groups: (i) sham-operated, (ii) I/R, (iii) I/R+CAPE, and (iv) I/R+glutathione. CAPE (10 micromol/kg) was infused i.v. 10 min before occlusion of the left anterior descending coronary artery (8 min) followed by reperfusion (8 min). RESULTS: SOD (p < 0.010) and CAT (p < 0.014) activities were increased and GSH-Px (p < 0.019) activity decreased in the I/R group in cardiac tissues compared with the sham-operated group. There were no effects of CAPE on antioxidant enzyme activities after I/R. Glutathione administration led to decreased SOD activity (p < 0.024) and increased GSH-Px (p < 0.014) activity after I/R. The most prominent effects of CAPE were seen in XO and ADA activities, which were increased after I/R compared with the sham-operated group (p < 0.029 and p < 0.001, respectively). When CAPE was administered, XO and ADA activities were decreased compared with the I/R group (p < 0.045 and p < 0.001). ADA activity was also decreased in the I/R+glutathione group compared with the I/R group. No differences in basal heart rate or systolic or diastolic pressure were noted among the experimental groups. CONCLUSIONS: This study demonstrates that CAPE exerts cardio-protective effects in short-term I/R of rat heart. This protective effect may be mediated by a combination of decreased XO activity and direct antioxidant effects.

Protective effect of caffeic acid phenethyl ester (CAPE) administration on cisplatin-induced oxidative damage to liver in rat.

Cisplatin is one of the most active cytotoxic agents in the treatment of cancer. High doses of cisplatin have also been known to produce hepatotoxicity. Several studies suggest that supplementation with an antioxidant can influence cisplatin-induced hepatotoxicity. The present study was designed to determine the effects of cisplatin on the liver oxidant/antioxidant system, and the possible protective effects of caffeic acid phenethyl ester (CAPE) on liver toxicity induced by cisplatin. Twenty-four adult female Wistar albino rats were divided into four groups of six rats each: control, cisplatin, CAPE, and cisplatin+CAPE. Cisplatin and CAPE were injected intraperitoneally. Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), xanthine oxidase (XO), adenosine deaminase (ADA), and the levels of malondialdehyde and nitric oxide (NO). The activities of SOD and GSH-Px increased in the cisplatin+CAPE and CAPE groups compared with the cisplatin group. CAT activity was higher in the cisplatin +CAPE group than the other three groups. XO activity was lower in the cisplatin group than the control group. MPO activity was also increased in the cisplatin group compared to the control and CAPE groups. It can be concluded that CAPE may prevent cisplatin-induced oxidative changes in liver by strengthening the antioxidant defence system by reducing reactive oxygen species and increasing antioxidant enzyme activities.

Nitric oxide, adenosine deaminase, xanthine oxidase and superoxide dismutase in patients with panic disorder: alterations by antidepressant treatment.

OBJECTIVE: In the present study, we aimed to investigate whether nitric oxide (NO) levels and activities of xanthine oxidase (XO), superoxide dismutase (SOD), and adenosine deaminase (ADA) are associated with Panic disorder (PD) as well as impact of psychopharmacological treatments on NO, SOD, ADA, and XO levels in PD. METHOD: In this study, 32 patients and 20 healthy controls were included. The serum levels of NO, XO, SOD, and ADA were measured in the patients and controls. The patients were treated with antidepressant. RESULTS: ADA and XO levels of the patients were significantly higher than the controls. SOD levels of the patients were significantly lower than the controls but the difference was not statistically significant. Although NO levels of the patients were higher than the controls, the difference was not statistically significant. There was no correlation between PAS and the parameters studied (SOD, ADA, XO, and NO) of the patients. After 8 weeks of antidepressant treatment, ADA and SOD activities were increased whereas NO and XO levels decreased significantly. CONCLUSION: ADA, XO activity may have a pathophysiological role in PD, and prognosis of PD. Activity of these enzymes may be used to monitor effects of the antidepressant treatment.

In vivo effects of caffeic acid phenethyl ester on myocardial ischemia-reperfusion injury and apoptotic changes in rats.

Ischemia/reperfusion (I/R) has been reported to induce apoptotic cellular death in myocardium. This study tested the hypothesis that caffeic acid phenethyl ester (CAPE), one of the active components of propolis, may ameliorate myocardial apoptosis and oxidative myocardial injury. Wistar rats were divided into 4 groups: (i) sham operated, (ii) I/R, (iii) I/R+CAPE, and (iv) I/R+glutathione (GSH). CAPE (10 micromol/kg) was infused iv 10 min before occlusion of the left anterior descending coronary artery (30 min) followed by reperfusion (120 min). GSH (5 mg/kg) was infused iv after the occlusion and immediately before reperfusion. The TdT-mediated in situ nick end-labeling (TUNEL) method was used to evaluate apoptotic activity. I/R resulted in myocardial apoptosis, alterations of antioxidant status, elevation of serum creatine kinase (CK) and aspartate aminotransferase (AST) activities, evidence of lipid peroxidation, and elevated nitric oxide levels, compared to the sham-operation group. No apoptotic cells were found in the myocardial tissue of sham-operated rats. The TUNEL-positive myocardial cells averaged 60%, 30%, and 40% in the I/R, I/R+CAPE, and I/R+GSH groups, respectively. This study demonstrates that pretreatment with CAPE provides cardio-protection from I/R injury. The I/R+CAPE group showed reduced apoptosis, attenuated NO production, elevated myocardial superoxide dismutase (SOD) activity, and diminished serum CK and AST activities, compared to the I/R group.

Antioxidant properties of propofol and erythropoietin after closed head injury in rats.

Reactive oxygen species play a role during brain injury due to closed head trauma. Enzymatic or nonenzymatic antioxidants may protect brain tissue against oxidative damage. The present study was performed to assess the changes of endogenous indices of oxidative stress in serum from rats subjected to head trauma and whether treatment with propofol and/or erythropoietin (EPO) modifies the levels of endogenous indices of oxidative stress. For these purposes, female Wistar Albino rats were divided into five groups: non-traumatic sham group, trauma performed control, trauma with propofol (i.p.), trauma with EPO (i.p.) and trauma with propofol and EPO performed study groups. At the end of the experimental procedure, blood was taken by cardiac puncture to determine superoxide dismutase (SOD) and xanthine oxidase (XO) activities as well as malondialdehyde (MDA) and nitric oxide (NO) levels in serum. Serum MDA level of control traumatic brain injury (TBI) group was significantly higher than sham operation group (p<0.012). Serum MDA levels in propofol, EPO and propofol+EPO groups were found to be decreased in comparison with control group (p<0.039, p<0.030 and p<0.018, respectively). Serum NO level was found to be increased in TBI group, but difference was not statistically significant when compared to sham-operated group (p=0.092). Propofol, EPO and propofol+EPO administration efficiently reduced serum NO levels to reach sham-operated group (p<0.002, p<0.001 and p<0.015, respectively). These results suggested that acute administration of both propofol and EPO altered the indices of oxidative stress similarly against brain injury due to trauma.

The protective effect of erdosteine against ototoxicity induced by cisplatin in rats.

The elimination of cisplatin ototoxicity is an ongoing concern. This experimental study was undertaken to investigate the effect of oral erdosteine in ameliorating cisplatin-induced ototoxicity. Twenty-eight adult female Wistar albino rats were randomly divided into four equal groups. Group A received an oral carrier vehicle of the drug erdosteine with 0.2 ml of 0.9% saline. Group B was administered only erdosteine (per oral 10 mg/kg twice a day) for 6 days. Group C was injected with cisplatin intraperitoneally (i.p.) on day 0 (16 mg/kg body weight), once only. Group D was given erdosteine (per oral 10 mg/kg/day) 1 day before and for 5 days consecutively after cisplatin injection (16 mg/kg, i.p.). Distortion product otoacoustic emissions (DPOAEs) were elicited in different frequency regions, ranging from 1,001 to 6,299 Hz as DPgram and input/output (I/O) functions from the control and experimental animals. All experimental animals were killed under general anesthesia on day 5, following the last otoacoustic emission measurements. Prior to death, blood samples were drawn for measurement of superoxide dismutase, xanthine oxidase (XO), malondialdehyde and nitric oxide. Initial DPgram and I/O function baseline measurements were similar in all groups prior to any drug administration ( P>0.05). On day 5, intra-subject measurement parameters of DPgrams and I/O functions in the cisplatin group showed significant deterioration ( P <0.05). The other groups revealed no differences between their pre- and post-test drug administration DPgrams and I/O functions at any test frequency ( P>0.05). Comparison of the amplitudes of DPgrams and I/O functions between the cisplatin and control groups showed significant changes ( P <0.05). Biochemical studies noted an increased XO activity following cisplatin administration ( P <0.007). The other biochemical results did not show significant differences between the study and control groups. This study demonstrates that, in rats, erdosteine is protective for cochlear function against the disruptive effects of cisplatin as measured by DPOAEs.

PCR/RFLP-based cost-effective identification of SOD2 signal (leader) sequence polymorphism (Ala-9Val) using NgoM IV: a detailed methodological approach.

BACKGROUND: Superoxide dismutases (SOD) play an important role in the protection of cells and extracellular space from the products of oxidative stress. Two allelic variants have been described for the SOD2 gene (Ile58Thr involves a C to T substitution at nucleotide residue 339 and Ala-9Val involves a T to C substitution at nucleotide residue 1183). The enzyme proteins encoded by the different alleles have been suggested to have different activity patterns. METHODS: The SOD2 polymorphism was determined using a polymerase chain reaction (PCR) and RFLP techniques with restriction endonuclease NgoM IV. RESULTS: The most available results were obtained from with 20 pmol primer final concentration in PCR reaction. A total of 20 pmol seems the cost-effective primer concentration with maximum quality. There were no difference between the band quality of 1-5 units of restriction endonucleases. On the other hand, short and long incubation times seem to be similar in order to obtain sharp bands on agarose gel. CONCLUSIONS: We have extended a method of SOD2 polymorphism (Ala-9Val) in mitochondrial sequence. This method provides the ability to genotype of SOD2, and it represents a fast, reliable, cost-effective and semi-automated methodology to determine SOD2 polymorphism in order to perform large-scale population studies.

Antioxidant enzyme activities and oxidative stress in affective disorders.

Recent data from several reports indicate that free radicals are involved in the biochemical mechanisms underlying neuropsychiatric disorders in human. The results of several reports suggest that lower antioxidant defences against lipid peroxidation exist in patients with depression and that there is a therapeutic benefit from antioxidant supplementation in unstable manic-depressive patients. We investigated the antioxidant enzyme status and the indices of oxidative stress and lipid peroxidation end products in erythrocytes from patients with affective disorder. For this purpose, we measured superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities, as well as malondialdehyde (MDA) and nitric oxide (NO) levels in patients with affective disorders (n=30) in both pre- and post-treatment periods, and in a control group (n=21). CAT activities were significantly decreased in both pre-, and post-treatment periods in patients compared to the control group. GSH-Px activity in the pre-treatment period in the patients was significantly lower than both post-treatment patient and control groups. MDA levels were increased in both pre-, and post-treatment patient groups compared to the control group. NO level was lower in the pre-treatment patient group than in the control group. There were statistically significant correlations between SOD and MDA, and SOD and NO in the pre-treatment patient and control groups. Because the overall study sample was small, and the post-treatment patient group was even smaller, it can tentatively be suggested that the antioxidant system is impaired during a mood episode in patients with affective disorders, normalizing at the end of the episode.

The comparison of nail and serum trace elements in patients with epilepsy and healthy subjects.

The objective of this prospective study was to determine the levels of manganese (Mn), copper (Cu), and zinc (Zn) levels in both nail and serum from patients with epilepsy. For this purpose, levels of these elements were measured in 31 patients with epilepsy and 19 healthy subjects. Element analyses were carried out by atomic absorption spectrophotometer (AAS). Increased Mn levels were detected in nail of patients with epilepsy compared to healthy controls (P<.008). The main nail Zn and Cu levels were found to be unchanged in epileptic patients compared to control subjects. There were no significant differences in serum Mn and Zn levels between epileptic patients and control subjects. However, there was a statistically significant increase in serum Cu levels in patients with epilepsy in comparison with control group (P<.009). Our results demonstrate that some trace element levels may vary in epileptic patients, and because of the more stable status, the analysis of these element levels in some tissues such as nail might be superior to serum analysis.

Protective role of alpha-tocopherol and caffeic acid phenethyl ester on ischemia-reperfusion injury via nitric oxide and myeloperoxidase in rat kidneys.

BACKGROUND: The aim of this study was to determine the acute effects of antioxidant caffeic acid phenethyl ester (CAPE) and alpha-tocopherol (vitamin E) on nitric oxide (NO) production, neutrophil infiltration, and antioxidant enzyme activities on an in vivo model of renal ischemia-reperfusion injury. METHODS: Rats were divided into five equal groups each consisting six rats: sham operation, ischemia, ischemia-reperfusion (I/R), I/R plus CAPE, and I/R plus vitamin E groups. CAPE or vitamin E was administered intraperitoneally before reperfusion. After experimental procedure, rats were sacrificed and both ipsilateral and contralateral kidneys were removed and prepared for NO concentrations, myeloperoxidase (MPO), catalase (CAT) and superoxide dismutase (SOD) activities. RESULTS: Acute administration of vitamin E decreased NO concentrations in both ipsilateral and contralateral renal tissues compared to I/R group. SOD activity was increased in I/R and I/R + CAPE groups compared to sham operation group. The most prominent results were encountered in MPO activities, which did not change in contralateral kidneys in both ischemia and I/R groups. There was a significant decrease in ipsilateral MPO activity in ischemia group and a significant increase in I/R group compared to sham operation group. Pretreatment with intraperitoneal CAPE significantly diminished the tissue MPO activity indicating the prevention of the neutrophil sequestration into the kidney. CONCLUSION: There is a role for CAPE in attenuation in renal damage after I/R injury of the kidney, in part at least by inhibition of neutrophil sequestration.

Adenosine deaminase, xanthine oxidase, superoxide dismutase, glutathione peroxidase activities and malondialdehyde levels in the sera of patients with head and neck carcinoma.

OBJECTIVES: Clinical and epidemiological findings have provided evidence supporting a role of free radicals in the etiology of cancer. Scavengers and inhibitors of free radical processes have been demonstrated to prevent or delay the neoplastic process. PATIENTS AND METHODS: Adenosine deaminase, xanthine oxidase, superoxide dismutase, and glutathione peroxidase activities and malondialdehyde levels were measured in the sera of 35 patients with head and neck cancers and were compared to those of healthy control subjects. RESULTS: Serum adenosine deaminase activity was found to be significantly increased in the patient group (p<0.001). Compared to the control group, glutathione peroxidase and xanthine oxidase activities and malondialdehyde levels were slightly higher and serum superoxide dismutase activity was slightly lower in the patient group, with none reaching statistical significance. CONCLUSION: The results indicate that serum adenosine deaminase activity may be helpful in the diagnosis and follow-up of head and neck cancers. Further studies with a larger cohort of patients are needed to clarify the exact mechanism of adenosine deaminase elevation.

The effects of single-dose dexamethasone on wound healing in rats.

UNLABELLED: Dexamethasone effectively decreases the incidence of nausea and vomiting among pediatric and adult patients. In this study, we evaluated the effects of single-dose dexamethasone on wound healing in a prospective, randomized, experimental animal model. Anesthesia was induced with thiopental 100 mg/kg intraperitoneally. Dexamethasone 1 mg/kg was administered intraperitoneally in a dexamethasone group, and physiological saline was administered in a control group. Collagenization, epithelization, and fibroblast content were significantly less in the dexamethasone group compared with the control group (P values of 0.002, 0.041, and 0.023, respectively). The vascularity and the degree of inflammatory cells were more intense in the dexamethasone group compared with the control group (P values of 0.023 and 0.002, respectively). The white blood cell count was similar in the control (7.84 +/- 2.09) and dexamethasone (6.98 +/- 2.12) groups. The mean hydroxyproline level was 0.72 +/- 0.13 mg/g in the dexamethasone and 1.03 +/- 0.19 mg/g in the control group. Hydroxyproline levels were significantly less in the dexamethasone group (P = 0.001). We conclude that dexamethasone at 1 mg/kg may have negative effects on wound healing. IMPLICATIONS: We evaluated the effects of dexamethasone on wound healing in a prospective, randomized, experimental animal model. Our results show that dexamethasone at 1 mg/kg may have negative effects on wound healing.

Effects of caffeic acid phenethyl ester and alpha-tocopherol on reperfusion injury in rat brain.

Oxygen-derived free radicals have been implicated in the pathogenesis of cerebral injury after ischaemia-reperfusion. Caffeic acid phenethyl ester (CAPE), an active component of propolis extract, exhibits antioxidant properties. The purpose of the present study was to investigate the effects of ischaemia and subsequent reperfusion on rat brain and to investigate the effects of two free radical scavengers, CAPE and alpha-tocopherol, on this in vivo model of cerebral injury. Ischaemia was induced by bilateral occlusion of the carotid arteries for 20 min and reperfusion was achieved by releasing the occlusion to restore the circulation for 20 min. Control rats underwent a sham operation. CAPE at 10 micromol kg(-1) or alpha-tocopherol at 25 micromol kg(-1) was administered intraperitoneally before reperfusion. Reperfusion led to significant increase in the activity of xanthine oxidase and higher malondialdehyde levels in the brain. Acute administration of both CAPE and alpha-tocopherol suppressed ischaemia-reperfusion-induced cerebral lipid peroxidation and injury, but CAPE seems to offer a better therapeutic advantage over alpha-tocopherol.

Adenosine deaminase and xanthine oxidase activities in bladder washing fluid from patients with bladder cancer: a preliminary study.

Activities of adenosine deaminase (AD), and xanthine oxidase (XO) enzymes were measured in bladder washing fluid (BWF) from 37 patients with bladder cancer. The patients were divided into several groups according to their sex; pattern, number, and depth of the tumors; and tumor grade. There was a statistically significant difference in XO activities between the patients having no tumor and papillary tumor (p < 0.002). The differences in XO values between the patients having no tumor and single tumor; and with no tumor and multiple tumors were statistically significant (p < 0.012, p < 0.016 respectively). XO activities were increased in patients with both papillary and multiple tumors compared to tumor-free group. Regarding to the depth of tumors, only the differences in XO values between the patients having no tumor and superficial tumor was statistically significant (p < 0.037). XO values of patients in grade1 were higher than the patients having no tumor (p < 0.010). AD activities in patients with multiple and invasive tumor were increased compared to patients with single and superficial tumor. AD values in grade 3 were lower than grade 2. However, we did not find any statistically significant differences in AD activities in all groups. As a conclusion, increased XO activity in BWF might be a potentially important finding as an additional diagnostic biochemical tool for bladder cancer. But we could not say this for AD activity. Further investigations in a larger cohort of patients with bladder cancer are needed to enlighten the possible diagnostic role of XO and AD in BWF.

Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant levels in rabbits.

The number of reports on the effects induced by electromagnetic radiation (EMR) in various cellular systems is still increasing. Until now no satisfactory mechanism has been proposed to explain the biological effects of this radiation. Oxygen free radicals may play a role in mechanisms of adverse effects of EMR. This study was undertaken to investigate the influence of electromagnetic radiation of a digital GSM mobile telephone (900 MHz) on oxidant and antioxidant levels in rabbits. Adenosine deaminase, xanthine oxidase, catalase, myeloperoxidase, superoxide dismutase (SOD) and glutathione peroxidase activities as well as nitric oxide (NO) and malondialdehyde levels were measured in sera and brains of EMR-exposed and sham-exposed rabbits. Serum SOD activity increased, and serum NO levels decreased in EMR-exposed animals compared to the sham group. Other parameters were not changed in either group. This finding may indicate the possible role of increased oxidative stress in the pathophysiology of adverse effect of EMR. Decreased NO levels may also suggest a probable role of NO in the adverse effect.

The protective role of caffeic acid phenethyl ester (CAPE) on testicular tissue after testicular torsion and detorsion.

Testicular artery occlusion causes an enhanced formation of reactive oxygen species, which contributes to the pathophysiology of tissue damage. Here, we have investigated the effects of caffeic acid phenethyl ester (CAPE), a new antioxidant and antiinflammatory agent, in rats subjected to testicular torsion/detorsion (T/D). Thirty-five male rats were divided into four groups: sham operation group ( n=8), torsion group ( n=9), T/D+saline group ( n=9) and T/D+CAPE group ( n=9). Rats, except the sham operation group, were subjected to left unilateral torsion (720 degrees rotation in the clockwise direction) without including the epididymis. After torsion (2 h) and detorsion (4 h) periods, rats were sacrificed and bilateral orchidectomy was performed. Testis tissues were washed with cold saline solution, cut into small pieces with scissors, placed into glass bottles and homogenised in four volumes of ice-cold Tris-HCl buffer. Clear supernatant fluid was used for biochemical analyses. Treating rats with CAPE (applied at 10 micro mol/kg, 30 min prior to T/D) attenuated the testicular injury, as well as the increase in the tissue levels of myeloperoxidase and thiobarbituric acid-reactant substances (TBARS) caused by T/D in the testis. Testis tissues showed a significant increase in glutathione peroxidase (GSH-Px) activity compared to the torsion group when CAPE was applied. Taken together, our results clearly demonstrate that CAPE treatment exerts a protective effect on testicular T/D, and part of this effect may be due to inhibiting the neutrophil-mediated cellular injury.