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The aim of this experimental study was to investigate the possible role of nitric oxide (NO) and the activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the pathogenesis of isoniazid (INH)-induced oxidative damage in red blood cells (RBCs), and also to show the effect of caffeic acid phenethyl ester (CAPE) and erdosteine, antioxidants, in decreasing this toxicity. A total of 25 adult male rats were divided into four experimental groups as follows: control group (n = 7), INH-treated group (n = 6), INH + CAPE-treated group (n = 6), and INH + erdosteine-treated group (n = 6). INH, INH-CAPE, and INH-erdosteine-treated groups were treated orally with INH 50 mg/kg daily and with the tap water for 15 days. Control group was given only tap water. CAPE was intraperitoneally injected for 15 days at a dose of 10 micromol/kg. Erdosteine was treated orally for 15 days at a dose of 10 mg/kg/day. The injection of INH led to a significant increase in the activities of ADA, XO, and NO levels in RBCs of rats. Co-treatment with CAPE caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. In addition, co-treatment with erdosteine caused a significant decrease in the activities of ADA and XO and the levels of NO in RBCs. The results of this study showed that ADA, XO, and NO may play an important role in the pathogenesis of INH-induced oxidative stress in RBCs. CAPE and erdosteine may have protective potential in this process and they may become a promising drug in the prevention of this undesired side effect of INH.

Background and Aims: Studies have already pointed out a possible pathophysiological role of oxidative and antioxidative molecules in bipolar disorder. We aimed to evaluate the activity and levels of antioxidant superoxide dismutase (SOD), and oxidant nitric oxide (NO), in bipolar I depressive episode (BD-DE) patients in a prospective design., Method: 30 BD-DE patients, diagnosed according to DSM IV, and 30 healthy volunteer controls were included. The serum levels of NO and SOD have been studied when admitted to hospital (1st) and on the 30th days. Clinical outcome was measured by Hamilton Depression Scale (HAM-D). The patients were allowed to have their treatments. One patient was dropped out due to insufficient sampling., Results: As in the previous studies, NO 1st day levels were significantly higher in patients and SOD 1st day activity was significantly low (p<0.01). NO levels significantly decreased (p<0.01) and normalized, as SOD activity significantly increased but did not reach to the controls' levels (p<0.01) on the 30th day., Conclusion: Despite normalized NO levels, persistent low SOD activity might point out an oxidative imbalance in BD-DE. Chronic low SOD activity may be associated with incapacity of coping with oxidative stress. This research connotes the probable oxidative imbalance in BD-DE and discusses that phenomenon within the continuum of the disease state.

Background: Essential hyperhidrosis (EH) is a disorder of excessive, bilateral, and relatively symmetric sweating occurring in the axillae, palms, soles, or craniofacial region without obvious etiology. The expression of endothelial nitric oxide synthase (eNOS) in eccrine clear cells, reported by an immunohistochemical technique, has suggested that nitric oxide (NO) may play a role in the physiology of production and/or excretion of sweat in the human skin eccrine gland., Aim: To determine plasma NO levels in patients with EH and healthy controls., Methods: We assessed the levels of plasma NO in patients with EH (n = 31) in comparison with those in age- and sex-matched healthy controls (n = 28). Total nitrite (nitrite + nitrate) was measured by a spectrophotometer at 545 nm after the conversion of nitrate to nitrite by copperized cadmium granules., Results: Plasma NO levels were found to be significantly increased in EH patients in comparison with the control group (P = 0.0001)., Conclusions: These findings indicate a possible role of increased plasma NO levels in the pathophysiology of EH.

The aim of the present study was to evaluate the effects of hyaluronan (HA) on nitric oxide (NO) levels and superoxide dismutase (SOD) enzyme activities in synovial fluid (SF) in the treatment of patients with knee osteoarthritis (OA). SF samples were aspirated from OA patients before the commencement of the treatment (n=23) and 6 weeks after they were treated with HA products. NO levels and SOD activities were compared between the pre- and post-treatment of OA patients and of the control group (n=10). SF NO levels were significantly higher in patients with OA before the commencement of the treatment compared with the post-treatment (p<0.001) and the control groups. The SF SOD activity of patients before the commencement of the treatment was lower than the values in the controls and post-treatment (p<0.001). There is no significant correlation between SF NO and SOD levels and the radiographic changes of the OA knee according to Kellgren-Lawrence grading (p>0.05). Also, the Western Ontario and McMaster Universities Osteoarthritis index (WOMAC) pain scores and physical function scores were gradually improved. These findings made us think that SF NO was a potent mediator in cartilage damage in OA, whereas SOD was an antioxidant mediator in the same process. Exogenous HA injections might reduce the NO levels and increase SOD activities in synovial fluid. These effects also do not seem to be dependent on the radiographic grading of the OA knee. More comprehensive studies are needed to clarify a possible clinical significance of this topic, and we suggest that this is an important area for further research into new treatment options.

Oxidant nitric oxide (NO) and antioxidant superoxide dismutase (SOD) have been implicated to play a role in the pathogenesis of bipolar disorders. This is the first prospective study aimed to evaluate NO levels and SOD activity in bipolar disorder (type I manic episode) (BD-ME). 29 inpatient subjects with BD-ME and 30 healthy controls were included. Serum NO levels and SOD activity have been studied at 1st (NO [1st] and SOD [1st] respectively) and 30th days (NO [30th] and SOD [30th] respectively) after treatment. The clinical outcome was measured by Bech-Rafaelson Mania Scale (BRMS). The mean NO [1st] (p<.001) and NO [30th] levels (p<.001) were higher than controls, but SOD [1st] (p<.001) and SOD [30th] (p<.001) activities in BD-ME were lower than controls. SOD(1) activity was higher than SOD [30th] (p<.001), while there was no significance in comparison between NO [1st] and NO [30th] (p>.05). SOD [30th] activity is negatively correlated with the number of previous manic attacks and NO [1st] was negatively correlated with sleep item score of BRMS at first day. Also there was a significant correlation between NO [1st] levels and with the existence of a delusion. NO and SOD appear to play a role in the pathophysiological events occurring in BD, especially in BD-ME. This study for the first time showed the possible role of NO on sleep and the generation of delusions in the pathophysiology of BD. In the light of literature, induced glutamate pathway might be responsible for delusions in BD. The results of this research need further investigation to understand the oxidative vs antioxidative process in BD.

The aim of this experimental study was to investigate the possible role of nitric oxide (NO) levels, and activities of adenosine deaminase (ADA) and xanthine oxidase (XO) in the pathogenesis of methotrexate-induced nephrotoxicity, and was the effect of caffeic acid phenethyl ester (CAPE), the potent free radical scavenger, in decreasing the toxicity. A total of 19 adult male rats were divided into three experimental groups, as follows: control group, MTX-treated group, and MTX+CAPE treated group. MTX were administered intraperitoneally (i.p.) with 20 mg/kg for single dose. CAPE was administered i.p. with a dose of 10 micromol//kg once daily for 7 days. The injection of MTX induced a significant increase in the activities of ADA and XO, and NO levels in renal tissue of rats (p < 0.0001). Co-treatment with CAPE caused a significantly decrease activities of ADA and XO, and the levels of NO in renal tissue (p < 0.0001). The results of this study revealed that NO, XO and ADA may play an important role in the pathogenesis of MTX-induced oxidative renal damage. CAPE may have protective potential in this process and it will become a promising drug in the prevention of this undesired side effect of MTX.

Evidence is accumulating for a possible role of nitric oxide (NO) in schizophrenia. Adrenomedullin (AM) induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of NO. AM immune reactivity is present in the brain consistent with a role as neurotransmitter. We aimed to examine plasma levels of nitrite (a metabolite of NO) and AM in schizophrenic patients. Eighty-two patients with schizophrenia and 21 healthy control subjects were included in this study. DSM-IV diagnosis of chronic schizophrenia was established on the basis of independent structured clinical interviews and review of records by two qualified psychiatrists which included the Brief Psychiatric Rating Scale (BPRS), The Scale for the Assessment of Negative Symptoms (SANS) and The Scale for the Assessment of Positive Symptoms (SAPS). Total nitrite and AM have been studied in plasma. The mean values of plasma nitrite and AM levels in schizophrenic group were significantly higher than control values, respectively (P=0.03, P<0.0001). AM levels of schizophrenic patients were three fold higher than controls. In correlation analyses, there were statistically significant positive correlations between AM level and SAPS-delusion subscale (r=0.27, P=0.04); SAPS-bizarre behavior subscale (r=0.28, P=0.03) and SAPS-total (r=0.36, P=0.005). There is no correlation between total nitrite and AM levels (r=0.11, P=0.31). Both NO and AM may have a pathophysiological role in schizophrenia, and clinically symptomatology and prognosis of schizophrenia. This subject needs further study including treatment response and subtypes of schizophrenia.

Nitric oxide (NO) has been implicated to play a role in the pathogenesis of depressive disorders. Adrenomedullin (AM) induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of NO. AM immune reactivity is present in the brain, consistent with a role as neurotransmitter. Therefore, it is suggested that these two molecules may play a role together in the brain. We aimed to examine AM and NO in bipolar affective disorder (BPAD). Forty-four patients with BPAD and 21 healthy control subjects were included in this study. DSM-IV diagnosis of bipolar affective disorder (type I, manic episodes) was independently established by two psychiatrists and the Turkish version of the Bech-Rafaelson Mania Scale was administered. Also, a semistructured form was used to ascertain several sociodemographic and clinical variables of the patients. AM and NO were studied in plasma. The mean value of plasma NO levels in the BPAD group of 46.58 +/- 13.97 micromol/l was significantly higher than that of controls (31.81 +/- 8.14 micromol/l) (z = -4.15, p = 0.000). Mean plasma AM levels were found to be increased in patients with BPAD (35.13 +/- 5.26 pmol/l) compared to controls (16.22 +/- 3.02 pmol/l) (z = -6.16, p = 0.000). AM levels of BPAD patients were approximately 2-fold higher than controls. AM levels were positively correlated with the duration of hospitalization for the current episode and negatively correlated with the total duration of illness. Both NO and AM may have a pathophysiological role in BPAD (type I, manic episodes) and the clinical symptomatology and prognosis of BPAD., (Copyright 2002 S. Karger AG, Basel)

Aims: To evaluate alteration of plasma malondialdehyde (MDA) and nitric oxide (NO) levels in patients with exudative age related macular degeneration (ARMD)., Methods: Plasma nitrite plus nitrate concentrations as an index of plasma NO levels and plasma MDA level as a marker of lipid peroxidation were measured in patients with exudative ARMD and age and sex matched healthy subjects., Results: Significantly higher MDA and lower NO levels were detected in plasma of patients with ARMD compared with their controls (p=0.01, p=0.001, respectively)., Conclusion: The results may support involvement of oxidative damage and vascular theory in the pathogenesis of ARMD as part of the ageing process.

Nitric oxide (NO) plays an important role in modulating blood flow in normal and in several pathological conditions, and its levels seem to change with ischemia-reperfusion injuries. Caffeic acid phenethyl ester (CAPE), an active component of propolis, exhibits antioxidant properties. This experimental study was designed to determine the changes in NO levels and the effect of CAPE on NO levels after testicular torsion/ detorsion in rats. Thirty-five adult male albino rats were divided into four groups: sham operation (n = 8), torsion (n = 9), saline/detorsion (n = 9), and CAPE/detorsion (n = 9). Rats in the sham operation group were killed after the testes were handled without torsion. Rats in the torsion group were killed after 720 degrees clockwise testicular torsion for 2 h. CAPE was administered 30 min before detorsion in the CAPE/detorsion group and saline was administered in the saline/detorsion group. After 4 h of testicular detorsion in both of these groups, the rats were killed and bilateral orchiectomy was performed to determine the tissue levels of NO. The level of NO in the torsion group (113.77 +/- 33.18 nmol/g protein) was significantly higher than that of the sham operation group (64.53 +/- 29.64 nmol/g protein). In the saline/detorsion group, the NO level (31.26 +/- 12.58 nmol/g protein) was significantly lower than in the torsion and sham operation groups. CAPE administration in the CAPE/detorsion group seemed to raise the NO level (72.63 +/- 23.87 nmol/g protein) above the level of the sham operation group. Contralateral testes were not affected by the torsion/detorsion processes performed on the ipsilateral testes. These results show that NO levels increase with torsion and decrease with detorsion. CAPE administration seems to increase tissue NO levels and this may be important for protecting the testes from torsion/detorsion injuries.