Arginase, NOS activities, and clinical features in fibromyalgia patients.

OBJECTIVES: Fibromyalgia (FM) is a form of nonarticular rheumatism characterized by chronic widespread musculoskeletal aching and tender points. The aim of the present study was to investigate the effect of arginase and nitric oxide synthase (NOS) enzyme activities in FM with respect to their importance in pathogenesis, and the relationship with FM-related clinical parameters. METHODS: After obtaining informed consent, 25 female FM patients were compared with 23 healthy female controls. NOS and arginase enzyme activities were measured spectrophometrically in sera. Tender points were examined using the protocol described by Wolfe et al. The health status of patients was assessed by Fibromyalgia Impact Questionnaire. Musculoskeletal pain was scored according to visual analog scale. Health Assessment Questionnaire, Beck depression and Beck anxiety scales, and dyspnea scores were administered to analyze functional, psychiatric, and respiratory status of the patients. RESULTS: We found that NOS activity was significantly higher whereas arginase activity was lower in patients with FM. In the correlation analysis, NOS levels showed statistically significant positive correlation with chest pain and dyspnea parameters. NOS enzyme activities were higher in subjects with positive history of migraine, pain, and morning stiffness. On the other hand, arginase levels were lower in subjects with positive history of irritable bowel syndrome and morning stiffness. CONCLUSION: Animal experiments have suggested that nitric oxide (NO) is an important transmitter in pain pathways. It can also stimulate cyclooxygenase activity. We observed increased NOS activity and reduced arginase activity in FM patients, which may be due to increased cyclooxygenase enzyme activity and oxidant/antioxidant imbalance. In conclusion, we think that future studies concerning clinical control of pain with selective NOS inhibitors are needed in order to determine new therapeutic approaches and the exact pathophysiologic mechanisms in FM patients.

The potential inflammatory role of arginase and iNOS in children with chronic adenotonsillar hypertrophy.

OBJECTIVE: Nitric oxide (NO) induced tissue damage has been implicated in the pathogenesis of several diseases. Although recurrent/chronic tonsillitis and hypertrophy are still the most frequent surgical procedures carried out on children in order to cure these pathologies, etiopathogenetic mechanisms underlying these entities are still unknown. We aimed to investigate the potential inflammatory role of NO regulatory enzymes, arginase and inducible nitric oxide synthase (iNOS), in children with adenotonsillar hypertrophy. MATERIALS AND METHODS: The study consisted of 22 children with chronic adenotonsillar hypertrophy and 30 control subjects with similar age and sex. All the patients and/or their parents had complaints of snoring, mouth breathing and pausing of breathe during sleep at least 6 months. All patients underwent an adenotonsillectomy operation under general anesthesia with curettage and cold dissection methods. Venous blood samples were taken pre-operatively and 4 weeks post-operatively. iNOS activity was based on the diazotization of sulfanilic acid by nitric oxide at acid pH and subsequent coupling to N-(1-naphthtyl)-ethylenediamine. Arginase activity was measured by the spectrophotometric method. RESULTS: The mean pre-operative and post-operative arginase activities in patient group were 4283.7 +/- 1823.7 and 2754.5 +/- 889.3 IU/L, respectively. In the control group, mean arginase activity was 2254.7 +/- 903 IU/L. When pre-, post-operative and control arginase values were compared with each other, the mean activity in pre-operative activity was significantly different from the post-operative and control values (p < 0.001). In the patient group, the mean levels of pre- and post-operative iNOS were 2.84 +/- 1.16 and 1.99 +/- 0.78 IU/ml, respectively. The difference was statistically significant (p = 0.007). Similarly, post-operative and control values were not significantly different (p > 0.05). CONCLUSION: The results of the present study supports that L-arginine:NO pathway may be key the participant in the pathogenesis of chronic adenotonsillar disease; arginase and iNOS activities are altered in children with adenotonsillar hypertrophy and this alteration improves after tonsillectomy.

Malondialdehyde and antioxidant enzymes in children with obstructive adenotonsillar hypertrophy.

OBJECTIVE: Free radical induced tissue damage has been implicated in the pathogenesis of several diseases. We aimed to investigate the role of free radicals and scavenging enzymes in children with obstructive adenotonsillar hypertrophy. MATERIALS AND METHODS: The study consisted of 29 children with obstructive adenotonsillar hypertrophy and 51 control subjects with similar age and sex. All the patients and/or their parents had complaints of snoring, mouth breathing, and pausing of breath during sleep for at least 6 months. All patients underwent an adenotonsillectomy operation under general anesthesia with curettage and cold dissection methods. Venous blood was taken preoperatively and 4 weeks postoperatively. After collection of blood samples into citrate (3.5 mg/ml blood) containing glass tubes, erythrocyte sediments were prepared for the analyses. Then malondialdehyde (MDA) level, and superoxide dismutase (SOD), glutathione peroxidase (GSHPx), and catalase (CAT) activities were measured. RESULTS: The levels of MDA and activities of SOD and GSHPx were significantly higher in the pre-tonsillectomy period than in the post-tonsillectomy period. However, CAT activity was not different in pre- and postoperative period. CONCLUSION: Our study supports the notion that oxidant and antioxidant defense mechanisms are altered in children with obstructive adenotonsillar hypertrophy, and this alteration improves after tonsillectomy.

Plasma reactive oxygen species activity and antioxidant potential levels in rosacea patients: correlation with seropositivity to Helicobacter pylori.

BACKGROUND: Recent studies have suggested that there might be an etiologic role for Helicobacter pylori (HP) in rosacea. HP is a Gram-negative bacterium that colonizes the gastric mucosa, increases the generation of reactive oxygen species (ROS), and decreases plasma antioxidants such as ascorbic acid. AIM: To investigate plasma ROS activities and antioxidant status, and their relationship with HP infection, in rosacea patients. METHODS: Twenty-nine rosacea patients and 20 age- and sex-matched healthy controls were examined for specific immunoglobulin G (IgG) and IgM against HP, plasma malondialdehyde (MDA), and antioxidant potential (AOP) levels. RESULTS: Compared with controls, the seropositivity of HP for IgM was significantly higher (P = 0.03) and the seropositivity of HP for IgG was significantly lower (P = 0.0001) in patients with rosacea. Plasma MDA levels were higher (P = 0.0001) and AOP levels were lower (P = 0.019) in patients than in controls, regardless of the severity of the disease. Plasma MDA and AOP levels were not affected by the seropositivity of HP for IgM and/or IgG in either group. CONCLUSION: Our results suggest that rosacea is an oxidative stress condition, as reflected by the increased ROS activity and decreased AOP, regardless of HP infection.

The effect of ethylenediaminetetraacetic acid on calcific degeneration in bovine pericardium.

Calcification is the most frequent cause of the clinical failure of bovine pericardium bioprosthetic valves, preventing their widespread application for surgical treatment. The aim of this study was to minimize calcific degeneration in bovine pericardium by using a chelating agent, ethylenediaminetetraacetic acid (EDTA). Freshly excised bovine pericardium was dissected free from adhering fat tissue and cut into 1-cm(2) pieces that were rinsed in phosphate-buffered saline solution (PBS) and transferred into 4 degrees C PBS containing 1% glutaraldehyde (GA) for initial fixation, then allocated into two groups. Group I received the same treatment in a fresh solution for 5 more days. Group II underwent an additional fixation step in PBS solution (pH 7.4, 37 degrees C) containing 11% EDTA for a period of 48 h (30 ml/g tissue) and was then transferred into freshly prepared PBS + 1% GA solution at 37 degrees C for another 3 days. To investigate the calcification rate, pericardial patches were inserted into the dorsal pouches of 25 male Wistar rats for 21 days. Calcium levels were measured with an atomic absorption spectrophotometer and examined histo-pathologically. The calcium content of EDTA-treated pericardium (Group II), 21 +/- 3.8 microg/mg, was significantly lower than that of Group I, 43.3 +/- 9.2 microg/mg. Assessment of the degree of calcification in the histological sections generally agreed well with the results of the chemical analyses. Calcium deposition in Group I samples were found to be solid mineral depositions, whereas in the Group II pericardial samples, only smaller traces of calcium were found. Calcific degeneration in bovine pericardium can be reduced by using chelates such as EDTA.