Neutrophil/Lymphocyte Ratio, Serum Endocan, and Nesfatin-1 Levels in Patients with Psoriasis Vulgaris Undergoing Phototherapy Treatment.

BACKGROUND Psoriasis is an autoimmune, inflammatory, and chronic disease. Recent studies have evaluated serum endocan and nesfatin-1 levels in patients with inflammatory disorders. The neutrophil-to-lymphocyte ratio (NLR) is an inflammatory marker currently used in many diseases. The aim of the present study was to evaluate NLR, serum endocan, and nesfatin-1 levels in psoriasis vulgaris before and after narrow-band ultraviolet B (NB-UVB) phototherapy treatment and compared to healthy controls. MATERIAL AND METHODS This study was conducted on a total of 88 cases, 39 of which had psoriasis vulgaris and 49 were healthy volunteers. Thirty-nine psoriasis vulgaris patients underwent NB-UVB phototherapy treatment for 3 months. NLR, serum endocan, and nesfatin-1 levels were measured in all psoriasis patients before and after NB-UVB phototherapy and in the control group. RESULTS Compared with the control group, neutrophil count and NLR were significantly higher (p<0.001) in psoriasis patients before NB-UVB phototherapy. Serum endocan levels were significantly correlated with disease activity before treatment. There was no significant difference in NLR, serum endocan, and nesfatin-1 levels in psoriasis patients before and after NB-UVB phototherapy (p>0.05). CONCLUSIONS The current study shows that NLR was higher in psoriasis vulgaris patients when compared with the control group, whereas serum endocan and nesfatin-1 levels were not significantly different. In addition, NB-UVB phototherapy did not affect NLR, serum endocan, or nesfatin-1 levels. Further larger-scale studies are required on this subject.

Prognostic significance of neutrophil gelatinase-associated lipocalin in ST-segment elevation myocardial infarction.

OBJECTIVES: This study investigated the prognostic value of neutrophil gelatinase-associated lipocalin (NGAL) in patients with ST-segment elevation myocardial infarction (STEMI). BACKGROUND: Neutrophil gelatinase-associated lipocalin is a promising biomarker for acute kidney injury. Recently, it was concluded that NGAL may be used beyond the boundaries of renal physiopathology. It was found to be an important factor indirectly contributing to the inflammatory processes. Little is known regarding its predictive role in STEMI. METHODS: One hundred six consecutive patients who underwent percutaneous coronary intervention (PCI) for STEMI and control group consisted of age- and sex-matched 60 consecutive patients with chest pain admitted to the hospital for elective PCI. According to median NGAL level, patients were classified into high- and low-NGAL groups. RESULTS: Neutrophil gelatinase-associated lipocalin levels were higher in patients with STEMI compared to the elective PCI group subjects. Inhospital and 1-year mortality rates were found to be significantly greater in patients with high NGAL. In addition, inhospital and 1-year major adverse cardiovascular event rates were significantly greater in the high-NGAL group, compared to the low NGAL group. High NGAL level on admission was a significant predictor for long-term mortality and major adverse cardiovascular events. The receiver operating characteristics curve analysis further illustrated that NGAL level on admission is a strong indicator of mortality, with an area under the curve of 0.76 (95% confidence interval, 0.62-0.89). CONCLUSIONS: High NGAL levels may be associated with poor prognosis after PCI in patients with STEMI. However, further studies with larger numbers of patients and longer follow-up are required to evaluate the usefulness of plasma NGAL level for predicting prognosis of STEMI.

Protective effects of omega-3 essential fatty acids against formaldehyde-induced cerebellar damage in rats.

This study aimed to investigate changes in the cerebellum of formaldehyde-exposed rats and the effects of omega-3 fatty acids on these changes. The study involved 21 male Wistar-Albino rats which were divided into three groups. The rats in Group I comprised the control group. The rats in Group II were injected with intraperitoneal 10% formaldehyde every other day. The rats in Group III received omega-3 fatty acids daily while exposed to formaldehyde. At the end of the 14-day experimental period, all rats were killed by decapitation and the cerebellum removed. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), xanthine oxidase (XO), and malondialdehyde (MDA) levels were determined in cerebellum specimens by using spectrophotometric methods. In our study, levels of SOD and CAT were significantly decreased, and GSH-Px, XO, MDA levels were significantly increased in rats treated with formaldehyde compared with those of the controls. Whereas, it was seen that there was an increase in SOD and CAT enzyme activities and decrease in MDA, XO, and GSH-Px levels in rats administered to omega-3 fatty acids with exposure of formaldehyde. It was determined that exposure of formaldehyde increased free radicals in cerebellum of rats and this increase was prevented by administration of omega-3 fatty acids.

Protective effects of edaravone on experimental spinal cord injury in rats.

BACKGROUND: Spinal cord injury (SCI) is a leading cause of morbidity and mortality among youth and adults. Secondary injury mechanisms within the spinal cord (SC) are well known to cause deterioration after an acute impact. Free radical scavengers are among the most studied agents in animal models of SCI. Edaravone is a scavenger of hydroxyl radicals. METHODS: We aimed to measure and compare the effects of both methylprednisolone and edaravone on tissue and on serum concentrations of nitric oxide (NO), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, and tissue total antioxidant capacity (TAC) in rats with SCI. SCI was induced in four groups of Wistar albino rats by a weight-drop method. The neurological function of the rats was periodically tested. At the end of the experiment, blood samples were collected, and SC tissue samples were harvested for biochemical evaluation. RESULTS: The tissue level of NO was decreased in the edaravone-treated group compared with the no-treatment group (p < 0.05). The tissue levels of SOD and GSH-Px were higher in the edaravone-treated group than in the no-treatment group (p < 0.05). The serum levels of NO were lower in the edaravone-treated and methylprednisolone-treated groups than in the no-treatment group (p < 0.05). The serum levels of SOD in the edaravone-treated group did not differ from those of any other group. The serum levels of MDA in the edaravone-treated and no-treatment groups were higher than in the two other groups (p < 0.05). Tissue levels of MDA in the edaravone-treated group were lower than in the no-treatment group (p < 0.05). Tissue levels of TAC in the edaravone-treated group were higher than in the no-treatment and methylprednisolone-treated groups (p < 0.05). The neurological outcome scores of the animals in treatment groups did not depict any statistically significant improvement in motor functions. However, edaravone seemed to prevent further worsening of the immediate post-SCI neurological status. CONCLUSION: Our biochemical analyses indicate that edaravone is capable of blunting the increased oxidative stress that follows SCI. We show, for the first time, that edaravone enhances the TAC in SC tissue. This beneficial effect of edaravone on antioxidant status may act to minimize the secondary neurological damage that occurs during the acute phase after SCI.

Effects of ß-glucan pretreatment on acetylsalicylic acid-induced gastric damage: An experimental study in rats.

BACKGROUND: NSAIDs have been found to induce gastrointestinal tract damage. Recently, it has been suggested that this might be mediated by lipid peroxidation. OBJECTIVE: The aim of this study was to assess the potential protective effects of ß-glucan against acetylsalicylic acid (ASA-induced gastric damage by means of its antioxidant capacity in an experimental rat model. METHODS: Thirty-two male Wistar albino rats (200-250 g) were randomized into 4 groups consisting of 8 rats each. The ß-glucan group received 50 mg/kg ß-glucan once a day for 10 days and 30 minutes before anesthesia. The ASA group received saline once a day for 10 days and 300 mg/kg (20 mg/mL) ASA as a single dose, 4 hours before anesthesia. The ASA+ß-glucan group was administered 50 mg/kg ß-glucan once a day for 10 days and 30 minutes before anesthesia. Additionally, 300 mg/kg (20 mg/mL) ASA was administered as a single dose, 4 hours before anesthesia. The control group received saline once a day for 10 days and 30 minutes before anesthesia. All medications were administered by intragastric gavage. The stomach from each rat was dissected and divided into 2 parts for histologic and biochemical analysis. Gastric tissue malondialdehyde (MDA), nitric oxide (NO) levels, catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were determined for oxidative parameter analysis. RESULTS: The gastroprotective and antioxidant effects of ß-glucan appeared to attenuate the ASA-induced gastric tissue damage. Compared with the control group, MDA and NO levels and CAT and GSH-Px activities were significantly increased in the stomachs of ASA-treated rats (MDA, 4.12 [0.44] to 13.41 [1.05] µmol/L; NO, 8.04 [7.25-9.10] vs 30.35 [22.34-37.95] µmol/g protein; CAT, 0.050 [0.004] to 0.083 [0.003] k/g protein; GSH-Px, 0.57 [0.42-0.66] to 1.55 [1.19-1.76] U/L; all, P < 0.001), whereas SOD activity was significantly decreased in the same group (291 [29] to 124 [6] U/mL; P < 0.001). In the ASA+ß-glucan group, MDA and NO levels and CAT and GSH-Px activities were found to be significantly lower, while SOD activity was found to be significantly higher, in comparison with the ASA-treated group (all, P < 0.001). CONCLUSION: ß-Glucan appeared to attenuate the gastric damage caused by ASA in these rats.

Protective effects of tadalafil on experimental spinal cord injury in rats.

Tadalafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Nitric oxide (NO) functions as a retrograde neurotransmitter in the spinal cord, and postsynaptic structures respond to NO by producing cGMP. The concentrations of cGMP in the spinal cord are controlled by the actions of PDE. The aim of the study was to evaluate and compare the effects of the use of both methylprednisolone and tadalafil on serum and tissue concentrations of NO, malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity, and tissue glutathione peroxidase (GSH-Px) activity in rats with spinal cord injury (SCI). SCI was induced in Wistar albino rats by dropping a 10 g rod from a 5.0 cm height at T8-10. The 28 rats were randomly divided into four equal groups: tadalafil, methylprednisolone, non-treatment and sham groups. Rats were neurologically tested at 24 hours after trauma. At the end of the experiment, blood samples were collected and spinal cord tissue samples were harvested for biochemical evaluation. The tissue level of NO was increased in the tadalafil group compared with the non-treatment and methylprednisolone groups (p<0.05). The tissue levels of SOD and GSH-Px did not differ between the groups. Serum levels of NO were higher in the tadalafil group than in the non-treatment group (p<0.05). The increase in serum SOD levels was greater in the tadalafil group than the methylprednisolone group. Serum MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group (p>0.05). Tissue MDA levels in the tadalafil and methylprednisolone groups tended to be lower than in the non-treatment group and sham groups (p>0.05). Although there was no difference in neurological outcome scores between the tadalafil, methylprednisolone and non-treatment groups (p>0.05), the animals in the tadalafil and methylprednisolone groups tended to have better scores than the non-treatment group. Thus, tadalafil appears to be beneficial in reducing the effects of injury to the spinal cord by increasing tissue levels of NO and serum activity of SOD.

Nitric oxide, lipid peroxidation, and antioxidant enzyme levels in epileptic children using valproic acid.

In the present study, we investigated the effects of valproic acid (VPA) on nitric oxide (NO) level, lipid peroxidation, and antioxidant enzyme activities in 21 epileptic children and 26 healthy controls. The subjects were selected from those who visited for a checkup or medical treatment at the Mustafa Kemal University Research Hospital. Serum levels of NO(-2), NO(-3), malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were analyzed by redox or enzymatic reactions and spectrophotometry. Based on the NO(-2) and NO(-3) levels, the NO concentration was about 10% higher in VPA group than in the control group (p<0.001). However, no significant difference was detected for serum MDA, SOD, and CAT levels. It is suggested that NO would play a role in the mechanism of antiepileptic effects by VPA treatment.

Effects of erdosteine on acetaminophen-induced hepatotoxicity in rats.

We investigated the effects of erdosteine on acetaminophen (APAP)-induced hepatotoxicity in rats. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), AST (aspartate aminotransferase), and ALT (alanine transaminase) activities, and malonyldialdehyde (MDA) and nitric oxide levels as oxidant/antioxidant biochemical parameters were investigated with light microscopic evaluation in adult female Wistar Albino rats. APAP administration produced a decrease in hepatic SOD, CAT, and GSH-Px activities, and coadministration of erdosteine (150 and 300 mg/kg) resulted in increases in the activities. MDA and NO levels increased in the APAP group, and erdosteine treatments prevented these increases. Significant elevations in serum AST and ALT levels were observed in the APAP group, and when erdosteine and APAP were coadministered, their serum levels were close to those in the control group. Light microscopic evaluation of livers showed that there were remarkable centrilobular (zone III) hepatic necrosis and mild to moderate sinusoidal congestion in the APAP group, whereas in the erdosteine group, cellular necrosis was minimal and the hepatocytes maintained a better morphology when compared to the APAP group. Erdosteine prevented APAP-induced liver injury and toxic side effects probably through the antioxidant and radical scavenging effects of erdosteine.

Protective effects of N-acetylcysteine on cyclosporine-A-induced nephrotoxicity.

OBJECTIVES: Cyclosporine A (CsA) is used for the treatment of autoimmune and inflammatory disorders. However, CsA-induced nephrotoxicity remains an important clinical problem, and oxidative stress has been implicated as a possible responsible mechanism. We assessed the protective ability of N-acetylcysteine (NAC), an antioxidant, against CsA-induced nephrotoxicity. MATERIALS AND METHODS: Wistar albino rats were randomly assigned into four groups. Group 1 rats were treated with sodium chloride as control, group 2 with CsA, group 3 with CsA and NAC, and group 4 with NAC alone. Animals were sacrificed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), malondialdehyde (MDA) and nitric oxide (NO) levels, and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. Kidney sections were analyzed for MDA and NO levels and SOD and GSH-Px activities, as well as histopathological changes. RESULTS: Overall, the treatment of rats with CsA alone produced significant increases in NO and MDA levels and significant decreases in SOD and GSH-Px activities in serum and renal samples. Morphological changes, including tubular epithelial atrophy, vacuolizations, and cellular desquamations, were clearly observed in the rats treated with CsA alone. Concurrent NAC administration with CsA improved renal function, as indicated by lower BUN and Cr values. Moreover, NAC significantly reduced MAD and NO levels and increased SOD and GSH-Px activities in serum and renal tissue, as well as provided a histologically proven protection against CsA-induced nephrotoxicity. CONCLUSION: These results indicate that NAC produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role for oxidative stress in pathogenesis.

From darkening urine to early diagnosis of alkaptonuria.

Alkaptonuria is a rare disorder of metabolism characterized by deficiency of homogentisic acid oxidase. Characteristic features include darkening of urine, ochronosis, and arthropathy. Darkening of urine is the only sign of the disorder in the pediatric age group, and it occurs at very early stage of the disorder, as reported by the parents. A 4-year-old boy presented to our clinic with the complaint of dark urine and bluish black staining of clothes. This darkening pointed to a positive physical history of bluish discoloration of sclerae which occurred off and on. We initiated treatment with ascorbic acid and a protein diet with restriction of phenylalanine and tyrosine (1.6 g/kg/d). This case report is significant because of the early diagnosis made.

The protective effect of N-acetylcysteine against cyclosporine A-induced hepatotoxicity in rats.

The immunosuppressive agent cyclosporine A (CsA) has been reported to exert measurable hepatotoxic effects. One of the causes leading to hepatotoxicity is thought to be reactive oxygen radical formation. The aim of this study was to investigate the effects of N-acetylcysteine (NAC) treatment on CsA-induced hepatic damage by both analysing superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), aspartate aminotransferase (AST) and alanine transaminase (ALT) activities with malondialdehyde (MDA) and nitric oxide (NO) levels, and using an histological approach. CsA administration produced a decrease in hepatic SOD activity, and co-administration of NAC with CsA resulted in an increase in SOD activity. MDA and NO levels increased in the CsA group and NAC treatment prevented those increases. A significant elevation in serum AST and ALT activities was observed in the CsA group, and when NAC and CsA were co-administered, the activities of AST and ALT were close to the control levels. CsA treatment caused evident morphological alterations. Control rats showed no abnormality in the cytoarchitecture of the hepatic parenchyma. The co-administration of NAC with CsA showed no signs of alteration and the morphological pattern was almost similar to the control group. In conclusion, CsA induced liver injury and NAC treatment prevented the toxic side effects induced by CsA administration through the antioxidant and radical scavenging effects of NAC.

Serum dehydroepiandrosterone sulphate level in age-related macular degeneration.

PURPOSE: To evaluate plasma dehydroepiandrosterone sulphate (DHEAS) levels in patients diagnosed with age-related macular degeneration (AMD) and controls. DESIGN: Case-controlled, prospective, comparative noninterventional study. METHODS: This study involved 32 men and 35 women with exudative AMD, 37 men and 38 women with nonexudative AMD, and 32 men and 32 women of an age-matched control group. The Wisconsin Age-Related Maculopathy Grading System was used to asses the severity of AMD lesions. DHEAS levels were measured and compared according to a gender based subdivision. Analysis of variance was used to assess the association between DHEAS and AMD. Linear regression model was used to examine the relation among DHEAS level and AMD severity scale. RESULTS: Mean +/- SD of DHEAS levels in exudative AMD, nonexudative AMD, and controls in men was 2.67 +/- 0.68 micromol/l, 2.89 +/- 0.95 micromol/l, and 4.43 +/- 1.44 micromol/l, respectively (P = .001), and in women was 1.64 +/- 0.72 micromol/l, 1.85 +/- 0.73 micromol/l, and 2.78 +/- 0.91 micromol/l, respectively (P = .001). Post hoc Tukey analyses revealed a significant reduction in serum DHEAS level in both AMD groups, compared with controls for men and women (P = .001), while no difference was found between AMD groups in both men and women (P = .668 and 0.49, respectively). Regression analyses revealed an inverse correlation among serum DHEAS level and AMD severity scale both in men and women (P = .006 and .007, respectively). CONCLUSIONS: This study suggests an inverse correlation between serum DHEAS level and AMD severity scale with a considerably reduced DHEAS level in AMD.

Effects of hyaluronan on nitric oxide levels and superoxide dismutase activities in synovial fluid in knee osteoarthritis.

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.

Androgen status of the nonautoimmune dry eye subtypes.

PURPOSE: To evaluate androgen levels of patients diagnosed with nonautoimmune dry eye, either with meibomian gland dysfunction (MGD) or without MGD (non-MGD), and normal control subjects. This is a prospective, comparative, case-control study. METHODS: Sixty-four (32 men and 32 women) subjects were enrolled for each of the three diagnostic groups. All dry eye patients were symptom positive. Nonfasting testosterone (T), sex hormone-binding globulin, serum albumin, dehydroepiandrosterone (DHEA), and DHEA sulphate levels of all study participants were determined using either automated immunoenzymatic assay, or standard radioimmunoassay. Analysis of variance was used to compare androgen levels among the three diagnostic groups in a gender-based design, followed by post-hoc multiple comparisons with the Tukey honestly significant difference test. RESULTS: Mean T levels in men and women of the three diagnostic groups were not significantly different (p = 0.808, p = 0.156, respectively; ANOVA). Statistical analyses of the three diagnostic groups revealed a significant difference for men and women in bioavailable T levels (p = 0.002, p = 0.014, respectively; ANOVA), DHEA levels (p = 0.009, p = 0.004, respectively; ANOVA), and DHEA sulphate levels (p = 0.001, p = 0.001, respectively; ANOVA), whereas there was no statistically significant difference between non-MGD dry eye patients and controls for any of the measured androgen levels according to the post-hoc tests. CONCLUSION: This study demonstrates that the androgen pool of nonautoimmune dry eye patients with MGD is significantly depleted compared with that of non-MGD and control cases.

Erdosteine against acetaminophen induced renal toxicity.

Acetaminophen (APAP) induced toxicities have been a major problem in clinical practice. The aim of the present study was to demonstrate a possible protective role of erdosteine, a mucolytic agent having antioxidant properties via its active metabolites, on APAP induced renal damage in rats. Female Wistar Albino rats were divided into groups including control, erdosteine (150 mg/kg, oral), APAP (1 g/kg, oral) APAP+erdosteine (150 mg/kg, oral) and APAP+erdosteine (300 mg/kg, oral). APAP treatment caused lipid peroxidation as well as high NO level in renal tissue. Also, APAP treated rats had decreased activities of CAT and GSH-Px, but not SOD. In addition, tubular epithelial degeneration, vacuolization and cell desquamation were clearly observed in the APAP treated rats. The cellular debris in the proximal tubules and cortical interstitial congestions were prominent in the kidneys of APAP treated rats. BUN and creatinine levels were increased after APAP administration. All these pathological changes were reversed after erdosteine treatments. Erdosteine treated APAP groups showed milder tubular degeneration, epithelial vacuolization in the proximal tubules, lesser cellular desquamation and better morphology when compared with APAP groups. In conclusion, erdosteine may be a choice of preventive treatment against APAP induced nephrotoxicity.

Current concepts in the pathophysiology of fibromyalgia: the potential role of oxidative stress and nitric oxide.

Fibromyalgia (FM) is a common chronic pain syndrome with an unknown etiology. Recent years added new information to our understanding of FM pathophysiology. Researches on genetics, biogenic amines, neurotransmitters, hypothalamic-pituitary-adrenal axis hormones, oxidative stress, and mechanisms of pain modulation, central sensitization, and autonomic functions in FM revealed various abnormalities indicating that multiple factors and mechanisms are involved in the pathogenesis of FM. Oxidative stress and nitric oxide may play an important role in FM pathophysiology, however it is still not clear whether oxidative stress abnormalities documented in FM are the cause or the effect. This should encourage further researches evaluating the potential role of oxidative stress and nitric oxide in the pathophysiology of FM and the efficacy of antioxidant treatments (omega-3 and -6 fatty acids, vitamins and others) in double blind and placebo controlled trials. These future researches will enhance our understanding of the complex pathophysiology of this disorder.

Antioxidant status, lipid peroxidation and nitric oxide in fibromyalgia: etiologic and therapeutic concerns.

We proposed to assess the oxidant/antioxidant status, lipid peroxidation and nitric oxide (NO) in untreated fibromyalgia (FM) patients and controls. The effect of amitriptyline (A, 20 mg daily) and sertraline (S, 100 mg daily) treatment on patients' superoxide dismutase (SOD), xanthine oxidase (XO), adenosine deaminase (ADA) enzyme activities, thiobarbituric acid reactive substances (TBARS) and NO levels was investigated. Thirty female patients with primary FM and age-matched 16 healthy female controls were included. Patients received an 8-week course of treatment with either A or S. FM patients had higher serum levels of TBARS (particularly malondialdehyde) and lower levels of nitrite compared to controls whereas enzyme activities were similar. A and S significantly improved Fibromyalgia Impact Questionnaire (FIQ) pain scores, Hamilton anxiety and depression rating scales. But neither A nor S had significant effects on measured oxidative stress parameters, except SOD activity that was significantly reduced after S treatment. Total myalgic scores negatively correlated with XO activity, and depression scales negatively correlated with levels of TBARS. Our results indicate that patients with FM are under oxidative stress. These findings represent a rationale for further research assessing the effect of free radical scavengers or antioxidant agents like vitamins and omega-3 fatty acids on peripheral and central mechanisms in FM.

The protective role of erdosteine on testicular tissue after testicular torsion and detorsion.

Testicular torsion and detorsion are important clinical problems for infertile man and oxidative stress may have a role in this clinical situation. The aim of this study was to investigate the protective role of erdosteine, an antioxidant, on unilateral testicular reperfusion injury in rats. The rats were divided into four groups including seven rats in each group: control, torsion, torsion/detorsion and torsion/detorsion+erdosteine. Rats, except the sham operation group, were subjected to left unilateral torsion (720( composite function) rotation in the clockwise direction) without including the epididymis. The experiments were finished after sham operation time for control, 120 min torsion for torsion group and 120 min torsion and 240 min detorsion for torsion/detorsion groups. Bilateral orchiectomy was performed for all groups of rats. The ipsilateral and controlateral testis were divided into two pieces to analyse biochemical parameters and to investigate the light microscopic view. Malondialdehyde level of ipsilateral testis was increased in torsion and torsion/detorsion groups in comparison with the other groups (p < 0.05). Erdosteine treatment ameliorated lipid peroxidation after torsion/detorsion in ipsilateral testis (p < 0.05). Also, xanthine oxidase activity of ipsilateral testis was increased in torsion/detorsion group in comparison with the others (p < 0.05). Nitric oxide (NO) level of ipsilateral testis was higher in all experimental groups than sham operated control group (p < 0.05). Also, NO level of torsion group was increased in comparison with detorsion groups (p < 0.05). Erdosteine treatment caused increased glutathione peroxidase activity in comparison with torsion and torsion/detorsion groups and catalase activity in comparison with the other groups in ipsilateral testis (p < 0.05). Superoxide dismutase activity of ipsilateral testis was higher in torsion/detorsion and torsion/detorsion+erdosteine groups than control and torsion groups (p < 0.05). The biochemical parameters were not affected in controlateral testis in all groups. Torsion, torsion/detorsion and torsion/detorsion+erdosteine groups showed ipsilateral testicular damage in the histological examination, but the specimens from torsion/detorsion had a significantly greater histological injury than those from the other groups (p < 0.05). Control rats showed normal seminiferous tubule morphology. Rats in torsion group had slight-to-moderate disruption of the seminiferous epithelium. Rats in torsion/detorsion group displayed moderate-to-severe disruption of the seminiferous epithelium. In all animals from torsion/detorsion+erdosteine group, the testicular tissues were affected with slight-to-moderate degenerative changes of the seminiferous epithelium. Administration of erdosteine resulted in a significantly reduced histological damage associated with torsion of the spermatic cord compared with torsion/detorsion. In all groups, the contralateral testes were histologically normal. In conclusion, the results clearly displayed that erdosteine treatment may have a protective role on testicular torsion/detorsion injury.

Protective agent, erdosteine, against cisplatin-induced hepatic oxidant injury in rats.

Cisplatin, one of the most active cytotoxic agents against cancer, has several toxicities. Hepatotoxicity is one of them occurred during high doses treatment. The aim of this study was to determine the effects of erdosteine against cisplatin-induced liver injury through tissue oxidant/antioxidant parameters and light microscopic evaluation. The rats were randomly divided into three groups: control (n=5), cisplatin (10 mg/kg, n=6) and cisplatin+erdosteine (50 mg/kg/day oral erdosteine, n=8) groups. The rats were sacrificed at the 5th day of cisplatin treatment. The liver tissues were examined with light microscopy and oxidant/antioxidant biochemical parameters. The malondialdehyde (MDA) and nitric oxide (NO) levels were increased in the cisplatin group in comparison with the control and cisplatin+erdosteine groups (p<0.05). There was no significant difference in MDA and NO levels between control and cisplatin+erdosteine groups. The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were higher in cisplatin+erdosteine group than cisplatin group (p<0.05). However, the CAT and GSH-Px activities were significantly lower in cisplatin group than in control group (p<0.05). The light microscopic examination revealed that cytoplasmic changes especially around cells of central vein were observed in cisplatin group. Hepatocellular vacuolization was seen in these cells. In the cisplatin plus erdosteine group, a decrease in cytoplasmic changes with the hepatocytes and sinusoidal dilatations around cells of central vein were noticed in as compared to cisplatin group. In the light of microscopic and biochemical results, it was concluded that cisplatin-induced liver damage in high dose and erdosteine prevented this toxic side effect by the way of its antioxidant and radical scavenging effects.

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.