Nitrosative Stress In Patients Research Articles

Oxidative and nitrosative stress in patients with meningitis

Introduction and aim. Meningitis is an acute inflammation of the protective membranes covering the brain and spinal cord, known as the meninges. In this study, oxidative and nitrosative stress were evaluated in cerebrospinal fluid (CSF) and blood samples that were taken from patients with meningitis. Our goal was to identify a fast and a reliable biomarker using these parameters in order to the early diagnose of bacterial meningitis. Material and methods. In this study, 37 bacterial meningitis, 30 tuberculous meningitis and 30 viral meningitis cases were included. Serum/CSF total oxidant status (TAS) and total antioxidant status (TOS) were measured by the Erel method. Nitrotyrosine concentrations were quantified by using ELISA in both serum and CSF Results. Serum nitrotyrosine, CSF TAS and TOS levels were not significantly different in three groups (p>0.05). CSF nitrotyrosine levels were significantly higher in bacterial meningitis than tuberculous meningitis group (p<0.05). Viral meningitis patients had higher serum TOS and TAS concentrations than tuberculous meningitis group (p<0.05). Conclusion. As a result, we can say that the oxidative and nitrosative stress markers studied are not a rapid and reliable biomarker in bacterial meningitis’s diagnosis.

Investigation of Dynamic Thiol/Disulfide Homeostasis and Nitrosative Stress in Patients with Wilson Disease.

Wilson disease (WD) is an autosomal recessive inherited disorder of copper (Cu2+) metabolism, resulting in Cu2+ accumulation and liver and central nervous system toxicity. Oxidative stress may have a role in the pathogenesis of Wilson disease, but the roles of thiol/disulfide homeostasis and nitrosative stress have not been examined. The purpose of this study was to evaluate whether there is a modification in thiol/disulfide homeostasis and nitrosative stress in patients with Wilson disease. A total of 50 patients with Wilson disease (42 under drug treatment and 8 newly diagnosed patients with no drug treatment) and 50 healthy gender- and age-matched controls were enrolled for this study. Serum native thiol and total thiol levels were measured with a spectrophotometric method. The number of disulfide bonds and the related ratios were determined from these measurements. Serum nitric oxide (NO) and 3-nitrotyrosine (3-NT) levels were analyzed using chemiluminescence and ELISA assays, respectively. The average native thiol levels of the patient group under drug treatment were found to be markedly higher than the levels of controls (P < .05). We detected no marked changes in total thiol and disulfide levels, and disulfide/total thiol, disulfide/native thiol, or native thiol/total thiol ratios between groups. We found significant elevations in NO levels in Wilson disease group before drug treatment, and the 3-NT levels in the Wilson disease groups prior to (P < .05) and under drug treatment (P < .01), when compared to controls. Our data are the first to show that nitrosative stress and thiol/disulfide homeostasis can contribute to the pathogenesis of Wilson disease.

Varicocoele and oxidative stress: New perspectives from animal and human studies.

Varicocoele (VCL), one of the main causes of male subfertility, negatively affects testicular function. Due to limited access to human testicular tissue, animal model studies have been used to evaluate molecular and, recently, epigenetic changes attributed to pathophysiology induced by VCL. This review aims to provide an update on the latest findings regarding the link between VCL-induced biochemical stress and molecular changes in germ cells and spermatozoa. Endocrine and antioxidant status, testicular chaperone-specific hemostasis failure, altered testicular ion balance, metabolic disorders, and altered carbon cycling during spermatogenesis are among the many features that will be presented. Literature review coupled with our own findings suggests that ionic imbalance, hypoxia, hyperthermia, and altered blood flow could lead to severe chronic oxidative and nitrosative stress in patients with VCL leading to defective spermatogenesis and impairment of the integrity of all sperm cell components and compartments down to the epigenetic information they carry. Since oxidative stress is an important feature of the reproductive pathology of VCL, therapeutic strategies such as the administration of appropriate antioxidants could be undertaken as a complementary non-invasive treatment line.

The levels of oxidative and nitrosative stress in patients who had 99mTc-MIBI myocardial perfusion scintigraphy and 99mTc-DMSA, 99mTc-MAG-3 renal scintigraphy.

Ionizing radiation is a strong stimulator of reactive oxygen specises (ROS) and reactive nitrogen species (RNS). These reactive species may cause oxidative and nitrosative stress. In this study, we aimed to evaluate possible effects of 99mTechnetium (99mTc)-methoxyisobuthylisonitrite (MIBI), 99mTc-dimercaptosuccinic acid (DMSA), 99mTc-mercaptoacetyltriglycine (MAG-3) on oxidative and nitrosative stress biomarkers in patients who were performed myocardial perfusion scintigraphy (MPS) and renal scintigraphy. Patients (n = 29) who were referred to nuclear medicine department were chosen as the patient group. They were divided into three subgroups according to the type of disease and 99mTc labelled agent. The first patient group had MPS (n = 9). The second patient group had 99mTc-DMSA renal scintigraphy (n = 12). The third patient group had 99mTc-MAG-3 renal scintigraphy (n = 8). The blood samples were taken from first, second and third patient groups 1 h, 3 h, 45 min after injection of the agent, respectively. The samples were taken from healthy volunteers (n = 25) as a control group. Alterations in catalase (CAT),superoxide dismutase (SOD), malondialdehyde (MDA) levels as oxidative stress biomarkers and nitric oxide (NO) and 3-Nitrotyrosine (3-NTx) levels as nitrosative stress biomarkers in all blood samples were evaluated. Results of MPS and renal scintigraphy performed patients were compared with control group separately. CAT, SOD, MDA and 3-NTx levels were higher in the first group than the control group (p < 0.05). Although NO levels were higher in the first group than the control group, it was not statistically significant (p > 0.05). CAT and SOD levels were lower in second and third groups than the control group (p < 0.0 5). However, MDA, NO, 3-NTx levels were higher in second and third groups than the control group (p < 0.05). These results show that oxidative and nitrosative balance is impaired due to ionization radiation. These reactive species might stimulate an adaptive and protective cellular defense mechanism in irradiated cells soon after exposure to radiation. Thereby, this mechanism protect organism from the effects of low dose ionizing radiation.

Determination of levels of oxidative stress and nitrosative stress in patients with epilepsy

BackgroundEpilepsy is one of the most common neurological diseases. The underlying pathophysiological mechanisms in epilepsy are still unknown. Oxidative stress is believed to be one of the factors involved in the pathogenesis of epileptogenesis. In various pathophysiological conditions, reactive nitrogen species (RNS) such as nitrogen and peroxynitrite are produced and these RNSs can bind to free nucleosides and nucleotides or to nucleosides and nucleotides existing in the DNA/RNA structure. 8-Nitroguanine (8-NG) is a typical DNA nucleobase product of nitrosative damage generated by RNS. It has been proposed that F2-isoprostanes, in particular 8-iso-Prostaglandin F2α (8-isoPGF2α), are specific, reliable and non-invasive biomarkers of lipid peroxidation in vivo. In the present study, we compared the levels of lipid oxidative stress biomarker 8-isoPGF2α and nitrosative stress DNA biomarker 8-NG in patients with epilepsy undergoing antiepileptic drug (AEDs) treatment and with those in healthy participants. MethodsThe present study comprised 90 patients aged between 17 and 53 who were admitted to the Neurology Clinic of Cumhuriyet University and diagnosed with epilepsy. The patients were assigned into the intervention (n = 45) and control (n = 45) groups. Of the participants in the intervention group, 37.7% (n = 17) were treated with levetiracetam (LEV), 33.3% (n = 15) with valproic acid (VA) and 29% (n = 13) with carbamazepine. Serum 8-iso-PGF2α and 8-NG levels of the participants in the intervention and control groups were determined by ELISA. ResultsThere was no significant difference between the medication (LEV, VA, Carbamazepine) used by the participants and their 8-iso-PGF2α and 8-NG levels (p > 0.05). However, 8-iso-PGF2α and 8-NG were significantly higher in the participants in the intervention than in the participants in the control group (p < 0.001). ConclusionOur study demonstrated that there was an increase in oxidative and nitrosative stres markers in patients with epilepsy. There was no significant difference between the 8-iso-PGF2α and 8-NG levels of the participants taking three different AEDs.

Nitrosative stress in patients with asthma–chronic obstructive pulmonary disease overlap

Asthma-chronic obstructive pulmonary disease overlap (ACO) has frequent exacerbations and a poor quality of life and prognosis compared with those of chronic obstructive pulmonary disease alone. However, the pathogenesis of ACO has not been fully elucidated yet. The aim of this study was to investigate nitrosative stress, which causes a redox imbalance and tissue inflammation in the airways of patients with ACO, and to evaluate the relationship between nitrosative stress and the clinical course in study subjects. Thirty healthy subjects and 56 asthmatic patients participated in this study. The asthmatic patients were divided into 33 asthmatic patients and 23 patients with ACO. The study subjects had been followed prospectively for 2years to evaluate the clinical course. Nitrosative stress was evaluated based on the production of 3-nitrotyrosine (3-NT) in sputum cells. Production of 3-NT was significantly enhanced in patients with ACO compared with that in asthmatic patients. Amounts of reactive persulfides and polysulfides, newly identified powerful antioxidants, were significantly decreased in the ACO group. Baseline levels of 3-NT were significantly correlated with the frequency of exacerbations and decrease in FEV1 adjusted by age, smoking history, and blood eosinophil count. The 3-NT-positive cells were also significantly correlated with amounts of proinflammatory chemokines and cytokines. These findings suggested that greater nitrosative stress occurred in the airways of patients with ACO, and the degree of nitrosative stress was correlated with an impairment in the clinical course. Nitrosative stress might be related to thepathogenesis of ACO.

Glutathione Metabolism, Mitochondria Activity, and Nitrosative Stress in Patients Treated for Mandible Fractures

The aim of the study was to evaluate the effect of titanium bone fixations on mitochondrial activity, reactive oxygen species (ROS) production, glutathione metabolism, and selected markers of oxidative/nitrosative stress in the periosteum-like tissue of patients treated with mandible fractures. The study group consisted of 30 patients with bilateral fractures of the mandible body eligible for surgical treatment. Our study is the first one that indicates disturbances of mitochondrial activity as well as a higher production of ROS in the periosteum-like tissue covering titanium fixations of the mandible. We also found significantly higher levels of reduced glutathione and enhanced activity of glutathione reductase in the periosteum homogenates of patients in the study group compared to the control group. Levels of nitrosative (S-nitrosothiols, peroxynitrite, nitrotyrosine) and oxidative stress biomarkers (malondialdehyde, protein carbonyls, dityrosine, kynurenine, and N-formylkynurenine) were statistically elevated in periosteum-like tissue covering titanium fixations. Although exposure to titanium fixations induces local antioxidant mechanisms, patients suffer oxidative damage, and in the periosteum-like tissue the phenomenon of metallosis was observed. Titanium implants cause oxidative/nitrosative stress as well as disturbances in mitochondrial activity.

Oxidative and nitrosative stress in patients with ischemic stroke

AbstractBackgroundOxidative and nitrosative stress is well believed to play a role in the pathogenesis of ischemic stroke. This study aims to evaluate the time course of oxidative and nitrosative stress in ischemic stroke.MethodsIn total, 27 healthy individuals, 22 individuals with high risk of ischemic stroke due to hypertension and diabetes mellitus, and 20 patients with acute ischemic stroke hospitalized at the Neurology Department of the Kırıkkale University School of Medicine were enrolled in the study. Venous blood was collected at admission (hour 0) and again at hours 24, 48, 72, and 96. Nitric oxide (NO), malondialdehyde (MDA), total oxidative stress (TOS), oxidative stress index (OSI), and total antioxidant status (TAS) were measured and compared among stroke patients and control groups.ResultsBlood NO was significantly higher in the patient group at 0, 24, 48, and 72 h compared to the healthy and high-risk control groups, and lower at 96 h than at early times within the patient group (p&lt;0.001). MDA was higher in patients than the healthy control group at all times. Conversely, TOS and OSI were significantly lower in the patient group than the healthy control group at 96 h and the high-risk control group at 72 and 96 h (p&lt;0.05). There was a significant correlation between initial NO (0 h) and duration of hospitalization (r=0.71; p=0.0003).ConclusionsThese findings suggest a substantial early increase in oxidative and nitrosative stress in ischemic stroke patients during the first 2 days post-admission. However, TOS was lower by days 3–4, likely due to pathological recovery and local/systemic defense systems. The correlation between elevated serum NO during the acute phase of stroke and duration of hospitalization suggests NO as a potentially valuable predictor of ensuing oxidative damage and clinical outcome.

Influence of disease-modifying antirheumatic drugs on oxidative and nitrosative stress in patients with rheumatoid arthritis.

Nitro-oxidative stress plays a central role in the pathogenesis of rheumatoid arthritis (RA) and several articles show correlation with disease activity. However, the influence and mechanisms by which disease-modifying antirheumatic drugs (DMARDs) may interfere with nitro-oxidative stress are poorly understood. To show the available data on the effect of the DMARDs on the nitro-oxidative stress in RA patients. A bibliographic search was carried out in the electronic databases PUBMED, Lilacs, Scientific Electronic Library Online (SCIELO), and Science Direct and the research was limited to human studies, independently of the publication date. Most studies were performed with infliximab (IFX, 4 articles), tocilizumab (TCZ, 3 articles) and methotrexate (MTX, 2 articles). MTX and leflunomide showed similar results with reduction of nitric oxide. The studies with TCZ verified a marked decrease of reactive oxygen and nitrogen species. Most studies with IFX found a reduction of protein oxidation, evaluated by protein carbonyl measurement. In the present review, the most remarkable results were observed with the increase of the antioxidant defenses through several markers and antioxidant systems. The only study with etanercept showed very similar results to those obtained with MTX, with decreased pentosidine and oxidative DNA damage. The majority of the studies reported in this work showed an improvement in the redox state, which could be related to success of the therapy. Thus, oxidative and nitrosative stress markers may be useful to early evaluate the response of DMARDs in patients with RA.

Intensity of oxidative and nitrosative stress in patients with nonalcoholic steatohepatitis and comorbid chronic kindney disease

Objective — to establish intensity of the oxidative and nitrosative stress at the comorbid course of nonalcoholic steatohepatitis (NASH) and chronic kidney disease (CKD) of the 1st and 2nd stages. Materials and methods. Investigation involved 105 patients (48 men and 57 women) with NASH, form them 52 had 1st degree obesity (group 1), and in 53 patients NASH was combined with 1st degree obesity and І - ІІ stages CKD (group 2). The average age of patients was (45.8 ± 3.81) years. The control group consisted of 30 practically healthy age- and sex-matched subjects. The functional endothelium state was studied by the blood levels of stable nitrogen monoxide (NO) metabolites (nitrites, nitrates) by L. C. Green et al. The number of desquamated endothelial cells in blood was determined by the method of J. Hladovec in the modification of N.N Petrischev et al. The state of the antioxidant protection system (AOP) was studied based on the erythrocyte levels of the restored glutathione (GSH), glutathione peroxidase (GPx), glutathione-S-transferase (GSTs), catalase, superoxide dismutase (SOD), ceruloplasmin (CP). Results. It has been established that in case of comorbidity of NASH and І - ІІ stages CKD, the oxidative stress intensity increased with accompanying accumulation of not only intermediate, but also final products of free radical lipid oxidation in all observation groups, testifying presence of the decompensated oxidative stress in this category of patients. The latter fact is an undeniable evidence of the involvement of oxidative stress in the NASH pathogenesis, and its intensity increases with the CKD comorbidity. The obtained results showed the significant increase in blood NO levels of NASH patients vs indices of practically healthy people. The raised number of desquamated endothelial cells in 1.9 times (p < 0.05) evidenced about the expressed endothelial dysfunction in NASH patients. Conclusions. The investigation showed that in case of comorbid course of NASH and І - ІІ stages CKD, the oxidative stress intensity increased with accompanying accumulation of the intermediate and final products of free radical lipid oxidation, early development of the endothelial dysfunction (increased blood number of desquamated endothelial cells and blood levels of the stable NO metabolites) against the background of the activity of the factors of antiradical defense (the decreased erythrocytic levels of the restored glutathione, superoxide dismutase activity, glutathione-dependent enzymes).

Mitochondrial DNA acquires immunogenicity on exposure to nitrosative stress in patients with vitiligo

Vitiligo is a common pigmentary skin disorder of unknown etiology. Many studies show the defective mitochondrial functionality in vitiligo patients, but the potential role of mitochondrial DNA (mtDNA) in the pathogenesis of vitiligo remains to be investigated. Recent evidences demonstrate that mitochondria possess their own nitric-oxide-synthase and can produce endogenous peroxynitrite (ONOO−). This study was undertaken to investigate the role of ONOO−-modified-mitochondrial-DNA (ONOO−-mtDNA) in vitiligo autoimmunity. Our data revealed that ONOO−-induced modifications in mtDNA caused structural alterations. Specificity of immunoglobulin G (IgG) from vitiligo patients (n=26) and controls (n=25) were analysed towards ONOO−-mtDNA. Vitligo-IgG samples (Vt-IgG) show preferential binding to ONOO−-mtDNA in comparison with native mtDNA (p<0.01). Anti-ONOO−-mtDNA–IgG show cross-reactivity with isolated DNA from vitiligo patients. Furthermore, levels of anti-ONOO−-mtDNA–IgG, inducible-nitric-oxide-synthase (iNOS), nitric oxide (NO) and nitrotyrosine were higher among vitiligo patients whose disease durations (DD) were ⩾5years as compared to patients with lower DD (DD<5years). In conclusion, this is the first study to demonstrate the role of ONOO−-modified mtDNA in vitiligo patients. Our data provide an important insight into the immunological mechanisms occur in vitiligo. The ONOO−-mtDNA may be useful in elucidating the mechanisms of disease pathogenesis.

NGF and nitrosative stress in patients with Huntington's disease

IntroductionHuntington's disease (HD) is a neurodegenerative genetic disorder caused by expansion of polyglutamine repeats in the huntingtin gene and characterised by the loss of striatal and cortical neurons. Few studies to date have focussed on peripheral neurotrophic-factor levels in patients with HD. ObjectiveTo measure plasma NGF levels in Huntington's disease and investigate their correlation with disease intensity. Materials and methodsNineteen patients with HD and nineteen age- and sex-matched healthy subjects took part in this cross-sectional study. Plasma levels of NGF, BDNF, GDNF, nitrotyrosine, and myeloperoxidase (MPO) were measured; lactate dehydrogenase (LDH) levels were determined and white blood cell (WBC) counts were evaluated. ResultsNGF levels were significantly lower, nitrotyrosine levels were higher and LDH activity was greater in HD patients than in healthy subjects. There was no significant difference in MPO levels or WBC counts, whereas the MPO/WBC ratio was considerably higher in HD patients. The data obtained suggested that biochemical and haematological changes correlated with disease severity. ConclusionNGF levels are lower in HD patients than in healthy subjects. However, further research is required to confirm the role of NGF in HD.

Increase of nitrosative stress in patients with eosinophilic pneumonia

BackgroundExhaled nitric oxide (NO) production is increased in asthma and reflects the degree of airway inflammation. The alveolar NO concentration (Calv) in interstitial pneumonia is reported to be increased. However, it remains unknown whether NO production is increased and nitrosative stress occurs in eosinophilic pneumonia (EP). We hypothesized that nitrosative stress markers including Calv, inducible type of NO synthase (iNOS), and 3-nitrotyrosine (3-NT), are upregulated in EP.MethodsExhaled NO including fractional exhaled NO (FENO) and Calv was measured in ten healthy subjects, 13 patients with idiopathic pulmonary fibrosis (IPF), and 13 patients with EP. iNOS expression and 3-NT formation were assessed by immunocytochemistory in BALf cells. The exhaled NO, lung function, and systemic inflammatory markers of the EP patients were investigated after corticosteroid treatment for 4 weeks.ResultsThe Calv levels in the EP group (14.4 ± 2.0 ppb) were significantly higher than those in the healthy subjects (5.1 ± 0.6 ppb, p < 0.01) and the IPF groups (6.3 ± 0.6 ppb, p < 0.01) as well as the FENO and the corrected Calv levels (all p < 0.01). More iNOS and 3-NT positive cells were observed in the EP group compared to the healthy subject and IPF patient. The Calv levels had significant positive correlations with both iNOS (r = 0.858, p < 0.05) and 3-NT positive cells (r = 0.924, p < 0.01). Corticosteroid treatment significantly reduced both the FENO (p < 0.05) and the Calv levels (p < 0.01). The magnitude of reduction in the Calv levels had a significant positive correlation with the peripheral blood eosinophil counts (r = 0.802, p < 0.05).ConclusionsThese results suggested that excessive nitrosative stress occurred in EP and that Calv could be a marker of the disease activity.

Effects of Darbepoetin Alfa on Plasma Mediators of Oxidative and Nitrosative Stress in Anemic Patients With Chronic Heart Failure Secondary to Ischemic or Idiopathic Dilated Cardiomyopathy

Increased oxidative and nitrosative stress are important mediators of left ventricular (LV) and vascular dysfunction in patients with chronic heart failure (CHF). This study investigated the effects of darbepoetin alfa on plasma markers of oxidative and nitrosative stress in patients with CHF with anemia. Thirty patients with CHF (LV ejection fraction [LVEF] <40%, hemoglobin <12.5 g/dl, and serum creatinine <2.5 mg/dl) were randomly assigned (1:1) to receive either a 3-month darbepoetin alfa regimen at 1.5 microg/kg every 20 days plus oral iron or placebo plus oral iron. Plasma B-type natriuretic peptide (BNP), markers of oxidative (oxidative, malondialdehyde, carbonyl proteins; antioxidative, glutathione) and nitrosative (nitrotyrosine) stress, LVEF, and 6-minute walked distance were assessed at baseline and after treatment. A significant improvement in LVEF and 6-minute walked distance was observed in only darbepoetin-treated patients. Plasma BNP (F = 14.8, p = 001), malondialdehyde (F = 9.4, p = 0.006), protein carbonyl (F = 9.2, p = 0.006), and nitrotyrosine (F = 4.4, p = 0.045) were significantly decreased, along with an increase in antioxidative glutathione (F = 4.2, p = 0.049) after darbepoetin alfa treatment. These factors were unaffected in placebo-treated patients. Darbepoetin-induced percentages of change in carbonyl protein significantly correlated with respective changes in plasma BNP (r = 0.55, p <0.05) and LVEF (r = -0.46, p <0.05). Finally, a drug-induced percentage of decrease in nitrotyrosine significantly correlated with the respective improvement in 6-minute walked distance (r = -0.63, p <0.05). In conclusion, darbepoetin alfa attenuated deleterious effects of oxidative and nitrosative stress into the cardiovascular system of anemic patients with CHF, improving also cardiac function and exercise capacity.

Chronic endurance exercise induces quadriceps nitrosative stress in patients with severe COPD

Background:Although exercise training has beneficial effects on skeletal muscle bioenergetics and exercise performance in patients with severe chronic obstructive pulmonary disease (COPD), it may also be associated with increased quadriceps...

Effects of Levosimendan on circulating markers of oxidative and nitrosative stress in patients with advanced heart failure

Background Oxidative stress is associated with maladaptive cardiac remodeling and vascular dysfunction and may be an important contributor to chronic heart failure (CHF) deterioration. We sought to investigate if the calcium sensitizer levosimendan beneficially modulates circulating markers of oxidative and nitrosative stress thus lessening their deleterious effects in patients with advanced CHF. Methods Thirty-nine patients with advanced CHF (mean NYHA 3.5 ± 0.4; ischemic/dilated: 23/16; mean left ventricular ejection fraction: 26 ± 7%) who were hospitalized due to syndrome worsening, were randomized (2:1) to receive either a 24-h levosimendan infusion of 0.1 μg/(kg min) ( n = 26) or placebo ( n = 13). Plasma b-type natriuretic peptide (BNP), circulating markers of oxidative [protein carbonyls, malondialdehyde (MDA)] and nitrosative (nitrotyrosine) stress, and cyclic GMP (cGMP) were measured at baseline and 48 h after each treatment. Results Baseline characteristics and medications were well balanced in the two treatment groups. A significant improvement in left ventricular ejection fraction ( P < 0.01), NYHA class ( P < 0.01), and plasma BNP ( P < 0.01) was observed post-treatment only in the levosimendan group. Markers such as MDA, protein carbonyls and nitrotyrosine remained stable in the levosimendan-treated group, but significantly increased ( P < 0.05) in the placebo-treated patients. Neither therapeutic intervention changed the levels of circulating cGMP. Conclusion Levosimendan does not increase markers of oxidative and nitrosative stress in contrast to the placebo treatment, thus, exerting cardioprotective effects in advanced CHF patients. Moreover, levosimendan may exert its biologic action through non-cGMP-dependent biochemical pathways.

Evidence of oxidative and nitrosative stress in patients with cervical squamous cell carcinoma

Background We conducted a study to evaluate reactive oxygen species (ROS) and reactive nitrogen species (RNS) simultaneously together with the antioxidant status in patients with cervical carcinoma. Methods We measured lipid peroxidation product, including malondialdehye (MDA), nitric oxide (NO) products, including nitrite (NO 2 −), nitrate (NO 3 −) and total nitrite (TNO 2 −) and antioxidant enzymes in 45 patients with cervical cancer and compared them against 30 healthy controls. Results Plasma as well as erythrocyte MDA and plasma NO levels was higher ( p < 0.001) in cervical cancer as compared to healthy controls. Antioxidant enzymes, Superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities, were decreased ( p < 0.001) whereas glutathione S-transferase (GST) activity was increased ( p < 0.001) in cervical cancer patients. Lipid peroxidation and NO products accumulation correlated significantly with a deranged antioxidant system. Conclusions We demonstrated a possible involvement of both oxidative and nitrosative stress, as evidenced by increased lipid peroxidation and NO levels with altered antioxidant defense system in the pathogenesis of cervical cancer.