scholarly journals Nitric oxide, lipid peroxidation products, and antioxidants in primary fibromyalgia and correlation with disease severity

2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Varsha Shukla ◽  
Siddharth Kumar Das ◽  
Abbas Ali Mahdi ◽  
Shweta Agarwal ◽  
Sukhanshi Khandpur
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Disease Severity ◽  
Pain Perception ◽  
High Plasma ◽  
Primary Fibromyalgia

Summary Background Fibromyalgia syndrome (FMS) is characterized by altered pain perception with chronic, widespread musculoskeletal pain. The relationship between nitric oxide, oxidative stress and the severity of FMS has not been studied. This study evaluated NO levels in plasma, LPO products and antioxidants in Red Cell lysate in patients of FMS and correlated it with disease severity. Methods 105 FMS patients who fulfilled 1990 ACR Criteria and 105 age- and sex-matched healthy controls were recruited over two years from 2013 to 2015. Antioxidative enzyme activity was assessed by the estimation of catalase, glutathione peroxidase (GPx) and glutathione reductase (GR) and superoxide dismutase (SOD). Nitric oxide in plasma, MDA marker of lipid peroxidation (LPO) in the lysate was donen for estimating oxidative stress. FIQR was used to assess the severity of fibromyalgia. Results The catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase levels were significantly low in patients than controls (p<0.001). Plasma NO levels and LPO were also significantly high (p<0.05). NO and LPO levels showed a significant positive correlation with FIQR (r: 0.57, 0.8 and p: <0.001) whereas a negative correlation was observed between antioxidants (Cat, GR and GPx, but not SOD) and FIQR. Conclusions Low antioxidants and raised LPO in RBC lysate in patients with FM together with high plasma NO correlated with the severity of FMS.

scholarly journals Effect of Cross-Sex Hormonal Replacement on Antioxidant Enzymes in Rat Retroperitoneal Fat Adipocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Alejandra Zúñiga-Muñoz ◽  
Rodrigo Velázquez Espejel ◽  
Alfredo Cabrera-Orefice ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Enzymatic Activities ◽  
Glutathione S Transferase ◽  
Control Groups ◽  
Intact Female ◽  
Hormonal Replacement

We report the effect of cross-sex hormonal replacement on antioxidant enzymes from rat retroperitoneal fat adipocytes. Eight rats of each gender were assigned to each of the following groups: control groups were intact female or male (F and M, resp.). Experimental groups were ovariectomized F (OvxF), castrated M (CasM), OvxF plus testosterone (OvxF + T), and CasM plus estradiol (CasM + E2) groups. After sacrifice, retroperitoneal fat was dissected and processed for histology. Adipocytes were isolated and the following enzymatic activities were determined: Cu-Zn superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and glutathione reductase (GR). Also, glutathione (GSH) and lipid peroxidation (LPO) were measured. In OvxF, retroperitoneal fat increased and adipocytes were enlarged, while in CasM rats a decrease in retroperitoneal fat and small adipocytes are observed. The cross-sex hormonal replacement in F rats was associated with larger adipocytes and a further decreased activity of Cu-Zn SOD, CAT, GPx, GST, GR, and GSH, in addition to an increase in LPO. CasM + E2exhibited the opposite effects showing further activation antioxidant enzymes and decreases in LPO. In conclusion, E2deficiency favors an increase in retroperitoneal fat and large adipocytes. Cross-sex hormonal replacement in F rats aggravates the condition by inhibiting antioxidant enzymes.

scholarly journals Oxidative Stress in Rats After 60 Days of Hypergalactosemia or Hyperglycemia

2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Insulin Treatment ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Glutathione Disulfide ◽  
Hepatic Lipid Peroxidation ◽  
Streptozotocin Diabetic Rats

Two of the models used in current diabetes research include the hypergalactosemic rat and the hyperglucosemic, streptozotocin-induced diabetic rat. Few studies, however, have examined the concurrence of these two models regarding the effects of elevated hexoses on biomarkers of oxidative stress. This study compared the activities of superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase and the concentrations of glutathione, glutathione disulfide, and thiobarbituric acid reactants (as a measure of lipid peroxidation) in liver, kidney, and heart of Sprague-Dawley rats after 60 days of either a 50% galactose diet or insulin deficiency caused by streptozotocin injection. Most rats from both models developed bilateral cataracts. Blood glucose and glycosy-lated hemoglobin A1c concentrations were elevated in streptozotocin diabetic rats. Streptozotocin diabetic rats exhibited elevated activities of renal superoxide dismutase, cardiac catalase, and renal and cardiac glutathione peroxidase, as well as elevated hepatic lipid peroxidation. Insulin treatment of streptozotocin-induced diabetic rats normalized altered markers. In galactosemic rats, hepatic lipid peroxidation was increased whereas glutathione reductase activity was diminished. Glutathione levels in liver were decreased in diabetic rats but elevated in the galactosemic rats, whereas hepatic glutathione disulfide concentrations were decreased much more in diabetes than in galactosemia. Insulin treatment reversed/prevented all changes caused by streptozotocin-induced diabetes. Lack of concomitance in these data indicate that the 60-day galactose-fed rat is not experiencing the same oxidative stress as the streptozotocin diabetic rat, and that investigators must be cautious drawing conclusions regarding the concurrence of the effects of the two animal models on oxidative stress biomarkers.

scholarly journals Gonadal Steroids Negatively Modulate Oxidative Stress in CBA/Ca Female Mice Infected withP. bergheiANKA

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Néstor Aarón Mosqueda-Romo ◽  
Ana Laura Rodríguez-Morales ◽  
Fidel Orlando Buendía-González ◽  
Margarita Aguilar-Sánchez ◽  
Jorge Morales-Montor ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Sexual Dimorphism ◽  
Stress Response ◽  
Glutathione Peroxidase ◽  
Oxidative Stress Response ◽  
Gonadal Steroids ◽  
Male Mice ◽  
Female Mice

We decreased the level of gonadal steroids in female and male mice by gonadectomy. We infected these mice withP. bergheiANKA and observed the subsequent impact on the oxidative stress response. Intact females developed lower levels of parasitaemia and lost weight faster than intact males. Gonadectomised female mice displayed increased levels of parasitaemia, increased body mass, and increased anaemia compared with their male counterparts. In addition, gonadectomised females exhibited lower specific catalase, superoxide dismutase, and glutathione peroxidase activities in their blood and spleen tissues compared with gonadectomised males. To further study the oxidative stress response inP. bergheiANKA-infected gonadectomised mice, nitric oxide levels were assessed in the blood and spleen, and MDA levels were assessed in the spleen. Intact, sham-operated, and gonadectomised female mice exhibited higher levels of nitric oxide in the blood and spleen compared with male mice. MDA levels were higher in all of the female groups. Finally, gonadectomy significantly increased the oxidative stress levels in females but not in males. These data suggest that differential oxidative stress is influenced by oestrogens that may contribute to sexual dimorphism in malaria.

Dietary supplementation with magnesium citrate may improve pancreatic metabolic indices in an alloxan-induced diabetes rat model

10.5219/1375 ◽  
2020 ◽  
Vol 14 ◽  
pp. 836-846
Author(s):  
Olena Shatynska ◽  
Oleksandr Tokarskyy ◽  
Petro Lykhatskyi ◽  
Olha Yaremchuk ◽  
Iryna Bandas ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Glutathione Reductase ◽  
Fasting Glucose ◽  
Reduced Glutathione ◽  
Pancreatic Tissue ◽  
Magnesium Supplementation ◽  
Metabolism Enzymes ◽  
Peroxidation Index

The purpose of the current study was to evaluate the protective properties of dietary magnesium supplementation on pancreatic tissue of rats with alloxan-induced diabetes mellitus. Twenty-five male Wistar rats were split into five groups (control, diabetes, diabetes with 100 mg Mg daily, diabetes with 250 mg Mg daily, diabetes with 500 mg Mg daily) with feeding supplementation starting on day 1, diabetes induction on day 21, and animal sacrifice on day 30. Fasting glucose in blood serum was measured on days 21, 25, 27, and day 30. Glucose metabolism enzymes, namely, lactate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in pancreatic tissue upon the sacrifice, as well as lipid peroxidation, antioxidant system protective enzymes (catalase and superoxide dismutase), and glutathione system components (glutathione reductase, glutathione peroxidase, and glutathione reduced). Pearson correlation coefficients showed strong negative correlation between serum glucose (control and diabetic animals) and glucose metabolism enzymes, catalase, superoxide dismutase, glutathione peroxidase in pancreatic tissue (r >-0.9, p <0.05), moderate negative correlation with reduced glutathione (r = -0.79, p <0.05), moderate positive correlation with lipid peroxidation index (r = +0.67, p <0.05), weak correlation with glutathione reductase (r = -0.57, p <0.05). Magnesium supplementation slowed down diabetes onset considering fasting glucose levels in rats (p <0.05), as well as partially restored investigated dehydrogenase levels in the pancreas of rats comparing to diabetes group (p <0.05). The lipid peroxidation index varied between treatments showing the dose-dependent influence of Mg2+. Magnesium supplementation partially restored catalase and superoxide dismutase activities in pancreatic tissue, as well as glutathione peroxidase and reduced glutathione levels (p <0.05), while glutathione reductase levels remained unaffected (p >0.05). The obtained results suggested a model, where magnesium ions may have a possible protective effect on pancreatic tissue against the negative influence of alloxan inside β cells of the pancreas.

scholarly journals Characterization of Oxidative Stress in Various Tissues of Diabetic and Galactose-fed Rats

2001 ◽  
Vol 2 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Robert M. Strother ◽  
Tonya G. Thomas ◽  
Mary Otsyula ◽  
Ruth A. Sanders ◽  
John B. Watkins III
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Rat Model ◽  
Catalase Activity ◽  
Diabetic Rats ◽  
Oxidized Glutathione ◽  
Hepatic Glutathione ◽  
Reduced And Oxidized Glutathione

Rats fed a galactose-rich diet have been used for several years as a model for diabetes to study, particularly in the eye, the effects of excess blood hexoses. This study sought to determine the utility of galactosemia as a model for oxidative stress in extraocular tissues by examining biomarkers of oxidative stress in galactose-fed rats and experimentally-induced diabetic rats. Sprague-Dawley rats were divided into four groups: experimental control; streptozotocin-induced diabetic; insulin-treated diabetic; and galactose-fed. The rats were maintained on these regimens for 30 days, at which point the activities of catalase, glutathione peroxidase, glutathione reductase, and superoxide dismutase, as well as levels of lipid peroxidation and reduced and oxidized glutathione were determined in heart, liver, and kidney. This study indicates that while there are some similarities between galactosemic and diabetic rats in these measured indices of oxidative stress (hepatic catalase activity levels and hepatic and renal levels of oxidized glutathione in both diabetic and galactosemic rats were significantly decreased when compared to normal), overall the galactosemic rat model is not closely parallel to the diabetic rat model in extra-ocular tissues. In addition, several effects of diabetes (increased hepatic glutathione peroxidase activity, increased superoxide dismutase activity in kidney and heart, decreased renal and increased cardiac catalase activity) were not mimicked in galactosemic rats, and glutathione concentration in both liver and heart was affected in opposite ways in diabetic rats and galactose- fed rats. Insulin treatment reversed/prevented the activity changes in renal and cardiac superoxide dismutase, renal and cardiac catalase, and hepatic glutathione peroxidase as well as the hepatic changes in lipid peroxidation and reduced and oxidized glutathione, and the increase in cardiac glutathione. Thus, prudence should be exercised in the use of experimentally galactosemic rats as a model for diabetes until the correspondence of the models has been more fully characterized.

scholarly journals Characteristics of lipid peroxidation processes and factors of the antioxidant defense system in chronic atrophic gastritis and gastric cancer

2022 ◽  
Vol 20 (4) ◽  
pp. 63-70
Author(s):  
O. V. Smirnova ◽  
V. V. Tsukanov ◽  
A. A. Sinyakov ◽  
O. L. Moskalenko ◽  
N. G. Elmanova ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastric Cancer ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Antioxidant Defense ◽  
Antioxidant Defense System ◽  
Control Group ◽  
Defense System ◽  
Glutathione S Transferase

Background. The problem of gastric cancer remains unresolved throughout the world, while chronic atrophic gastritis (CAG) increases the likelihood of its development by 15 times. In the Russian Federation, the incidence of gastric cancer (GC) is among the highest, with it prevailing among males. One of the leading mechanisms in molecular pathology of membranes is lipid peroxidation (LPO). The severity of oxidative membrane damage depends on concomitant diseases, contributing to emergence and progression of pathological processes and development of cancer. Currently, the problem of LPO is unsolved in biological systems.The aim of this study was to investigate the state of LPO and antioxidant defense system in CAG and GC. Materials and methods. The parameters were studied in 45 patients with CAG and 50 patients with GC. The control group included 50 practically healthy volunteers without gastrointestinal complaints, who did not have changes in the gastric mucosa according to the fibroesophagogastroduodenoscopy (FEGDS) findings.Results. In patients with CAG, an increase in malondialdehyde, superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase was found in the blood plasma compared with the control group. In patients with CAG, lipid peroxidation was activated, and the malondialdehyde level increased by 3.5 times relative to normal values. At the same time, the body fought against oxidative stress by increasing the activity of antioxidant enzymes, such as superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase. All patients with GC showed pronounced oxidative stress in the blood plasma in the form of a 45-fold increase in malondialdehyde. The activity of the main antioxidant enzyme superoxide dismutase was reduced in GC. Catalase was activated, which indicated pronounced oxidative stress, significant damage to blood vessels, and massive cell death. Glutathione-related enzymes (glutathione S-transferase and glutathione peroxidase) and the antioxidant protein ceruloplasmin were activated, which also indicated significant oxidative stress and severe intoxication in patients with GC.Conclusion. Depending on the stage and type of cancer, an in-depth study of lipid peroxidation and factors of the antioxidant defense system can be used to correct therapy and prevent cancer and can serve as markers of progression and prognosis in gastric cancer. 

Oxidative stress profile during postpartum period in Surti goats

2016 ◽  
Author(s):  
Tanvi D. Manat ◽  
Sandhya S. Chaudhary ◽  
Virendra Kumar Singh ◽  
Sanjay B. Patel ◽  
Kuldeep Kumar Tyagi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Critical Care ◽  
Uric Acid ◽  
Glutathione Peroxidase ◽  
Postpartum Period ◽  
Reduced Glutathione ◽  
Stress Profile ◽  
Blood Samples

Present study was conducted to investigate postpartum oxidative stress in 20 Surti goats. Blood samples were collected on 0, 7th, 14th, 21st, 30th and 45th days postpartum and analysed for Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx), lipid peroxidation (LPO), reduced Glutathione (GSH) and uric acid. SOD differed significantly between 0, 14th and 21st day postpartum. GPx was significantly low on 14th day and then increased significantly (P<0.01) up to 45th day. Significant (P<0.01) difference was observed between days except 0 and 21st. LPO increased significantly (P<0.01) from 0 to 14th day and then decreased non-significantly up to 45th day. Reduced glutathione was significantly (P<0.05) higher on 0 day. Uric acid was lowest on 0 day and highest on 45th day however they were non-significantly different on 7th, 14th, 30th and 45th day. It can be summarized that on 14th day post kidding, the values of SOD, GPx and GSH were lowest while LPO was highest. Uric acid was significantly (P<0.01) low on the day of kidding. Thus it may be concluded that in Surti goats the period from 0 day to 14th day postpartum is most stressful and critical care should be taken during this period. GPx, SOD along with LPO and GSH can be used as marker of stress during postpartum period.

Oxidative stress in the testis of hyperglycemic rabbits treated with repaglinide

2007 ◽  
Vol 2 (4) ◽  
pp. 538-546
Author(s):  
Anna Gumieniczek ◽  
Hanna Hopkała ◽  
Marcin Pruchniak
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Protective Effect ◽  
Protein Carbonyl ◽  
Carbonyl Groups ◽  
Protein Carbonyl Groups ◽  
Diabetic Rabbits

AbstractIn the present study, the induction of oxidative stress was examined in the testis of alloxan-induced diabetic rabbits. In addition, the protective effect of repaglinide, an oral anti-diabetic, at a dose of 1 mg daily was studied after four and eight weeks of the treatment. For these purposes, the levels of superoxide dismutase (Cu,Zn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), glutathione (GSH), ascorbic acid (AA), lipid peroxidation products (LPO) and protein carbonyl groups (PCG) were quantified. Hyperglycemia resulted in significant increases in the antioxidative enzymes, Cu, Zn-SOD, CAT, GSH-Px, and GSSG-R after four and eight weeks, respectively. There was also an increase in GSH level, and a decrease in the level of AA. These effects were accompanied by an elevation in testicular LPO levels and PCG levels. Repaglinide was found to normalize the activity of GSSG-R and levels of GSH and AA, and blunted the increased lipid peroxidation, however no decrease in PCG levels were observed. In conclusion, some oxidative changes provoked in the testis of rabbits by hyperglycemia, were found to be reduced with repaglinide treatment at therapeutic dose.

scholarly journals Tocotrienol-Rich Fraction Ameliorates Antioxidant Defense Mechanisms and Improves Replicative Senescence-Associated Oxidative Stress in Human Myoblasts

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Shy Cian Khor ◽  
Wan Zurinah Wan Ngah ◽  
Yasmin Anum Mohd Yusof ◽  
Norwahidah Abdul Karim ◽  
Suzana Makpol
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radical ◽  
Glutathione Peroxidase ◽  
Defense Mechanisms ◽  
Antioxidant Defense ◽  
Replicative Senescence ◽  
Ros Generation ◽  
Tocotrienol Rich Fraction

During aging, oxidative stress affects the normal function of satellite cells, with consequent regeneration defects that lead to sarcopenia. This study aimed to evaluate tocotrienol-rich fraction (TRF) modulation in reestablishing the oxidative status of myoblasts during replicative senescence and to compare the effects of TRF with other antioxidants (α-tocopherol (ATF) andN-acetyl-cysteine (NAC)). Primary human myoblasts were cultured to young, presenescent, and senescent phases. The cells were treated with antioxidants for 24 h, followed by the assessment of free radical generation, lipid peroxidation, antioxidant enzyme mRNA expression and activities, and the ratio of reduced to oxidized glutathione. Our data showed that replicative senescence increased reactive oxygen species (ROS) generation and lipid peroxidation in myoblasts. Treatment with TRF significantly diminished ROS production and decreased lipid peroxidation in senescent myoblasts. Moreover, the gene expression of superoxide dismutase(SOD2), catalase(CAT),and glutathione peroxidase(GPX1)was modulated by TRF treatment, with increased activity of superoxide dismutase and catalase and reduced glutathione peroxidase in senescent myoblasts. In comparison to ATF and NAC, TRF was more efficient in heightening the antioxidant capacity and reducing free radical insults. These results suggested that TRF is able to ameliorate antioxidant defense mechanisms and improves replicative senescence-associated oxidative stress in myoblasts.

scholarly journals Antioxidants-Related Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPX), Glutathione-S-Transferase (GST), and Nitric Oxide Synthase (NOS) Gene Variants Analysis in an Obese Population: A Preliminary Case-Control Study

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 595
Author(s):  
Amani M. T. Gusti ◽  
Safaa Y. Qusti ◽  
Eida M. Alshammari ◽  
Eman A. Toraih ◽  
Manal S. Fawzy
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Superoxide Dismutase ◽  
Nitric Oxide Synthase ◽  
Glutathione Peroxidase ◽  
Disease Risk ◽  
Nucleotide Polymorphisms ◽  
Obesity Risk ◽  
Glutathione S Transferase ◽  
Oxide Synthase

Oxidative stress and antioxidants play an important role in obesity etiopathology. Genetic variants, including single nucleotide polymorphisms (SNPs) of the antioxidant-related genes, may impact disease risk in several populations. This preliminary study aimed to explore the association of 12 SNPs related to superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione-S-transferase (GST), and nitric oxide synthase (NOS) genes with obesity susceptibility in a Saudi population. A total of 384 unrelated participants, including 154 (40.1%) obese individuals, were enrolled. TaqMan OpenArray Genotyping assays were used. Six SNPs were significantly more prevalent in obese cohorts: (1) GSTM1 rs1056806*C/T; (2) SOD1 rs2234694*A; (3) SOD2 rs4880*G; (4) SOD3 rs2536512*A; (5) GPX1 rs1800668*A; (6) NOS3 rs1799983*G. Four SNPs were associated with higher obesity risk under heterozygote and dominant models for GSTM1 rs1056806 (C/T), homozygote model for SOD2 rs4880 (A/G), and homozygote and recessive models for GPX1 rs1800668 (A/G). In contrast, SOD3 rs2536512 (A/G) were less likely to be obese under heterozygote and dominant models. The CGAG, CAAA, TGGG, and CGAG combined genotypes showed a higher risk of obesity. In conclusion, the present results suggest that oxidative-stress-related genetic determinants could significantly associate with obesity risk in the study population.

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