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

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.

Open Medicine ◽  
2011 ◽  
Vol 6 (5) ◽  
pp. 588-594 ◽  
Author(s):  
Anna Łukaszewicz-Hussain

AbstractOrganophosphate pesticides are known to induce oxidative stress and cause oxidative tissue damage, as has been reported in studies concerning acute and chronic intoxication with these compounds.Our objective was to investigate the activities of brain antioxidant enzymes and malonyldialdehyde, as well as the level of carbonyl groups, in rats sub-chronically intoxicated with chlorpyrifos at doses of 0.2, 2 and 5 mg per kg of body weight per day. It was found that chlorpyrifos induces change in brain antioxidant enzymes, such as superoxide dismutase, catalase and glutathione peroxidise, but to a different degree in comparison to proper control values; however, the elevated antioxidant enzymes activities failed to check lipid and protein peroxidation in the brains of rats. Thus, in sub-chronic intoxication with chlorpyrifos, as evidenced by increased level of malonyldialdehyde and carbonyl groups, oxidative stress is induced.Measurements of protein carbonyl groups appeared to give more consistent responses in the rats’ brains when compared to the malonyldialdehyde level after sub-chronic chlorpyrifos treatment.


2003 ◽  
Vol 22 (6) ◽  
pp. 423-427 ◽  
Author(s):  
Mary Otsyula ◽  
Matthew S. King ◽  
Tonya G. Ketcham ◽  
Ruth A. Sanders ◽  
John B. Watkins

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.


2003 ◽  
Vol 12 (4) ◽  
pp. 247-249 ◽  
Author(s):  
S. Gangemi ◽  
A. Saija ◽  
A. Tomaino ◽  
F. Cimino ◽  
R. A. Merendino ◽  
...  

Familiar chronic nail candidiasis (FCNC) is a rare disorder characterized by early-onset infections caused by different species of Candida, restricted to the nail of the hands and feet, and associated with a low serum concentration of intercellular adhesion molecule 1. Host defense mechanisms against candidiasis require the cooperation of many immune cells through several candidacidal mechanisms, including oxygen-dependent killing mechanisms, mediated by a superoxide anion radical myeloperoxidase-H2O2-halide system, and reactive nitrogen intermediates. We analyzed protein carbonyl groups (considered a useful marker of oxidative stress) in the serum of patients belonging to a five-generation Italian family with an isolated form of FCNC.Serum protein carbonyl groups in FCNC patients were significantly lower than those measured in healthy donors.Also, if this hypothesis is merely speculative, we could suggest that the decreased circulating level of protein carbonyl groups in these patients is not a marker of a lower oxidative stress condition, but might be linked to a lower protease activity.


2001 ◽  
Vol 2 (3) ◽  
pp. 211-216 ◽  
Author(s):  
Robert M. Strother ◽  
Tonya G. Thomas ◽  
Mary Otsyula ◽  
Ruth A. Sanders ◽  
John B. Watkins III

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.


2016 ◽  
Vol 27 (2) ◽  
pp. 55 ◽  
Author(s):  
Deepti Pande ◽  
Reena Negi ◽  
Ranjana S. Khanna ◽  
Hari D. Khanna

Objective: To evaluate the oxidative stress and antioxidant defense in patients with chronic myeloid leukemia.Background: Chronic myeloid leukemia is a myeloproliferative disorder associated with a characteristic chromosomal translocation called the Philadelphia chromosome. Reactive oxygen species and other free radicals mediate phenotypic and genotypic changes leading from mutation to neoplasia in all cancers, including chronic myeloid leukemia. We evaluated patients with chronic myeloid leukemia by observing their oxidative status and antioxidant defense.Methods: Using serum from 40 clinically diagnosed cases of chronic myeloid leukemia as well as 40 healthy controls, we measured the concentration of thiobarbituric acid, levels of protein carbonylation, total antioxidant status, catalase, superoxide dismutase, glutathione peroxidase, vitamins A and E, and the trace elements zinc, magnesium, and selenium. Results: We found significantly increased levels of serum malonyldialdehyde and protein carbonyl in patients with chronic myeloid leukemia in comparison to healthy individuals, and significantly decreased levels of the antioxidants and micronutrients thiobarbituric acid, catalase, superoxide dismutase, glutathione peroxidase, vitamins A and E, zinc, magnesium, and selenium. These data suggest cellular damage occurring at the level of lipids and proteins.Conclusion: These findings indicate a link between low levels of antioxidants and cellular damage in patients with chronic myeloid leukemia, supporting the idea that oxidative stress may play a role in the pathogenesis of chronic myeloid leukemia.


Author(s):  
Udedi Stanley Chidi ◽  
Ani Onuabuchi Nnenna ◽  
Asogwa Kingsley Kelechi ◽  
Maduji Fitzcharles Chijindu ◽  
Okafor Clinton Nebolisa

This study investigated the in-vitro antioxidant activity of ethanol leaf extract of Justicia carnea and its effect on antioxidant status of alloxan-induced diabetic albino rats. The in-vitro antioxidant activity was assayed by determining the total phenol, flavonoids, ascorbic acid, β-carotene and lycopene contents and by using 2,2 diphenyl-1-picrylhydrazyl (DPPH) radical, reducing antioxidant power and inhibition of lipid peroxidation antioxidant systems. Oxidative stress was produced in rats by single intraperitoneal injection of 150 mg/kg alloxan and serum concentration of malonaldehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) were determined. Five experimental groups of rats (n=6) were used for the study. Two groups of diabetic rats received oral daily doses of 100 and 200 mg/kg Justicia carnea leaf extract respectively while gilbenclamide (5 mg/ml); a standard diabetic drug was also given to a specific group for 14 days. From the result, the leaf extract contained a higher concentration of flavonoids followed byphenols, ascorbic acid, lycopene and β-carotene. The extract displayed more potent reducing power ability with EC50 of 40 µg/ml compared to BHA (EC50 of 400µg/ml). The percentage DPPH radical scavenging activity of the extract was also higher with EC50 of 200µg/ml and increased with increase in concentration while BHA had EC50of 320µg/ml. The inhibition of lipid peroxidation also increased with increase in concentration with EC50 of 58µg/ml and comparable with BHA (EC50=60µg/ml). The effect of the plant extract on antioxidant enzyme activities was concentration-dependent. Administration of 100mg/kg of the plant extract resulted in a significant decrease (p<0.05) in serum MDA concentration, while 200 mg/kg of the extract caused a significant (p˂0.05) increase in superoxide dismutase (SOD) and catalase activities with a non-significant increase (p>0.05) in the serum level of MDA when compared with the diabetic untreated group. These findings suggest that ethanol leaf extract of Justicia carnea have antioxidant properties and could handle diabetes-induced oxidative stress.


2022 ◽  
Vol 20 (4) ◽  
pp. 63-70
Author(s):  
O. V. Smirnova ◽  
V. V. Tsukanov ◽  
A. A. Sinyakov ◽  
O. L. Moskalenko ◽  
N. G. Elmanova ◽  
...  

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. 


2019 ◽  
Vol 0 (0) ◽  
Author(s):  
Varsha Shukla ◽  
Siddharth Kumar Das ◽  
Abbas Ali Mahdi ◽  
Shweta Agarwal ◽  
Sukhanshi Khandpur

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.


Author(s):  
Tanvi D. Manat ◽  
Sandhya S. Chaudhary ◽  
Virendra Kumar Singh ◽  
Sanjay B. Patel ◽  
Kuldeep Kumar Tyagi

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.


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