scholarly journals Changes in the Rate of Lipid Peroxidation in Plasma and Selected Blood Antioxidants before and during Pregnancy in Ewes

2009 ◽  
Vol 78 (2) ◽  
pp. 237-242 ◽  
Author(s):  
Mine Erişir ◽  
Fulya Benzer ◽  
Fatih M. Kandemir
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Glutathione Peroxidase ◽  
Antioxidant Status ◽  
Healthy Male ◽  
Blood Samples ◽  
Awassi Sheep ◽  
Healthy Female

Pregnancy is a condition that favours oxidative stress. The aim of this study was to evaluate the oxidant and antioxidant status by measuring glutathione peroxidase (GSH-Px), catalase (CAT) activities and malondialdehyde (MDA) and glutathione (GSH) concentrations before and during pregnancy in ewes. Twelve healthy female and two healthy male Awassi sheep, aged 4-5 years, weighing approximately 50 - 55 kg each, were used in the study. The ewes’ blood samples were taken before synchronization and during pregnancy (on 25th days of each month of pregnancy). Plasma MDA concentrations in the 2nd and 3rd months of pregnancy in ewes were lower than in the 1st, 4th, 5th months of pregnancy and in the non-pregnant ewes. GSH concentrations and GSH-Px activities during pregnancy were increased (P < 0.01). GSH concentrations and GSH-Px activities were the highest in the 2nd and 3rd months of pregnancy. CAT activities were decreased after the 1st month of pregnancy in ewes (P < 0.001). They were the lowest in the 2nd and 3rd months of pregnancy. The findings of our study show decreased CAT activities and elevated GSH concentrations and GSH-Px activities after the 1st month of pregnancy in ewes. These changes in the indicators under study may indicate a predisposition to oxidative stress in the 2nd and 3rd month of pregnancy in ewes.

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.

scholarly journals Prospects of Vitamin C as an Additive in Plasma of Stored Blood

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
R. Vani ◽  
R. Soumya ◽  
H. Carl ◽  
V. A. Chandni ◽  
K. Neha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Vitamin C ◽  
Antioxidant Status ◽  
Oxidation Products ◽  
Blood Storage ◽  
Advanced Oxidation Protein Products ◽  
Blood Samples ◽  
Storage Solutions ◽  
Stored Blood

There is a dire necessity to improve blood storage and prolong shelf-life of blood. Very few studies have focused on oxidative stress (OS) in blood and its influence on plasma with storage. This study attempts to (i) elucidate the continuous changes occurring in plasma during storage through oxidant levels and antioxidant status and (ii) evaluate the influence of vitamin C (VC) as an additive during blood storage. Blood was drawn from maleWistarrats and stored for 25 days at 4°C. Blood samples were divided into control and experimental groups. Plasma was isolated every 5 days and the OS markers, antioxidant enzymes, lipid peroxidation, and protein oxidation products, were studied. Catalase activity increased in all groups with storage. Lipid peroxidation decreased in VC (10) but was maintained in VC (30) and VC (60). Although there were variations in all groups, carbonyls were maintained towards the end of storage. Advanced oxidation protein products (AOPP) increased in VC (30) and were maintained in VC (10) and VC (60). Sulfhydryls were maintained in all groups. Vitamin C could not sufficiently attenuate OS and hence, this opens the possibilities for further studies on vitamin C in combination with other antioxidants, in storage solutions.

Safety of Antitheilerial Drug Buparvaquone in Rams

2018 ◽  
Vol 46 (1) ◽  
Author(s):  
Nermin Isik ◽  
Ozlem Derinbay Ekici ◽  
Ceylan Ilhan ◽  
Devran Coskun
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Alkaline Phosphatase ◽  
Blood Cell ◽  
Blood Urea Nitrogen ◽  
Troponin I ◽  
Oxidative Status ◽  
Blood Samples ◽  
Heart Damage

 Background: Theileriosis is a tick-borne disease caused by Theileria strains of the protozoan species. Buparvaquone is the mostly preferred drug in the treatment theileriosis, while it is safety in sheep, has not been detailed investigated. It has been hypothesized that buparvaquone may show side effects and these effects may be defined some parameters measured from blood in sheep when it is used at the recommended dose and duration. The aim of this research was to determine the effect of buparvaquone on the blood oxidative status, cardiac, hepatic and renal damage and bone marrow function markers.Materials, Methods & Results: In this study, ten adult (> 2 years) Akkaraman rams were used. Healthy rams were placed in paddocks, provided water ad libitum, and fed with appropriate rations during the experiment. Buparvaquone was ad­ministered at the dose of 2.5 mg/kg (IM) intramuscularly twice at 3-day intervals. Blood samples were obtained before (0. h, Control) and after drug administration at 0.25, 0.5, 1, 2, 3, 4 and 5 days. The blood samples were transferred to gel tubes, and the sera were removed (2000 g, 15 min). During the study, the heart rate, respiratory rate, and body temperature were measured at each sampling time. In addition, the animals were clinically observed. Plasma oxidative status mark­ers (Malondialdehyde, total antioxidant status, catalase, glutathione peroxidase, superoxide dismutase), serum cardiac (Troponin I, creatine kinase-MBmass, lactate dehydrogenase), hepatic (Alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, gamma glutamyltransferase, total protein, albumin, globulin) and renal (Creatinine, blood urea nitrogen) damage markers and hemogram values (white blood cell, red blood cell, platelet, hemogram, hematocrit) were measured. Buparvaquone caused statistically significantly (P < 0.05) increases in the troponin I and blood urea nitrogen levels and fluctuations in alkaline phosphatase activity, but there was no any statistically significance difference determined in the other parameters.Discussion: In this study, buparvaquone was administered two times at a dose of 2.5 mg/kg (IM) at 3-day intervals. Al­though the result was not statistically significant (P > 0.05), it was determined that buparvaquone gradually increased the levels of the main oxidative stress marker, MDA, by approximately 2.8 fold. CAT and GPX levels were also found to have decreased by 2.2 fold. Buparvaquone may cause lipid peroxidation by producing free radicals. Some other antiprotozoal drugs may affect the oxidative status and may increase MDA level and decrease SOD level. In this study, MDA, which is an indicator of lipid peroxidation in vivo, was used to partially detect developing lipid peroxidation. Changes in the levels of reduced GPX and CAT enzymes could be attributed to their use in mediating the hydrogen peroxide detoxification mechanisms. The absence of significant changes in the TAS levels in this study suggests that buparvaquone may partially induce oxidative stress by producing hydrogen peroxide, but no significant changes occurred in the oxidative stress level because of the high antioxidant capacity of sheep. In this study, buparvaquone caused a statistically significant increase (P < 0.05) in the level of Tn-I, which is a marker of specific cardiac damage (P < 0.05), whereas there was no statistically (P > 0.05) significant increase in CK-MBmass. Tn-I and CK-MB levels, which are used to define heart damage in humans, have been successfully used to determine heart damage in sheep. In this research study, the statistically significant increases in Tn-I but not CK-MBmass levels could be considered indicative of mild cardiac damage.Keywords: ram, buparvaquone, safety.

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.

The Impact of Concomitant Chronic Pancreatitis on Prooxidant-antioxidant Status and Other Conditions in Osteoarthritis

2016 ◽  
pp. 75-78
Author(s):  
Liliia Babynets ◽  
Tetiana Maevska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Chronic Pancreatitis ◽  
Functional Capacity ◽  
Antioxidant Status ◽  
Activation Parameters ◽  
Tissue Destruction ◽  
The Impact ◽  
Stress Accumulation

The study proved that patients with combined progress of osteoarthritis and chronic pancreatitis have reliable top-level activation of lipid peroxidation in terms of malonyc aldehyde and tissue destruction in terms of oxyproline, weakening of the antioxidant level (in terms of superoxide dismutase and SH-groups) and activation parameters of catalase and ceruloplasmin (p<0,05). The authentic predictority of patients biological age, duration of combined clinical courses, the functional capacity of the pancreas in terms of fecal α-elastase, structural state by ultrasound criteria for progression effects of oxidative stress, accumulation oxyproline activation parameters catalase and ceruloplasmin, which statistically was reflected by the presence of mainly moderate of significant correlations between these groups of indicators have been identified.

scholarly journals Antioxidants in erythrocytes in aging and dementia

2013 ◽  
Vol 59 (4) ◽  
pp. 443-451 ◽  
Author(s):  
E.A. Kosenko ◽  
L.A. Tikhonova ◽  
A.C. Poghosyan ◽  
Y.G. Kaminsky
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glutathione Peroxidase ◽  
Antioxidant Status ◽  
Transferase Activity ◽  
Glutathione S Transferase ◽  
Age Related ◽  
Organic Hydroperoxides

Age of patients and brain oxidative stress may contribute to pathogenesis of Alzheimer's disease (AD). Erythrocytes (red blood cells, RBC) are considered as passive “reporter cells” for the oxidative status of the whole organism and are not well studied in AD. The aim of this work was to assess whether the antioxidant status of RBC changes in aging and AD. Blood was taken from AD and non-Alzheimer's dementia patients, aged-matched and younger controls. In vivo antioxidant status was assessed in each of the study subjects by measuring RBC levels of Н О , organic hydroperoxides, glutathione (GSH) and glutathione disulfide (GSSG), activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, and glucose-6-phosphate dehydrogenase. In both aging and dementia, oxidative stress in RBC was shown to increase and to be expressed in elevated concentrations of H O and organic hydroperoxides, decreased the GSH/GSSG ratio and glutathione S-transferase activity. Decreased glutathione peroxidase activity in RBC may be considered as a new peripheral marker for Alzheimer’s disease while alterations of other parameters of oxidative stress reflect age-related events.

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 Protein Damage and Antioxidant Status Alterations Caused by Oxidative Injury in Chronic Myeloid Leukemia

2016 ◽  
Vol 27 (2) ◽  
pp. 55 ◽  
Author(s):  
Deepti Pande ◽  
Reena Negi ◽  
Ranjana S. Khanna ◽  
Hari D. Khanna
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Chronic Myeloid Leukemia ◽  
Glutathione Peroxidase ◽  
Myeloid Leukemia ◽  
Antioxidant Status ◽  
Philadelphia Chromosome ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Cellular Damage

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.

scholarly journals Lapatinib protects against epileptic seizures via halting glutathione peroxidase 4-dependent ferroptosis

2020 ◽  
Author(s):  
Jining Jia ◽  
Qin Li ◽  
Qianyi Sun ◽  
Nan Yang ◽  
Kangni Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Glutathione Peroxidase ◽  
Western Blot ◽  
Neuronal Death ◽  
Epileptic Seizures ◽  
List Type ◽  
Dominant Form ◽  
Neuroprotective Strategy

ABSTRACTBackground and PurposeRepetitive epileptic seizures trigger massive neuronal death. Therefore, neuroprotection plays a role in preventing neuronal death and inversely suppresses seizure generation. Additionally, some studies have shown ferroptosis, featured by lipid peroxidation (a dominant form of oxidative stress in the brain), is of paramount importance in epileptic seizures. Lapatinib can play a first-line anti-tumor role by targeting oxidative stress and a recent work illustrates the improvement of encephalomyelitis in rodent models after lapatinib treatment. We hypothesize whether lapatinib can protect against ferroptosis in epileptic seizures via regulating lipid peroxidation.Experimental ApproachThe epileptic behavior of the mice was recorded after intracranial injection of KA. Western blot and RT-qPCR were used to detect the protein expression of 4-hydroxynonenal (4-HNE) and glutathione peroxidase 4 (GPX4) and the mRNA expression of prostaglandin endoperoxide synthase 2 (PTGS2) in vivo and in vitro. The level of lipid reactive oxygen species (lipid ROS) in cells pretreated with lapatinib was analyzed by flow cytometry.Key ResultsLapatinib remarkably prevented KA-induced epileptic seizures in mice and ferroptosis was involved in the neuroprotection of lapatinib. Compared with the model group, western blot showed that lapatinib significantly upregulated the levels of GPX4. In the ferroptotic cell death model, lapatinib exerted neuroprotection via up-regulating GPX4. Treatment with Ras-selective lethal small molecule 3 (RSL3), a selective GPX4 inhibitor abrogated its anti-ferroptotic potential.Conclusions and ImplicationsThese results illustrated that lapatinib has neuroprotective potential against KA-triggered epileptic seizures via suppressing GPX4-dependent ferroptosis.What is already knownActivation of ferroptosis occurs in epileptic seizures.What this study addsLapatinib protects brain against epileptic seizures via blocking ferroptosis.GPX4-dependent ferroptosis is involved in the neuroprotection of lapatinib.What is the clinical significanceInhibition of ferroptosis by lapatinib represents a potential neuroprotective strategy for epileptic patients.

Sign in / Sign up

Export Citation Format

Share Document