scholarly journals Fortified Extract of Red Berry,Ginkgo biloba, and White Willow Bark in Experimental Early Diabetic Retinopathy

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Claudio Bucolo ◽  
Giuseppina Marrazzo ◽  
Chiara Bianca Maria Platania ◽  
Filippo Drago ◽  
Gian Marco Leggio ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Diabetic Retinopathy ◽  
Ginkgo Biloba ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Sprague Dawley ◽  
White Willow ◽  
Willow Bark

Diabetic retinopathy is a complex condition where inflammation and oxidative stress represent crucial pathways in the pathogenesis of the disease. Aim of the study was to investigate the effects of a fortified extract of red berries,Ginkgo bilobaand white willow bark containing carnosine andα-lipoic acid in early retinal and plasma changes of streptozotocin-induced diabetic rats. Diabetes was induced by a single streptozotocin injection in Sprague Dawley rats. Diabetics and nondiabetic (control) rats were treated daily with the fortified extract for the ten days. Retina samples were collected and analyzed for their TNF-αand VEGF content. Moreover, plasma oxidative stress was evaluated by thiobarbituric acid reacting substances (TBARS). Increased TNF-αand VEGF levels were observed in the retina of diabetic rats. Treatment with the fortified extract significantly lowered retinal cytokine levels and suppressed diabetes-related lipid peroxidation. These data demonstrate that the fortified extract attenuates the degree of retinal inflammation and plasma lipid peroxidation preserving the retina in early diabetic rats.

scholarly journals Plasma Lipid Peroxidation as a Marker for Seminal Oxidative Stress in Stallion

2019 ◽  
Vol 11 (6) ◽  
pp. 401
Author(s):  
Patricia Wolkmer ◽  
Andressa M. G. Stumm ◽  
Luiz F. K. Borges ◽  
Eduarda P. T. Ferreira ◽  
Bruna Favaretto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Seminal Plasma ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Semen Collection ◽  
Semen Storage ◽  
Plasma Lipid Peroxidation ◽  
Antioxidant Enzyme Catalase

This experiment aims to evaluate the correlation between lipid peroxidation levels in serum and seminal plasma in equines. Also, it investigates the lipid peroxidation in extended semen samples and its effects and sperm motility during a 72 hr refrigeration period. Blood and semen were collected from fertile Crioulo stallions. Serum and seminal plasma lipid peroxidation levels were analyzed by thiobarbituric acid reactive substances (TBARS) immediately after semen collection. After addition of extender (hour = 0), diluted semen was refrigerated and stored at 5 °C. Semen analyses, TBARS and catalase activity were performed in extended semen at 0, 24, 48, and 72 hours. We noted that levels of plasma lipid peroxidation can be used as an indicative of seminal oxidative stress. Also, lipid peroxidation does not increase substantially during semen storage. Lipid peroxidation and the antioxidant enzyme catalase do not seem to be the major cause of loss and motility and consequently reduction in fertility in stallion semen during storage for 72 h at 5 °C.

scholarly journals Antioxidant Status and Lipid Peroxidation in Diabetic Rats under Hyperbaric Oxygen Exposure

2010 ◽  
pp. 97-104 ◽  
Author(s):  
T Matsunami ◽  
Y Sato ◽  
T Sato ◽  
M Yukawa
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Glucose ◽  
Hyperbaric Oxygen ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Enhanced Production ◽  
Comprehensive Evaluations ◽  
Hyperbaric Oxygen Exposure ◽  
Oxidative Effects

Hyperglycemia is known to cause oxidative stress that leads mainly to enhanced production of mitochondrial reactive oxygen species (ROS). It has been demonstrated that hyperbaric oxygen (HBO) treatment also increases the formation of ROS. There are, however, no comprehensive evaluations of such oxidative effects in diabetes which requires HBO treatment. The purpose of this study is to investigate the influence of a clinically-recommended HBO treatment on glucose homeostasis and oxidative stress in rats with streptozotocin (STZ)-induced diabetes. Under the clinically-used HBO exposure protocol, the levels of blood glucose, thiobarbituric acid reactive substances (TBARS) as a lipid peroxidation marker, and the activity of superoxide dismutase (SOD) as an antioxidant enzyme marker were investigated in the erythrocytes, liver, pancreas, skeletal muscle, and brain of rats with STZ-induced diabetes. The levels of blood glucose and TBARS increased significantly (p<0.05), and the activity of SOD decreased significantly (p<0.05) in the erythrocytes and all organs of rats with diabetes subjected to HBO exposure. These results suggested that HBO exposure might boost glucose autoxidation and increase ROS production in STZ-induced diabetes as side-effects of administering HBO treatment for the first time.

scholarly journals Protective Effects of Melatonin on Retinal Inflammation and Oxidative Stress in Experimental Diabetic Retinopathy

2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Tingting Jiang ◽  
Qing Chang ◽  
Jiyang Cai ◽  
Jiawen Fan ◽  
Xiaozhe Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Biological Effects ◽  
Interleukin 1 ◽  
Diabetic Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Akt Phosphorylation ◽  
Pathogenic Factors ◽  
And Oxidative Stress

Oxidative stress and inflammation are important pathogenic factors contributing to the etiology of diabetic retinopathy (DR). Melatonin is an endogenous hormone that exhibits a variety of biological effects including antioxidant and anti-inflammatory functions. The goals of this study were to determine whether melatonin could ameliorate retinal injury and to explore the potential mechanisms. Diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (60 mg/kg) in Sprague-Dawley rats. Melatonin (10 mg kg−1daily, i.p.) was administered from the induction of diabetes and continued for up to 12 weeks, after which the animals were sacrificed and retinal samples were collected. The retina of diabetic rats showed depletion of glutathione and downregulation of glutamate cysteine ligase (GCL). Melatonin significantly upregulated GCL by retaining Nrf2 in the nucleus and stimulating Akt phosphorylation. The production of proinflammatory cytokines and proteins, including interleukin 1β, TNF-α, and inducible nitric oxide synthase (iNOS), was inhibited by melatonin through the NF-κB pathway. At 12 weeks, melatonin prevented the significant decrease in the ERG a- and b-wave amplitudes under the diabetic condition. Our results suggest potent protective functions of melatonin in diabetic retinopathy. In addition to being a direct antioxidant, melatonin can exert receptor-mediated signaling effects to attenuate inflammation and oxidative stress of the retina.

scholarly journals Polyphenols from Berries ofAronia melanocarpaReduce the Plasma Lipid Peroxidation Induced by Ziprasidone

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Anna Dietrich-Muszalska ◽  
Justyna Kopka ◽  
Bogdan Kontek
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Healthy Subjects ◽  
Plasma Lipid ◽  
Thiobarbituric Acid ◽  
Tbars Level ◽  
Polyphenol Compounds ◽  
Aronia Melanocarpa ◽  
Plasma Lipid Peroxidation

Background. Oxidative stress in schizophrenia may be caused partially by the treatment of patients with antipsychotics. The aim of the study was to establish the effects of polyphenol compounds derived from berries ofAronia melanocarpa(Aronox) on the plasma lipid peroxidation induced by ziprasidonein vitro.Methods. Lipid peroxidation was measured by the level of thiobarbituric acid reactive species (TBARS). The samples of plasma from healthy subjects were incubated with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) alone and with Aronox (5 ug/ml; 50 ug/ml).Results. We observed a statistically significant increase of TBARS level after incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) (after 24 h incubation:P=7.0× 10−4,P=1.6× 10−3, andP=2.7× 10−3, resp.) and Aronox lipid peroxidation caused by ziprasidone was significantly reduced. After 24-hour incubation of plasma with ziprasidone (40 ng/ml; 139 ng/ml; and 250 ng/ml) in the presence of 50 ug/ml Aronox, the level of TBARS was significantly decreased:P=6.5× 10−8,P=7.0× 10−6, andP=3.0× 10−5, respectively.Conclusion. Aronox causes a distinct reduction of lipid peroxidation induced by ziprasidone.

Administration of beta-carotene Suppresses Lipid Peroxidation in Tissues and Improves the Glucose Tolerance Ability of Streptozotocin-Induced Diabetic Rats

2002 ◽  
Vol 72 (2) ◽  
pp. 71-76 ◽  
Author(s):  
Tadasu Furusho ◽  
Eiko Kataoka ◽  
Tadashi Yasuhara ◽  
Masahiro Wada ◽  
Satoshi Innami
Keyword(s):  
Lipid Peroxidation ◽  
Body Weight Gain ◽  
Beta Carotene ◽  
Thiobarbituric Acid ◽  
Diabetic Rats ◽  
Standard Diet ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sprague Dawley ◽  
Antioxidative Effect ◽  
Sd Rats

The present study attempted to examine the antioxidative effect of dietary beta-carotene (BC) on lipid peroxidation (LPO) in the streptozotocin (STZ)-induced diabetic rats. Male Sprague-Dawley (SD) rats were fed on the AIN76 standard diet with or without 0.1% BC. On the 21st day after introduction of these diets, STZ was intraperitoneally injected in half the subjects of both groups. All animals were sacrificed seven days after the STZ injection.Glucose tolerance and thiobarbituric acid reactive substance (TBARS) in the tissues or serum were measured. Body weight gain in the BC + STZ group was significantly higher than that in the STZ group (p < 0.05). Blood glucose and TBARS concentrations of the liver, pancreas, and serum in the BC + STZ group were significantly lower than those in the STZ group. The blood insulin concentration in the BC + STZ group was significantly higher than that in the STZ group. The hepatic and serum beta-carotene concentrations in the BC + STZ group were significantly lower than those in the BC group. Moreover, the synthesis and oxidation of glutathione (GSH) in the BC + STZ group were reduced when compared to the STZ group. These results suggest that the administration of beta-carotene suppresses the elevation of LPO and reduces the symptoms of diabetes mellitus (DM) in the STZ-induced diabetic rats.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

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.

Attenuation of erythrocyte membrane oxidative stress bySesbania grandiflorain streptozotocin-induced diabetic rats

2015 ◽  
Vol 93 (4) ◽  
pp. 385-395 ◽  
Author(s):  
Chandrabose Sureka ◽  
Thiyagarajan Ramesh ◽  
Vavamohaideen Hazeena Begum
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Blood Glucose ◽  
Erythrocyte Membrane ◽  
Osmotic Fragility ◽  
Diabetic Rats ◽  
Glycosylated Haemoglobin ◽  
Albino Rats ◽  
Enzymatic Antioxidants ◽  
Protective Effects

The aim of the present study was to investigate the protective effects of Sesbania grandiflora flower (SGF) extract on erythrocyte membrane in Streptozotocin (STZ)-induced diabetic rats. Adult male albino rats of Wistar strain, weighing 190–220 g, were made diabetic by an intraperitonial administration of STZ (45 mg/kg). Normal and diabetic rats were treated with SGF, and diabetic rats were also treated with glibenclamide as drug control, for 45 days. In this study plasma insulin and haemoglobin levels were decreased and blood glucose, glycosylated haemoglobin, protein oxidation, lipid peroxidation markers, and osmotic fragility levels were increased in diabetic rats. Moreover, erythrocytes antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxide, glutathione reductase, glutathione-S-transferase, and glucose-6-phosphate dehydrogenase activities and non-enzymatic antioxidants such as vitamin C, vitamin E, reduced glutathione (GSH), and oxidized glutathione (GSSG) levels were altered. Similarly, the activities of total ATPases, Na+/K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase were also decreased in the erythrocytes of diabetic rats. Administration of SGF to STZ-induced diabetic rats reduced blood glucose and glycosylated haemoglobin levels with increased levels of insulin and haemoglobin. Moreover, SGF reversed the protein and lipid peroxidation markers, osmotic fragility, membrane-bound ATPases activities, and antioxidant status in STZ-induced diabetic rats. These results suggest that SGF could provide a protective effect on diabetes by decreasing oxidative stress-associated diabetic complications.

Expression Analysis of 4-Hydroxynonenal Modified Proteins in Schizophrenia Brain; Relevance to Involvement in Redox Dysregulation

2021 ◽  
Vol 18 ◽  
Author(s):  
Sobia Manzoor ◽  
Ayesha Khan ◽  
Beena Hasan ◽  
Shamim Mushtaq ◽  
Nikhat Ahmed
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thiobarbituric Acid ◽  
Brain Regions ◽  
Protein Adducts ◽  
Antioxidant Systems ◽  
Control Group ◽  
Tbars Level ◽  
Elevated Expression ◽  
Modified Proteins

Background: Oxidative damage contributes to the pathophysiology of schizophrenia (SZ). Redox imbalance may lead to increased lipid peroxidation, which produces toxic aldehydes like 4-hydroxynonenal (4-HNE) ultimately leading to oxidative stress. Conversely, implications of oxidative stress points towards an alteration in HNE-protein adducts and activities of enzymatic and antioxidant systems in schizophrenia. Objectives: Present study focuses on identification of HNE-protein adducts and its related molecular consequences in schizophrenia pathology due to oxidative stress, particularly lipid peroxidation. Material and Methods: Oxyblotting was performed on seven autopsied brain samples each from cortex and hippocampus region of schizophrenia patients and their respective normal healthy controls. Additionally, thiobarbituric acid substances (TBARS), reduced glutathione (GSH) levels and catalase (CAT) activities associated with oxidative stress, were also estimated. Results: Obtained results indicates substantially higher levels of oxidative stress in schizophrenia patients than healthy control group represented by elevated expression of HNE-protein adducts. Interestingly, hippocampus region of schizophrenia brain shows increased HNE protein adducts compared to cortex. An increase in catalase activity (4.8876 ± 1.7123) whereas decrease in antioxidant GSH levels (0.213 ± 0.015µmol/ml) have been observed in SZ brain. Elevated TBARS level (0.3801 ± 0.0532ug/ml) were obtained in brain regions SZ patients compared with their controls that reflects an increased lipid peroxidation (LPO). Conclusion: Conclusion: We propose the role of HNE modified proteins possibly associated with the pathology of schizophrenia. Our data revealed increase lipid peroxidation as a consequence of increased TBARS production. Furthermore, altered cellular antioxidants pathways related to GSH and CAT also highlight the involvement of oxidative stress in schizophrenia pathology.

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