scholarly journals Chronic Hyperinsulinaemic Hypoglycaemia in Rats Is Accompanied by Increased Body Weight, Hyperleptinaemia, and Decreased Neuronal Glucose Transporter Levels in the Brain

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Vivi F. H. Jensen ◽  
Anne-Marie Mølck ◽  
Melissa Chapman ◽  
Lene Alifrangis ◽  
Lene Andersen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Food Consumption ◽  
Glucose Transporter ◽  
Redox Homeostasis ◽  
Hyperinsulinaemic Hypoglycaemia ◽  
Lipid Peroxidation Products ◽  
Glucose Levels ◽  
The Brain

The brain is vulnerable to hypoglycaemia due to a continuous need of energy substrates to meet its high metabolic demands. Studies have shown that severe acute insulin-induced hypoglycaemia results in oxidative stress in the rat brain, when neuroglycopenia cannot be evaded despite increased levels of cerebral glucose transporters. Compensatory measures in the brain during chronic insulin-induced hypoglycaemia are less well understood. The present study investigated how the brain of nondiabetic rats copes with chronic insulin-induced hypoglycaemia for up to eight weeks. Brain level of different substrate transporters and redox homeostasis was evaluated. Hyperinsulinaemia for 8 weeks consistently lowered blood glucose levels by 30–50% (4–6 mM versus 7–9 mM in controls). The animals had increased food consumption, body weights, and hyperleptinaemia. During infusion, protein levels of the brain neuronal glucose transporter were decreased, whereas levels of lipid peroxidation products were unchanged. Discontinued infusion was followed by transient systemic hyperglycaemia and decreased food consumption and body weight. After 4 weeks, plasma levels of lipid peroxidation products were increased, possibly as a consequence of hyperglycaemia-induced oxidative stress. The present data suggests that chronic moderate hyperinsulinaemic hypoglycaemia causes increased body weight and hyperleptinaemia. This is accompanied by decreased neuronal glucose transporter levels, which may be leptin-induced.

scholarly journals Effects ofBauhinia forficataTea on Oxidative Stress and Liver Damage in Diabetic Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Andréia Caroline Fernandes Salgueiro ◽  
Vanderlei Folmer ◽  
Marianne Pires da Silva ◽  
Andreas Sebastian Loureiro Mendez ◽  
Ana Paula Pegoraro Zemolin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Liver Damage ◽  
Weight Ratio ◽  
Protein Carbonyl ◽  
Diabetic Mice ◽  
Body Weight Ratio ◽  
Glucose Levels ◽  
Nonprotein Thiols

This study was designed to evaluate the effects ofBauhinia forficataLink subsp.pruinosa(BF) tea on oxidative stress and liver damage in streptozotocin (STZ)-induced diabetic mice. Diabetic male mice have remained 30 days without any treatment. BF treatment started on day 31 and continued for 21 days as a drinking-water substitute. We evaluated (1) BF chemical composition; (2) glucose levels; (3) liver/body weight ratio and liver transaminases; (4) reactive oxygen species (ROS), lipid peroxidation, and protein carbonylation in liver; (5) superoxide dismutase (SOD) and catalase (CAT) activities in liver; (6)δ-aminolevulinate dehydratase (δ-ALA-D) and nonprotein thiols (NPSH) in liver; (7) Nrf2, NQO-1, and HSP70 levels in liver and pancreas. Phytochemical analyses identified four phenols compounds. Diabetic mice present high levels of NQO-1 in pancreas, increased levels of ROS and lipid peroxidation in liver, and decrease in CAT activity. BF treatment normalized all these parameters. BF did not normalize hyperglycemia, liver/body weight ratio, aspartate aminotransferase, protein carbonyl, NPSH levels, andδ-ALA-D activity. The raised oxidative stress seems to be a potential mechanism involved in liver damage in hyperglycemic conditions. Our results indicated that BF protective effect could be attributed to its antioxidant capacity, more than a hypoglycemic potential.

scholarly journals Failure of the Brain Glucagon-Like Peptide-1-Mediated Control of Intestinal Redox Homeostasis in a Rat Model of Sporadic Alzheimer’s Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1118
Author(s):  
Jan Homolak ◽  
Ana Babic Perhoc ◽  
Ana Knezovic ◽  
Jelena Osmanovic Barilar ◽  
Melita Salkovic-Petrisic
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Redox Homeostasis ◽  
Brain State ◽  
Gastrointestinal Hormone ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

The gastrointestinal system may be involved in the etiopathogenesis of the insulin-resistant brain state (IRBS) and Alzheimer’s disease (AD). Gastrointestinal hormone glucagon-like peptide-1 (GLP-1) is being explored as a potential therapy as activation of brain GLP-1 receptors (GLP-1R) exerts neuroprotection and controls peripheral metabolism. Intracerebroventricular administration of streptozotocin (STZ-icv) is used to model IRBS and GLP-1 dyshomeostasis seems to be involved in the development of neuropathological changes. The aim was to explore (i) gastrointestinal homeostasis in the STZ-icv model (ii) assess whether the brain GLP-1 is involved in the regulation of gastrointestinal redox homeostasis and (iii) analyze whether brain-gut GLP-1 axis is functional in the STZ-icv animals. Acute intracerebroventricular treatment with exendin-3(9-39)amide was used for pharmacological inhibition of brain GLP-1R in the control and STZ-icv rats, and oxidative stress was assessed in plasma, duodenum and ileum. Acute inhibition of brain GLP-1R increased plasma oxidative stress. TBARS were increased, and low molecular weight thiols (LMWT), protein sulfhydryls (SH), and superoxide dismutase (SOD) were decreased in the duodenum, but not in the ileum of the controls. In the STZ-icv, TBARS and CAT were increased, LMWT and SH were decreased at baseline, and no further increment of oxidative stress was observed upon central GLP-1R inhibition. The presented results indicate that (i) oxidative stress is increased in the duodenum of the STZ-icv rat model of AD, (ii) brain GLP-1R signaling is involved in systemic redox regulation, (iii) brain-gut GLP-1 axis regulates duodenal, but not ileal redox homeostasis, and iv) brain-gut GLP-1 axis is dysfunctional in the STZ-icv model.

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

scholarly journals Local and systemic oxidative stress in chronic suppurative otitis media

2021 ◽  
pp. 148-156
Author(s):  
I. D. Dubinets ◽  
M. Yu. Korkmazov ◽  
A. I. Sinitskii ◽  
E. I. Danshova ◽  
I. N. Skirpichnikov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Surgical Treatment ◽  
Temporal Bone ◽  
Otitis Media ◽  
Local Level ◽  
Chronic Suppurative Otitis Media ◽  
Suppurative Otitis Media ◽  
Lipid Peroxidation Products ◽  
Systemic Level

Introduction. According to the literature, oxidative stress is described as one of the main factors in the pathogenesis of chronic suppurative otitis media, supporting the inflammatory process at the local level. The transition of inflammatory mediators to the systemic level is associated with the risk of developing ear purulent-destructive complications. The study of the products of lipid peroxidation in comparison with morphological changes in the structures of the temporal bone will justify the tactics of the operation.Aim. Comparison of the levels of lipid peroxidation products at the local and systemic levels in chronic suppurative otitis media, depending on the nature of pathomorphological changes in the structures of the temporal bone.Materials and methods. A prospective study of 130 patients with chronic suppurative otitis media at the age of 20-62 years with a verified diagnosis of chronic suppurative otitis media, admitted for surgical treatment, was carried out. To study the indicators of oxidative stress at the systemic level, the blood serum of patients was used; at the local level, the bone biomaterial obtained from patients during the surgical treatment of chronic suppurative otitis media was used. The quantitative determination of the primary, secondary and final products of peroxidation was carried out in the groups of patients with separate registration of lipoperoxides in the heptane and isopropanol phases of the lipid extract by spectrophotometry.Results and discussion. In the observation of patients with morphological signs of purulent destruction of the temporal bone, not only a local level of inflammation activity, but also a systemic level of an unfavorable outcome was revealed in two variants: osteoproliferation or osteonecrosis of the bone tissue of the temporal bone in chronic purulent otitis media with a constant threat to the patient's life due to intracranial purulent complications.Conclusion. The appearance in low concentrations of lipid peroxidation products in serum in patients with chronic purulent otitis media substantiates the need for a behind-the-ear approach in reconstructive-sanitizing otosurgery even with minimal clinical manifestations and CT scan data, since at the preclinical level it confirms the osteonecrotic type of bone remodeling with the risk of delayed death.

Butylated hydroxyanisole alleviates ferric nitrilotriacetate induced nephrotoxicity in rats by abrogation of oxidative stress

2013 ◽  
Vol 3 (2) ◽  
pp. 65-70
Author(s):  
Sabah Ansar ◽  
Mohammad Iqbal ◽  
Noura Al Jameil
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Antioxidant Enzymes ◽  
Control Group ◽  
Butylated Hydroxyanisole ◽  
Chemopreventive Agent ◽  
Microsomal Lipid Peroxidation ◽  
Hydrogen Peroxide Generation

In this study the effect of butylated hydroxyanisole (BHA), a phenolic antioxidantused in food on Ferric‐Nitrilotriacetate (Fe–NTA) induced nephrotoxicity is reported. Fe‐NTA (9 mg Fe/kg body weight, intraperitoneally) treatment enhanced the renal microsomal lipid peroxidation and hydrogen peroxide generation to ~2‐2.5 folds compared to saline‐treated control and glutathione levels and the activities of antioxidant enzymes decreased to a range of 2–2.5 fold in kidney. These changes were reversed significantly in animals receiving a pretreatment of BHA. Pretreatment with BHA prior to Fe‐ NTA treatment reduced microsomal lipid peroxidation and hydrogen peroxide generation to 1.3‐1.5 fold compared to control group and glutathione and the activities of antioxidant enzymes increased to a range of 1.5‐2 folds in kidney. Fe‐NTA administration enhanced value of blood urea nitrogen and creatinine to 3.7 and 2.5 fold respectively as compared to their corresponding control group. Administration of Fe‐NTA to rats receiving a pretreatment of BHA led to a significant diminution in both of these values. The results indicate that BHA is a potent chemopreventive agent and suppresses Fe‐NTA induced nephrotoxicity in rats.

scholarly journals Reversal of age-associated oxidative stress in mice by PFT, a novel kefir product

2020 ◽  
Vol 34 ◽  
pp. 205873842095014
Author(s):  
Mamdooh Ghoneum ◽  
Shaymaa Abdulmalek ◽  
Deyu Pan
Keyword(s):  
Oxidative Stress ◽  
Low Density Lipoprotein ◽  
Redox Homeostasis ◽  
Density Lipoprotein ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Age Related ◽  
Total Antioxidant ◽  
The Brain

Introduction: Oxidative stress is a key contributor to aging and age-related diseases. In the present study, we examine the protective effects of PFT, a novel kefir product, against age-associated oxidative stress using aged (10-month-old) mice. Methods: Mice were treated with PFT orally at a daily dose of 2 mg/kg body weight over 6 weeks, and antioxidant status, protein oxidation, and lipid peroxidation were studied in the brain, liver, and blood. Results: PFT supplementation significantly reduced the oxidative stress biomarkers malondialdehyde (MDA) and nitric oxide; reversed the reductions in glutathione (GSH) levels, total antioxidant capacity (TAC), and anti-hydroxyl radical (AHR) content; enhanced the antioxidant enzyme activities of glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD); inhibited the liver enzyme levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT); significantly reduced triglyceride (TG), total cholesterol (TC), and low density lipoprotein (LDL) levels; and significantly elevated high density lipoprotein (HDL) levels. Interestingly, PFT supplementation reversed the oxidative changes associated with aging, thus bringing levels to within the limits of the young control mice in the brain, liver, and blood. We also note that PFT affects the redox homeostasis of young mice and that it is corrected post-treatment with PFT. Conclusion: Our findings show the effectiveness of dietary PFT supplementation in modulating age-associated oxidative stress in mice and motivate further studies of PFT’s effects in reducing age-associated disorders where free radicals and oxidative stress are the major cause.

Antioxidant Responses and Lipid Peroxidation of Penaeus Indicus Postlarvae Subjected to Sublethal Copper Exposure

Crustaceana ◽  
2011 ◽  
Vol 84 (10) ◽  
pp. 1197-1210 ◽  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Copper Toxicity ◽  
Sod Activity ◽  
Lipid Peroxidation Products ◽  
Coastal Marine ◽  
Potential Biomarker ◽  
Penaeus Indicus

AbstractThe objective of this study was to determine the effect of sublethal copper concentrations on certain antioxidant enzymes and lipid peroxidation products in the postlarvae (PL) of Penaeus indicus when subjected to short- and long-term exposure in the laboratory. The PL of P. indicus were exposed to 0.1641 ppm (sublethal) copper for a period of 30 days along with a parallel control. Sampling was carried out at six different time intervals, i.e., 24, 48, and 96 hrs (shortterm), and 10, 20, and 30 days (long-term). Variations in the activity of the antioxidant enzymes, namely, catalase (CAT) and superoxide dismutase (SOD), as well as lipid peroxidation products (LPP) were measured as biomarkers of metal toxicity. Our results showed a significant (P < 0.05) increase in LPP (indicating oxidative stress) and CAT activity (indicating an adaptive response of the PL for protection against oxidative stress) in the exposed PL for all periods of exposure. However, SOD activity significantly (P < 0.05) decreased on 20 and 30 days exposure, indicating susceptibility of the PL to oxidative stress upon long-term exposure. Therefore, CAT can serve as a better biomarker of oxidative stress than SOD to long-term copper toxicity. Our results indicate that copper contamination causes oxidative stress even at sublethal doses in Penaeus indicus PL, which can thus be used as a potential biomarker of copper toxicity for long-term monitoring of coastal marine ecosystems.

The effects of oral glutamine on cyclophosphamide-induced nephrotoxicity in rats

2010 ◽  
Vol 30 (7) ◽  
pp. 616-623 ◽  
Author(s):  
Premila Abraham ◽  
Bina Isaac
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Renal Damage ◽  
Neutrophil Infiltration ◽  
Protein Carbonyl ◽  
Male Rats ◽  
Glutathione Depletion ◽  
Myeloperoxidase Activity ◽  
Protein Carbonyl Content

Nephrotoxicity is one of the adverse side effects of cyclophosphamide (CP) chemotherapy. In a recent study, we have demonstrated that oxidative stress and glutathione depletion play important roles in CP-induced renal damage. The aim of the study was to verify whether glutamine, the precursor for glutathione synthesis, prevents CP-induced oxidative stress and renal damage using a rat model. Adult male rats were administered a single dose of 150 mg/ kg body weight of CP intraperitoneally. The glutamine-pretreated rats were administered 1 gm/kg body weight of glutamine orally 2 h before the administration of CP. Vehicle/glutaminetreated rats served as controls. All the rats were killed 16 h after the dose of CP/vehicle. The kidneys were removed and used for light microscopic and biochemical studies. The markers of oxidative stress including malondialdehyde content, protein carbonyl content, protein thiol, reduced glutathione and myeloperoxidase activity, a marker of neutrophil infiltration, were measured in kidney homogenates. CP treatment-induced damage to kidney involved the glomeruli and the tubules. Pretreatment with glutamine reduced CP-induced glutathione depletion and increased myeloperoxidase activity. However, it did not prevent CP-induced lipid peroxidation, protein carbonylation and renal damage. The results of the present study suggest that glutamine pretreatment does not prevent CP-induced lipid peroxidation and renal damage, although it prevents CP-induced glutathione depletion and neutrophil infiltration significantly. It is suggested that mechanisms other than oxidative stress may also be involved and/or oxidative stress may be consequence and not the cause of CP induced renal damage.

Application of lipid peroxidation products as biomarkers for flutamide-induced oxidative stress in vitro

2015 ◽  
Vol 238 (3) ◽  
pp. 53-59 ◽  
Author(s):  
Marieke Teppner ◽  
Franziska Böss ◽  
Beat Ernst ◽  
Axel Pähler
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Peroxidation Products
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