scholarly journals The influence of natural dicarbonils on the antioxidant enzymes activity in vitro and in vivo

2012 ◽  
Vol 58 (6) ◽  
pp. 727-736 ◽  
Author(s):  
V.Z. Lankin ◽  
G.G. Konovalova ◽  
A.K. Tikhaze ◽  
L.V. Nedosugova
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Antioxidant Enzymes ◽  
Carbonyl Stress ◽  
Diabetic Patients ◽  
Glutathione S Transferase ◽  
Liver Glutathione ◽  
Bovine Erythrocytes

Natural dicarbonyls, which may be accumulated during oxidative stress in atherosclerosis (e.g. malondialdehyde) or carbonyl stress in diabetes mellitus (glyoxal and methylglyoxal) effectively inhibited the activities of commercial preparations of antioxidant enzymes: catalase, Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and Se-contained glutathione peroxidase from human and bovine erythrocytes and also rat liver glutathione-S-transferase. After incubation of human erythrocytes with 10 mM of each investigated dicarbonyls the decrease of intracellular Cu,Zn-SOD was observed. The decreased activity of erythrocyte Cu,Zn-SOD was also detected in diabetic patients with carbohydrate metabolism disturbance but effective sugar-lowered therapy was accompanied by the increase of this enzyme activity. The increase of erythrocytes activity of Cu,Zn-SOD of diabetic patients theated with metformin (which may utilize methylglyoxal) was higher than in erythrocytase of diabetic patients subjected to traditional therapy.

Abstract 460: Characterization of Glycated Albumin Isolated From Poorly Controlled Diabetic Patients and Its Role in Macrophage Cholesterol Efflux

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Adriana Machado-Lima ◽  
Erika R Oliveira ◽  
Rodrigo T Iborra ◽  
Gabriela Castilho ◽  
Edna R Nakandakare ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Cholesterol Efflux ◽  
Glycated Albumin ◽  
Maldi Mass Spectrometry ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Macrophage Cholesterol Efflux

Advanced glycation end products (AGE) are elevated in diabetes mellitus (DM) and predict the development of atherosclerosis. In vitro produced AGE-albumin induces oxidative stress that is linked to the reduction in ABCA-1 levels and cholesterol efflux mediated by apo A-I and HDL-subfractions, leading to macrophage cholesterol accumulation. We characterized the glycation level/profile of human serum albumin (HSA) isolated by fast protein liquid chromatography from poorly controlled type 1 (DM1) and type 2 (DM2) diabetes mellitus patients (HbA1c > 8%) in comparison to control (C) individuals, and how these AGE-albumin can interfere in macrophage lipid accumulation. The glycation level of HSA from C, DM1 and DM2 was analyzed by MALDI mass spectrometry and was similar between DM1 and DM2-HSA. An increased mean mass was observed in DM1-HSA (68,544 ± 192 Da; n=6) and DM2-HSA (68,547 ± 132 Da; n=6) compared to C-HSA (67,846 ± 301 Da; n=6), reflecting the condensation of at least 8 and 5 units of glucose, respectively. The tryptic digestion of C-HSA generated a number of peptide species higher than those originated from DM1 and DM2-HSA. Macrophages isolated from peritoneal wild-type mice were treated for 18 h with C, DM1 or DM2-HSA in order to measure the 14C-cholesterol efflux and the mRNA expression of NOX-4 (NADPHoxidase4), ABCA-1 (Abca1) and ABCG-1 (Abcg1). Data were compared by one-way ANOVA and Dunnet′s post test. In comparison to cells treated with C-HSA the expression of NADPHoxidase4 (p<0.05; n=3) mRNA was increased after cell treatment with DM1 (3.2x) and DM2-HSA (0.7x), confirming oxidative stress. Abcg1 mRNA was reduced by DM2-HSA (26%; p<0.05; n=3); Abca1 mRNA was unchanged but ABCA-1 protein content was greatly reduced (82 and 25%, respectively in DM1 and DM2-HAS; p<0.05; n=12). The % of apo A-I mediated cholesterol efflux was impaired in DM1 (1.3 ± 0.3) and DM2-HSA-treated cells (2.4 ± 0.5) as compared to C-HSA (4.4 ± 0.5; n= 5; p<0.05). The level of advanced glycation that takes place in vivo was similar between DM1 and DM2-HSA and induced macrophage oxidative stress and impairment in cholesterol efflux that may contribute to atherogenesis in DM. Funding: FAPESP, Brazil (2012/19112-0)

scholarly journals The Functionality of Endothelial-Colony-Forming Cells from Patients with Diabetes Mellitus

Cells ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 1731
Author(s):  
Caomhán J. Lyons ◽  
Timothy O'Brien
Keyword(s):  
Diabetes Mellitus ◽  
Cell Therapy ◽  
Diabetic Patients ◽  
Angiogenic Potential ◽  
Endothelial Colony Forming Cells ◽  
Allogeneic Cell Therapy ◽  
Patients With Diabetes ◽  
Pre Treatment

Endothelial-colony-forming cells (ECFCs) are a population of progenitor cells which have demonstrated promising angiogenic potential both in vitro and in vivo. However, ECFCs from diabetic patients have been shown to be dysfunctional compared to ECFCs from healthy donors. Diabetes mellitus itself presents with many vascular co-morbidities and it has been hypothesized that ECFCs may be a potential cell therapy option to promote revascularisation in these disorders. While an allogeneic cell therapy approach would offer the potential of an ‘off the shelf’ therapeutic product, to date little research has been carried out on umbilical cord-ECFCs in diabetic models. Alternatively, autologous cell therapy using peripheral blood-ECFCs allows the development of a personalised therapeutic approach to medicine; however, autologous diabetic ECFCs are dysfunctional and need to be repaired so they can effectively treat diabetic co-morbidities. Many different groups have modified autologous diabetic ECFCs to improve their function using a variety of methods including pre-treatment with different factors or with genetic modification. While the in vitro and in vivo data from the literature is promising, no ECFC therapy has proceeded to clinical trials to date, indicating that more research is needed for a potential ECFC therapy in the future to treat diabetic complications.

scholarly journals P38 Initiates Diabetic Neurodegeneration Through Glutamatergic and GABAergic Neurons

2020 ◽  
Author(s):  
Aisan Farhadi ◽  
Mehdi Totonchi ◽  
Seyed Masood Nabavi ◽  
Hossein Baharvand ◽  
Hossein Pakdaman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Diabetic Mouse ◽  
Gabaergic Neurons ◽  
Expression Data ◽  
Tau Pathology

Abstract Background: Diabetes mellitus may cause neurodegeneration, but the exact mechanism by which diabetic conditions induce neuronal cell death remains unclear. Tau protein hyperphosphorylation is considered to be a major pathological hallmark of neurodegeneration and can be triggered by diabetes. Various tau-directed kinases, including P38, can be activated upon diabetic stress and induce tau hyperphosphorylation. Despite extensive research efforts and the known importance of tau pathology in neurodegeneration, the exact tau specie(s) and kinases driving neurodegeneration in diabetes mellitus have not been clearly elucidated. Methods: We herein employed protein expression data analysis as well as immunofluorescence and immunoblotting techniques to determine the exact molecular mechanism of tau pathology triggered by diabetes in both in vitro and in vivo systems.Results: We found that P38, a major tau kinase, was increased in Glutamatergic & GABAergic neuron subtypes under diabetic conditions. This rendered them more responsive to oxidative stress caused by diabetes. We observed that oxidative stress activated P38, which in turn directly and indirectly drove tau pathology in the brainstem (enriched by Glutamatergic & GABAergic neurons), which gradually spread to neighboring brain areas. Notably, P38 inhibition suppressed tau pathogenicity and neurodegeneration in diabetic mouse models. Conclusion: The data establish P38 as a central mediator of diabetes mellitus induced tau pathology. Furthermore, the inhibition of P38 at early stages of diabetes-induced stress can inhibit tau pathology. Our findings provide mechanistic insight on the consequences of this metabolic disorder on the nervous system.

scholarly journals S-glutathionylation: relevance in diabetes and potential role as a biomarker

2013 ◽  
Vol 394 (10) ◽  
pp. 1263-1280 ◽  
Author(s):  
Francisco J. Sánchez-Gómez ◽  
Cristina Espinosa-Díez ◽  
Megha Dubey ◽  
Madhu Dikshit ◽  
Santiago Lamas
Keyword(s):  
Oxidative Stress ◽  
Vascular Complications ◽  
Redox Balance ◽  
Diabetic Patients ◽  
Sulfenic Acid ◽  
Diabetic Vascular Complications ◽  
Main Regulator ◽  
Species Production

Abstract Glutathione is considered the main regulator of redox balance in the cellular milieu due to its capacity for detoxifying deleterious molecules. The oxidative stress induced as a result of a variety of stimuli promotes protein oxidation, usually at cysteine residues, leading to changes in their activity. Mild oxidative stress, which may take place in physiological conditions, induces the reversible oxidation of cysteines to sulfenic acid form, while pathological conditions are associated with higher rates of reactive oxygen species production, inducing the irreversible oxidation of cysteines. Among these, neurodegenerative disorders, cardiovascular diseases and diabetes have been proposed to be pathogenetically linked to this state. In diabetes-associated vascular complications, lower levels of glutathione and increased oxidative stress have been reported. S-glutathionylation has been proposed as a posttranslational modification able to protect proteins from over-oxidizing environments. S-glutathionylation has been identified in proteins involved in diabetic models both in vitro and in vivo. In all of them, S-glutathionylation represents a mechanism that regulates the response to diabetic conditions, and has been described to occur in erythrocytes and neutrophils from diabetic patients. However, additional studies are necessary to discern whether this modification represents a biomarker for the early onset of diabetic vascular complications.

scholarly journals Neural Oxidant-stress by Azadirachtin Induces Anti-oxidative Enzymes Evincing Biomarker Potential in Paddy Pest, Spathosternum prasiniferum prasiniferum (Orthoptera:Acridoidea)

2019 ◽  
pp. 1-10
Author(s):  
Balaram Manna ◽  
Smarajit Maiti ◽  
Amlan Das
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Growth Regulation ◽  
Oxidant Stress ◽  
Oxidative Enzymes ◽  
Oxidative Stress Marker ◽  
Stress Marker ◽  
The Impact

Azadirachtin (C35H44O16/AZT) develops antifeedancy/growth-regulation/fecundity-suppression/ sterilization/oviposition/repellence and deformity in insect via biochemical/cellular changes and causes their death. Agricultural productivity/quality/eco-sustainability is concerned to this issue. ROS are cytotoxic-factors generated in invertebrates in stress-conditions. The present in-vivo/in-vitro study aimed to investigate the impact of dose dependant AZT toxicity on oxidative-stress-marker (alkaline-phosphatise/ALP; thiobarbituric-acid-reactive-substances/TBARS; non-protein-soluble-thiols/NPSH; acetyl-cholinesterase/AChE) and antioxidant-enzyme activity (superoxide-dismutase/SOD; catalase/CAT; glutathione-peroxidise/GPx; amylase) in brain/hemolymph of Spathosternum prasiniferum prasiniferum (Walker,1871) (Orthoptera:Acridoidea). Acridids are highly abundant and bio-indicator of grassland-ecosystem. During cultivation, insects are exposed (dose/time dependant) to AZT. AZT developed restlessness, jerky-movements and swarming-movements in the insects. It promoted oxidative-stress-marker in brain/hemolymphin both sexes but female had significantly stimulated antioxidant-enzymes to overcome cellular-stress. Increase of brain TBARS, antioxidant-enzymes and decrease in NPSH by AZT indicates oxidative-stress induction in this species. In several instances damage to the brain DNA was noticed. In general female insect responded more intensely with some prominent adaptive strategies.

scholarly journals Antioxidant Activity of Pigmented Rice and Impact on Health

JURNAL PANGAN ◽  
2019 ◽  
Vol 28 (1) ◽  
pp. 11-22
Author(s):  
Arfina Sukmawati Arifin
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Antioxidant Activity ◽  
Vascular Function ◽  
Healthy Lifestyle ◽  
Cell Damage ◽  
The Body ◽  
Food Sources

The high number of free radicals that are not balanced with the amount of antioxidants in the body triggers oxidative stress. Oxidative stress causes impaired vascular function, damage to proteins and lipids in membrane cell, and nucleic acid (DNA) mutations. Chronic cell damage has a negative effect on tissue that triggers various diseases such as neurodegenerative diseases (Alzheimer's, Parkinson's), cardiovascular diseases (hypertension, arteriosclerosis, and others), cataracts, retinal damage, maculopathy, rheumatoid arthritis, asthma, stroke, diabetes mellitus , immunodepression, cancer, aging, hyperoxia, dermatitis, and others. The application of a healthy lifestyle for example by consuming food sources of bioactive compounds can minimize health risks. Rice is the staple food of the Indonesian people. Some types of rice contain red and black pigments which are known to have high antioxidant activity compared to white rice. The pigment comes from anthocyanin and proanthocyanidin. Various studies in vitro and in vivo prove that anthocyanin and proantocyanidine act as antioxidants and potency as a preventative for various diseases such as cardiovascular, diabetes mellitus, and etc.

scholarly journals Polyphenols and Oxidative Stress in Atherosclerosis-Related Ischemic Heart Disease and Stroke

2017 ◽  
Vol 2017 ◽  
pp. 1-16 ◽  
Author(s):  
Yu-Chen Cheng ◽  
Jer-Ming Sheen ◽  
Wen Long Hu ◽  
Yu-Chiang Hung
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Heart Disease ◽  
Platelet Aggregation ◽  
Ischemic Heart Disease ◽  
Radical Scavenging ◽  
Ischemic Heart ◽  
Vsmc Proliferation

Good nutrition could maintain health and life. Polyphenols are common nutrient mainly derived from fruits, vegetables, tea, coffee, cocoa, mushrooms, beverages, and traditional medicinal herbs. They are potential substances against oxidative-related diseases, for example, cardiovascular disease, specifically, atherosclerosis-related ischemic heart disease and stroke, which are health and economic problems recognized worldwide. In this study, we reviewed the risk factors for atherosclerosis, including hypertension, diabetes mellitus, hyperlipidemia, obesity, and cigarette smoking as well as the antioxidative activity of polyphenols, which could prevent the pathology of atherosclerosis, including endothelial dysfunction, low-density lipoprotein oxidation, vascular smooth muscle cell proliferation, inflammatory process by monocytes, macrophages or T lymphocytes, and platelet aggregation. The strong radical-scavenging properties of polyphenols would exhibit antioxidative and anti-inflammation effects. Polyphenols reduce ROS production by inhibiting oxidases, reducing the production of superoxide, inhibiting OxLDL formation, suppressing VSMC proliferation and migration, reducing platelet aggregation, and improving mitochondrial oxidative stress. Polyphenol consumption also inhibits the development of hypertension, diabetes mellitus, hyperlipidemia, and obesity. Despite the numerousin vivoandin vitrostudies, more advanced clinical trials are necessary to confirm the efficacy of polyphenols in the treatment of atherosclerosis-related vascular diseases.

scholarly journals Neither Excessive Nitric Oxide Accumulation nor Acute Hyperglycemia Affects the N-Acetylaspartate Network in Wistar Rat Brain Cells

2020 ◽  
Vol 21 (22) ◽  
pp. 8541
Author(s):  
Marlena Zyśk ◽  
Piotr Pikul ◽  
Robert Kowalski ◽  
Krzysztof Lewandowski ◽  
Monika Sakowicz-Burkiewicz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Wistar Rat ◽  
Diabetic Patients ◽  
Mrna Levels ◽  
Male Adult ◽  
The Impact

The N-acetylaspartate network begins in neurons with N-acetylaspartate production catalyzed by aspartate N-acetyltransferase from acetyl-CoA and aspartate. Clinical studies reported a significant depletion in N-acetylaspartate brain level in type 1 diabetic patients. The main goal of this study was to establish the impact of either hyperglycemia or oxidative stress on the N-acetylaspartate network. For the in vitro part of the study, embryonic rat primary neurons were treated by using a nitric oxide generator for 24 h followed by 6 days of post-treatment culture, while the neural stem cells were cultured in media with 25–75 mM glucose. For the in vivo part, male adult Wistar rats were injected with streptozotocin (65 mg/kg body weight, ip) to induce hyperglycemia (diabetes model) and euthanized 2 or 8 weeks later. Finally, the biochemical profile, NAT8L protein/Nat8l mRNA levels and enzymatic activity were analyzed. Ongoing oxidative stress processes significantly affected energy metabolism and cholinergic neurotransmission. However, the applied factors did not affect the N-acetylaspartate network. This study shows that reduced N-acetylaspartate level in type 1 diabetes is not related to oxidative stress and that does not trigger N-acetylaspartate network fragility. To reveal why N-acetylaspartate is reduced in this pathology, other processes should be considered.

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