Pipecolic acid induces oxidative stress in vitro in cerebral cortex of young rats and the protective role of lipoic acid

2013 ◽  
Vol 29 (1) ◽  
pp. 175-183 ◽  
Author(s):  
Giovana Reche Dalazen ◽  
Melaine Terra ◽  
Carlos Eduardo Diaz Jacques ◽  
Juliana G. Coelho ◽  
Raylane Freitas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Cortex ◽  
Lipoic Acid ◽  
Protective Role ◽  
Pipecolic Acid ◽  
Young Rats

scholarly journals A Protective Role of Paeoniflorin in Fluctuant Hyperglycemia-Induced Vascular Endothelial Injuries through Antioxidative and Anti-Inflammatory Effects and Reduction of PKCβ1

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jing-Shang Wang ◽  
Ye Huang ◽  
Shuping Zhang ◽  
Hui-Jun Yin ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Umbilical Vein ◽  
Protective Role ◽  
Vascular Endothelial ◽  
Glucose Levels ◽  
Umbilical Vein Endothelial Cells

Hyperglycemia fluctuation is associated with diabetes mellitus (DM) complications when compared to persistent hyperglycemia. Previous studies have shown that paeoniflorin (PF), through its antiapoptosis, anti-inflammation, and antithrombotic properties, effectively protects against cardiovascular and cerebrovascular disease. However, the mechanism underlying the protection from PF against vascular injuries induced by hyperglycemia fluctuations remains poorly understood. Herein, we investigated the potential protective role of PF on human umbilical vein endothelial cells (HUVECs) subjected to intermittent glucose levels in vitro and in DM rats with fluctuating hyperglycemia in vivo. A remarkable increased apoptosis associated with elevated inflammation, increased oxidative stress, and high protein level of PKCβ1 was induced in HUVECs by intermittently changing glucose for 8 days, and PF recovered those detrimental changes. LY333531, a potent PKCβ1 inhibitor, and metformin manifested similar effects. Additionally, in DM rats with fluctuating hyperglycemia, PF protected against vascular damage as what has been observed in vitro. Taken together, PF attenuates the vascular injury induced by fluctuant hyperglycemia through oxidative stress inhibition, inflammatory reaction reduction, and PKCβ1 protein level repression, suggesting its perspective clinical usage.

scholarly journals The Protective Role of Prenatal Alpha Lipoic Acid Supplementation against Pancreatic Oxidative Damage in Offspring of Valproic Acid-Treated Rats: Histological and Molecular Study

Biology ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 239
Author(s):  
Fatma M. Ghoneim ◽  
Hani Alrefai ◽  
Ayman Z. Elsamanoudy ◽  
Salwa M. Abo El-khair ◽  
Hanaa A. Khalaf
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Lipoic Acid ◽  
Caspase 3 ◽  
Protective Role ◽  
Alpha Lipoic Acid ◽  
Group Iii ◽  
Rat Offspring ◽  
Group I

Background: Sodium valproate (VPA) is an antiepileptic drug (AED) licensed for epilepsy and used during pregnancy in various indications. Alpha-lipoic acid (ALA) is a natural compound inducing endogenous antioxidant production. Our study aimed to investigate the effect of prenatal administration of VPA on the pancreas of rat offspring and assess the potential protective role of ALA co-administration during pregnancy. Methods: Twenty-eight pregnant female albino rats were divided into four groups: group I (negative control), group II (positive control, ALA treated), group III (VPA-treated), and group IV (VPA-ALA-treated). The pancreases of the rat offspring were removed at the fourth week postpartum and prepared for histological, immune-histochemical, morphometric, molecular, and oxidative stress marker studies. Results: In group III, there were pyknotic nuclei, vacuolated cytoplasm with ballooning of acinar, α, and β cells of the pancreas. Ultrastructural degeneration of cytoplasmic organelles was detected. Additionally, there was a significant increase in oxidative stress, a decrease in insulin-positive cell percentage, and an increase in glucagon positive cells in comparison to control groups. Moreover, VPA increased the gene expression of an apoptotic marker, caspase-3, with a decrease in anti-apoptotic Bcl2 and nuclear factor erythroid 2-related factor 2 (Nrf2) transcriptional factor. Conversely, ALA improved oxidative stress and apoptosis in group VI, and a consequent improvement of the histological and ultrastructure picture was detected. Conclusion: ALA co-administration with VPA significantly improved the oxidative stress condition, histological and morphometric picture of the pancreas, and restored normal expression of related genes, including Nrf2, caspase-3, and Bcl-2. Administration of α-lipoic acid has a protective effect against VPA-induced pancreatic oxidative damage via its cytoprotective antioxidant effect.

scholarly journals Manganese Induces Oxidative Stress, Redox State Unbalance and Disrupts Membrane Bound ATPases on Murine Neuroblastoma Cells In Vitro: Protective Role of Silymarin

2011 ◽  
Vol 36 (8) ◽  
pp. 1546-1557 ◽  
Author(s):  
Yassine Chtourou ◽  
Khaled Trabelsi ◽  
Hamadi Fetoui ◽  
Ghada Mkannez ◽  
Héla Kallel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Redox State ◽  
Neuroblastoma Cells ◽  
Protective Role ◽  
Murine Neuroblastoma ◽  
Membrane Bound

scholarly journals The antioxidant effects of melatonin in blood platelets during exposure to electromagnetic radiation – an in vitro study

2021 ◽  
Vol 75 (1) ◽  
pp. 889-895
Author(s):  
Małgorzata Lewicka ◽  
Magdalena Zawadzka ◽  
Gabriela Henrykowska ◽  
Maciej Rutkowski ◽  
Andrzej Buczyński
Keyword(s):  
Oxidative Stress ◽  
Electromagnetic Radiation ◽  
Blood Platelets ◽  
In Vitro Study ◽  
Oxygen Metabolism ◽  
Protective Role ◽  
Negative Effect ◽  
Antioxidant Effects

Abstract Objectives The article presents the results of an in vitro study aimed at identifying changes in parameters of oxidative stress – concentration of malondialdehyde (MDA), enzymatic activity of superoxide dismutase (SOD-1) and protective antioxidant role of melatonin (MLT) during the exposure of blood platelets to electromagnetic radiation (EMR) emitted by monitors. Methods Platelets were exposed to an EMR for 30- and 60 min. generated by monitors (1 kHz frequency, 220 V/m intensity). In each sample the level of SOD-1 activity and concentration of MDA were determined. Results The MDA concentration increased significantly after 30-and 60-min. irradiation, as compared to control values (2.53 vs 1.36; 3.64 vs 1.36 nmol/109 blood platelets) and after the addition of MLT it decreased (2.53 vs 1.55; 3.64 vs 1.12 nmol/109 blood platelets). The activity of SOD-1 increased significantly compared to control values after 30 min. and 60 min. of exposure to EMR (1.97vs 0.75; 2.08 vs 0.75 U/g of protein), and significantly decreased after the addition of MLT only in samples exposed for 60 min. (2.08 vs 0.95 U/g of protein). Discussion The results demonstrated the possibly negative effect of EMR on oxygen metabolism of blood platelets and indicated a possible protective role of melatonin in this process.

scholarly journals Dexmedetomidine Attenuates Orthotopic Liver Transplantation-Induced Acute Gut Injury via α2-Adrenergic Receptor-Dependent Suppression of Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Peibiao Lv ◽  
Tufeng Chen ◽  
Peibin Liu ◽  
Lei Zheng ◽  
Jingling Tian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Transplantation ◽  
Orthotopic Liver Transplantation ◽  
Adrenergic Receptor ◽  
Protective Role ◽  
Intestinal Injury ◽  
Protective Effects ◽  
Barrier Dysfunction

Patients with orthotopic liver transplantation (OLT) frequently develop acute gut injury (AGI), and dexmedetomidine (Dex) has been reported to exert a protective effect against AGI. We investigated whether Dex protects against AGI through antioxidative stress effects by the Nrf2/HO-1 antioxidative signaling pathway. Rats were randomly allocated into a sham group and six orthotopic autologous liver transplantation (OALT) groups receiving different doses of Dex together with/without α2-adrenergic receptor (AR) blockers. Intestinal tissues were collected to visualize the barrier damage and to measure the indexes of oxidative stress. For in vitro studies, rat intestinal recess epithelial cells (IEC-6) underwent hypoxia/reoxygenation (H/R), and the protective role of Dex was evaluated after α2A-AR siRNA silencing. OALT resulted in increased oxidative stress, significant intestinal injury, and barrier dysfunction. Dex attenuated OALT-induced oxidative stress and intestinal injury, which was abolished by the pretreatment with the nonspecific α2A-AR siRNA blocker atipamezole and the specific α2A-AR siRNA blocker BRL-44408, but not by the specific 2B/C-AR siRNA blocker ARC239. Silencing of α2A-AR siRNA also attenuated the protective role of Dex on alleviating oxidative stress in IEC-6 cells subjected to H/R. Dex exerted its protective effects by activating Nrf2/HO-1 antioxidative signaling. Collectively, Dex attenuates OALT-induced AGI via α2A-AR-dependent suppression of oxidative stress, which might be a novel potential therapeutic target for OALT-induced AGI.

Boron Compounds Counteracts Oxidative Stress Mediated Genotoxicity Induced by Fe3O4 Nanoparticles In Vitro

2016 ◽  
Vol 835 ◽  
pp. 84-90 ◽  
Author(s):  
Hasan Türkez ◽  
Erdal Sönmez ◽  
Abdulgani Tatar
Keyword(s):  
Oxidative Stress ◽  
Boric Acid ◽  
Antioxidant Capacity ◽  
Blood Cells ◽  
Defense Mechanisms ◽  
Human Lymphocytes ◽  
Protective Role ◽  
Boron Compounds

Due to rapid growing of nanotechnology, it is currently being used in many areas including biotechnology, electronics, drug delivery systems, cosmetics, material science and biosensors. Oxidative stress is considered as main cause behind the toxicity of nanoparticles (NPs). Recent reports indicate that boron is effective in protecting cells or organisms against oxidative damages by enhancing antioxidant defense mechanisms. However, protective role of boron compounds in nanotoxicity is not investigated yet. Therefore we assessed the potential protective role of boric acid (BA) and borax (BX) against the toxic responses of nano-Fe3O4 particles (IO NPs) in cultured human whole blood cells. Our results showed that IO NPs induced genotoxicity in human lymphocytes demonstrated by sister chromatid exchange (SCE) and 8-hydroxy-2′-deoxyguanosine (8-OH-dG) assays. Again, IO NPs caused decreases of total antioxidant capacity (TAC) and decreases of total oxidative stress (TOS) levels in vitro. Co-application of boric acid and borax (2.5 to 10 ppm) into the cell cultures significantly ameliorated genotoxicity and oxidative stress caused by IO NPs. In a conclusion, this study is the first report revealing that BA and BX significantly protected human blood cells from the toxicity of IO NPs, which is mediated through the generation of oxidative stress and depletion of antioxidant capacity.

Modulatory role of lipoic acid on lipopolysaccharide-induced oxidative stress in adult rat Sertoli cells in vitro

2009 ◽  
Vol 182 (2-3) ◽  
pp. 112-118 ◽  
Author(s):  
Hamdy A.A. Aly ◽  
David A. Lightfoot ◽  
Hany A. El-Shemy
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Sertoli Cells ◽  
Adult Rat

scholarly journals Oxidative Stress in Graves Disease and Graves Orbitopathy

2020 ◽  
Vol 9 (Suppl. 1) ◽  
pp. 40-50
Author(s):  
Giulia Lanzolla ◽  
Claudio Marcocci ◽  
Michele Marinò
Keyword(s):  
Oxidative Stress ◽  
Clinical Studies ◽  
Therapeutic Option ◽  
Protective Role ◽  
Beneficial Effects ◽  
Antioxidant Agents ◽  
Graves Orbitopathy

Oxidative stress is involved in the pathogenesis of Graves hyperthyroidism (GH) and Graves orbitopathy (GO) and an antioxidant approach has been proposed for both. In GH, a disbalance of the cell redox state is associated with thyroid hyperfunction and antithyroid medications may reduce oxidative stress. Tissue hypoxia participates in the pathogenesis of GO, and oxygen free radicals are involved in the typical changes of orbital tissues as reported by in vitro and clinical studies. Antioxidant agents, especially selenium, have been proposed as a therapeutic option for GH and GO. A clinical study regarding the use of selenium in mild GO has provided evidence for a beneficial effect in the short term, even though its beneficial effects in the long term are still to be investigated. In addition to selenium, a protective role of other antioxidant agents, i.e., quercetin, enalapril, vitamin C, <i>N</i>-acetyl-L-cysteine and melatonin has been suggested by in vitro studies, although clinical studies are lacking. Here, we review the role of oxidative stress and antioxidant agents in GH and GO.

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