scholarly journals Metallothionein-I/II Knockout Mice Aggravate Mitochondrial Superoxide Production and Peroxiredoxin 3 Expression in Thyroid after Excessive Iodide Exposure

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Na Zhang ◽  
Lingyan Wang ◽  
Qi Duan ◽  
Laixiang Lin ◽  
Mohamed Ahmed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Urinary Iodine ◽  
In Vitro Study ◽  
Superoxide Production ◽  
Mitochondrial Oxidative Stress ◽  
Mitochondrial Superoxide ◽  
Iodine Level ◽  
Significant Difference

Purpose. We aim to figure out the effect of metallothioneins on iodide excess induced oxidative stress in the thyroid.Methods. Eight-week-old MT-I/II knockout (MT-I/II KO) mice and background-matched wild-type (WT) mice were used. Mitochondrial superoxide production and peroxiredoxin (Prx) 3 expression were measured.Results. In in vitro study, more significant increases in mitochondrial superoxide production and Prx 3 expression were detected in the MT-I/II KO groups. In in vivo study, significantly higher concentrations of urinary iodine level were detected in MT-I/II KO mice in 100 HI group. Compared to the NI group, there was no significant difference existing in serum thyroid hormones level in either groups (P>0.05), while the mitochondrial superoxide production was significantly increased in 100 HI groups with significantly increased LDH activity and decreased relative cell viability. Compared to WT mice, more significant changes were detected in MT-I/II KO mice in 100 HI groups. No significant differences were detected between the NI group and 10 HI group in both the MT-I/II KO and WT mice groups (P>0.05).Conclusions. Iodide excess in a thyroid without MT I/II protection may result in strong mitochondrial oxidative stress, which further leads to the damage of thyrocytes.

scholarly journals ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia

2016 ◽  
Vol 113 (43) ◽  
pp. E6669-E6678 ◽  
Author(s):  
Mark A. Gregory ◽  
Angelo D’Alessandro ◽  
Francesca Alvarez-Calderon ◽  
Jihye Kim ◽  
Travis Nemkov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Mitochondrial Oxidative Stress ◽  
Flt3 Inhibitor ◽  
A Genome ◽  
Flt3 Inhibitors ◽  
Acute Myeloid

Activating mutations in FMS-like tyrosine kinase 3 (FLT3) are common in acute myeloid leukemia (AML) and drive leukemic cell growth and survival. Although FLT3 inhibitors have shown considerable promise for the treatment of AML, they ultimately fail to achieve long-term remissions as monotherapy. To identify genetic targets that can sensitize AML cells to killing by FLT3 inhibitors, we performed a genome-wide RNA interference (RNAi)-based screen that identified ATM (ataxia telangiectasia mutated) as being synthetic lethal with FLT3 inhibitor therapy. We found that inactivating ATM or its downstream effector glucose 6-phosphate dehydrogenase (G6PD) sensitizes AML cells to FLT3 inhibitor induced apoptosis. Examination of the cellular metabolome showed that FLT3 inhibition by itself causes profound alterations in central carbon metabolism, resulting in impaired production of the antioxidant factor glutathione, which was further impaired by ATM or G6PD inactivation. Moreover, FLT3 inhibition elicited severe mitochondrial oxidative stress that is causative in apoptosis and is exacerbated by ATM/G6PD inhibition. The use of an agent that intensifies mitochondrial oxidative stress in combination with a FLT3 inhibitor augmented elimination of AML cells in vitro and in vivo, revealing a therapeutic strategy for the improved treatment of FLT3 mutated AML.

scholarly journals Protective Effect of Coconut Oil Meal Phenolic Antioxidants against Macromolecular Damage: In Vitro and In Vivo Study

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
A. N. Karunasiri ◽  
C. M. Senanayake ◽  
H. Hapugaswatta ◽  
N. Jayathilaka ◽  
K. N. Seneviratne
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Stress Responses ◽  
Coconut Oil ◽  
Oral Feeding ◽  
Phenolic Antioxidants ◽  
Significant Difference ◽  
Macromolecular Damage

Coconut oil meal, a cheap by-product of coconut oil production, is a rich source of phenolic antioxidants. Many age-related diseases are caused by reactive oxygen species- (ROS-) induced damage to macromolecules such as lipids, proteins, and DNA. In the present study, the protective effect of the phenolic extract of coconut oil meal (CMPE) against macromolecular oxidative damage was evaluated using in vitro and in vivo models. Sunflower oil, bovine serum albumin (BSA), and plasmid DNA were used in the in vitro study, and thiobarbituric acid reactive substances (TBARS), protein carbonyl, and nicked DNA were evaluated as oxidation products. The inhibitory effect of CMPE against H2O2-induced macromolecular damage was evaluated using cultured HEp-2 cells. The results indicate that CMPE inhibits macromolecular damage both in vitro and in vivo. In addition, CMPE regulates redox status of HEp-2 cells under oxidative stress conditions by maintaining higher reduced glutathione levels. There was no significant difference in the expression of glutathione peroxidase in stressed and unstressed cells suggesting that CMPE regulates the cellular oxidative stress responses without affecting the expression of oxidative stress response genes. Oral feeding of Wistar rats with CMPE improves the serum and plasma antioxidant status without causing any toxic effects.

scholarly journals Solid Lipid Nanoparticles of Myricitrin Have Antioxidant and Antidiabetic Effects on Streptozotocin-Nicotinamide-Induced Diabetic Model and Myotube Cell of Male Mouse

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Akram Ahangarpour ◽  
Ali Akbar Oroojan ◽  
Layasadat Khorsandi ◽  
Maryam Kouchak ◽  
Mohammad Badavi
Keyword(s):  
Oxidative Stress ◽  
C2c12 Cell ◽  
In Vitro Study ◽  
Homogenization Method ◽  
Solid Lipid ◽  
Muscle Tissues ◽  
Diabetic Model ◽  
Cellular Apoptosis

Type 2 diabetes mellitus (T2DM) may occur via oxidative stress. Myricitrin is a plant-derived antioxidant, and its solid lipid nanoparticle (SLN) may be more potent. Hence, the present study was conducted to evaluate the effects of myricitrin SLN on streptozotocin-nicotinamide- (STZ-NA-) induced T2DM of the mouse and hyperglycemic myotube. In this experimental study, cold homogenization method was used to prepare SLN. Then, 120 adult male NMRI mice were divided into 7 groups: control, vehicle, diabetes (received STZ 65 mg/kg 15 min after injected NA 120 mg/kg), diabetes + SLN containing myricitrin 1, 3, and 10 mg/kg, and diabetes + metformin. For in vitro study, myoblast (C2C12) cell line was cultured and divided into 6 groups (n=3): control, hyperglycemia, hyperglycemia + SLN containing myricitrin 1, 3, and, 10 μM, and hyperglycemia + metformin. After the last nanoparticle treatment, plasma samples, pancreas and muscle tissues, and myotubes were taken for experimental assessments. Diabetes increased lipid peroxidation and reduced antioxidant defense along with the hyperglycemia, insulin resistance, and pancreas apoptosis. Hyperglycemia induced oxidative stress, antioxidant impairment, and cellular apoptosis. Myricitrin SLN improved diabetes and hyperglycemia complications in the in vivo and in vitro studies. Therefore, SLN of myricitrin showed antioxidant, antidiabetic, and antiapoptotic effects in the mouse and myotube cells.

scholarly journals Plant-Derived Natural Biomolecule Picein Attenuates Menadione Induced Oxidative Stress on Neuroblastoma Cell Mitochondria

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 552 ◽  
Author(s):  
Kavindra Kumar Kesari ◽  
Anupam Dhasmana ◽  
Shruti Shandilya ◽  
Neeraj Prabhakar ◽  
Ahmed Shaukat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroblastoma Cell ◽  
Water Extract ◽  
Subsequent Treatment ◽  
Hot Water ◽  
Superoxide Production ◽  
Mitochondrial Activity ◽  
Mitochondrial Superoxide ◽  
In Silico Studies

Several bioactive compounds are in use for the treatment of neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease. Historically, willow (salix sp.) bark has been an important source of salisylic acid and other natural compounds with anti-inflammatory, antipyretic and analgesic properties. Among these, picein isolated from hot water extract of willow bark, has been found to act as a natural secondary metabolite antioxidant. The aim of this study was to investigate the unrevealed pharmacological action of picein. In silico studies were utilized to direct the investigation towards the neuroprotection abilities of picein. Our in vitro studies demonstrate the neuroprotective properties of picein by blocking the oxidative stress effects, induced by free radical generator 2-methyl-1,4-naphthoquinone (menadione, MQ), in neuroblastoma SH-SY5Y cells. Several oxidative stress-related parameters were evaluated to measure the protection for mitochondrial integrity, such as mitochondrial superoxide production, mitochondrial activity (MTT), reactive oxygen species (ROS) and live-cell imaging. A significant increase in the ROS level and mitochondrial superoxide production were measured after MQ treatment, however, a subsequent treatment with picein was able to mitigate this effect by decreasing their levels. Additionally, the mitochondrial activity was significantly decreased by MQ exposure, but a follow-up treatment with picein recovered the normal metabolic activity. In conclusion, the presented results demonstrate that picein can significantly reduce the level of MQ-induced oxidative stress on mitochondria, and thereby plays a role as a potent neuroprotectant.

scholarly journals Alpha-1-antitrypsin suppresses oxidative stress in preeclampsia by inhibiting the p38MAPK signaling pathway: An in vivo and in vitro study

PLoS ONE ◽  
2017 ◽  
Vol 12 (3) ◽  
pp. e0173711 ◽  
Author(s):  
Ya-Ling Feng ◽  
Yong-Xiang Yin ◽  
Jian Ding ◽  
Hua Yuan ◽  
Lan Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
In Vitro Study ◽  
Vitro Study ◽  
P38mapk Signaling ◽  
Alpha 1 Antitrypsin

scholarly journals Compromised dental cells viability following teeth-whitening exposure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ola Redha ◽  
Morteza Mazinanian ◽  
Sabrina Nguyen ◽  
Dong Ok Son ◽  
Monika Lodyga ◽  
...  
Keyword(s):  
Protein Content ◽  
In Vitro Study ◽  
Organic Content ◽  
Time Dependent ◽  
Gingival Fibroblast ◽  
Direct Exposure ◽  
Significant Difference ◽  
Enamel Protein

AbstractThis study aimed to assess the viability of dental cells following time-dependent carbamide peroxide teeth-whitening treatments using an in-vitro dentin perfusion assay model. 30 teeth were exposed to 5% or 16% CP gel (4 h daily) for 2-weeks. The enamel organic content was measured with thermogravimetry. The time-dependent viability of human dental pulp stem cells (HDPSCs) and gingival fibroblast cells (HGFCs) following either indirect exposure to 3 commercially available concentrations of CP gel using an in-vitro dentin perfusion assay or direct exposure to 5% H2O2 were investigated by evaluating change in cell morphology and by hemocytometry. The 5% and 16% CP produced a significantly lower (p < 0.001) enamel protein content (by weight) when compared to the control. The organic content in enamel varied accordingly to the CP treatment: for the 16% and 5% CP treatment groups, a variation of 4.0% and 5.4%, respectively, was observed with no significant difference. The cell viability of HDPSCs decreased exponentially over time for all groups. Within the limitation of this in-vitro study, we conclude that even low concentrations of H2O2 and CP result in a deleterious change in enamel protein content and compromise the viability of HGFCs and HDPSCs. These effects should be observed in-vivo.

scholarly journals Endometriosis Susceptibility to Dapsone-Hydroxylamine-Induced Alterations Can Be Prevented by Licorice Intake: In Vivo and In Vitro Study

2021 ◽  
Vol 22 (16) ◽  
pp. 8476
Author(s):  
Chiara Sabbadin ◽  
Alessandra Andrisani ◽  
Gabriella Donà ◽  
Elena Tibaldi ◽  
Anna Maria Brunati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Carbonic Anhydrase Activity ◽  
Control Group ◽  
Beneficial Effects ◽  
Licorice Extract ◽  
Anti Oxidant ◽  
Gynecological Disease

Endometriosis, an estrogen-dependent chronic gynecological disease, is characterized by a systemic inflammation that affects circulating red blood cells (RBC), by reducing anti-oxidant defenses. The aim of this study was to investigate the potential beneficial effects of licorice intake to protect RBCs from dapsone hydroxylamine (DDS-NHOH), a harmful metabolite of dapsone, commonly used in the treatment of many diseases. A control group (CG, n = 12) and a patient group (PG, n = 18) were treated with licorice extract (25 mg/day), for a week. Blood samples before (T0) and after (T1) treatment were analyzed for: i) band 3 tyrosine phosphorylation and high molecular weight aggregates; and ii) glutathionylation and carbonic anhydrase activity, in the presence or absence of adjunctive oxidative stress induced by DDS-NHOH. Results were correlated with plasma glycyrrhetinic acid (GA) concentrations, measured by HPLC–MS. Results showed that licorice intake decreased the level of DDS-NHOH-related oxidative alterations in RBCs, and the reduction was directly correlated with plasma GA concentration. In conclusion, in PG, the inability to counteract oxidative stress is a serious concern in the evaluation of therapeutic approaches. GA, by protecting RBC from oxidative assault, as in dapsone therapy, might be considered as a new potential tool for preventing further switching into severe endometriosis.

scholarly journals The Pluripotency Factor Nanog Protects against Neuronal Amyloid β-Induced Toxicity and Oxidative Stress through Insulin Sensitivity Restoration

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1339
Author(s):  
Ching-Chi Chang ◽  
Hsin-Hua Li ◽  
Sing-Hua Tsou ◽  
Hui-Chih Hung ◽  
Guang-Yaw Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Stem Cell ◽  
Amyloid Β ◽  
Protective Effects ◽  
Mitochondrial Superoxide ◽  
Nanog Expression ◽  
Pluripotency Factor

Amyloid β (Aβ) is a peptide fragment of the amyloid precursor protein that triggers the progression of Alzheimer’s Disease (AD). It is believed that Aβ contributes to neurodegeneration in several ways, including mitochondria dysfunction, oxidative stress and brain insulin resistance. Therefore, protecting neurons from Aβ-induced neurotoxicity is an effective strategy for attenuating AD pathogenesis. Recently, applications of stem cell-based therapies have demonstrated the ability to reduce the progression and outcome of neurodegenerative diseases. Particularly, Nanog is recognized as a stem cell-related pluripotency factor that enhances self-renewing capacities and helps reduce the senescent phenotypes of aged neuronal cells. However, whether the upregulation of Nanog can be an effective approach to alleviate Aβ-induced neurotoxicity and senescence is not yet understood. In the present study, we transiently overexpressed Nanog—both in vitro and in vivo—and investigated the protective effects and underlying mechanisms against Aβ. We found that overexpression of Nanog is responsible for attenuating Aβ-triggered neuronal insulin resistance, which restores cell survival through reducing intracellular mitochondrial superoxide accumulation and cellular senescence. In addition, upregulation of Nanog expression appears to increase secretion of neurotrophic factors through activation of the Nrf2 antioxidant defense pathway. Furthermore, improvement of memory and learning were also observed in rat model of Aβ neurotoxicity mediated by upregulation of Nanog in the brain. Taken together, our study suggests a potential role for Nanog in attenuating the neurotoxic effects of Aβ, which in turn, suggests that strategies to enhance Nanog expression may be used as a novel intervention for reducing Aβ neurotoxicity in the AD brain.

scholarly journals Anti-glycation, anti-hemolysis, and ORAC activities of demethylcurcumin and tetrahydroxycurcumin in vitro and reductions of oxidative stress in d-galactose-induced BALB/c mice in vivo

2019 ◽  
Vol 60 (1) ◽  
Author(s):  
Yuh-Hwa Liu ◽  
Tai-Lin Lee ◽  
Chuan-Hsiao Han ◽  
Yi-Shan Lee ◽  
Wen-Chi Hou
Keyword(s):  
Oxidative Stress ◽  
Functional Foods ◽  
Antioxidant Activities ◽  
Animal Experiments ◽  
Lower Serum ◽  
Significant Difference ◽  
Protein Expressions ◽  
Brain Extracts

Abstract Background There were few report concerning anti-glycation and antioxidant activities of the minor amounts of components in curcuminoids, demethylcurcumin and tetrahydroxycurcumin, in vitro and in vivo. Results The bovine serum albumin/galactose of non-enzymatic glycation models, radical-induced hemolysis, and oxygen radical absorbance capacity (ORAC) were studied in vitro, and the d-galactose-induced oxidative stress in BALB/c mice and then demethylcurcumin or tetrahydroxycurcumin interventions in vivo. The parameters of oxidative stress in plasma and brain extracts were determined among animal groups with or without both curcuminoids interventions. The demethylcurcumin and tetrahydroxycurcumin exhibited anti-glycation, anti-hemolysis, and ORAC activities, and showed much better and significant difference (P < 0.05) compared to those of curcumin in vitro. In animal experiments, the intervened two curcuminoids at both concentrations showed to lower serum malondialdehyde (MDA), brain MDA levels and iNOS protein expressions, and elevate serum ORAC activities, and showed difference (P < 0.05) compared to the galactose-induced control. Conclusion The demethylcurcumin and tetrahydroxycurcumin showed potentials in developing functional foods for antioxidant-related purposes.

Sign in / Sign up

Export Citation Format

Share Document