scholarly journals Long-term in vivo polychlorinated biphenyl 126 exposure induces oxidative stress and alters proteomic profile on islets of Langerhans

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Rodrigo Azevedo Loiola ◽  
Fabyana Maria dos Anjos ◽  
Ana Lúcia Shimada ◽  
Wesley Soares Cruz ◽  
Carine Cristiane Drewes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Islets Of Langerhans ◽  
Polychlorinated Biphenyl ◽  
Proteomic Profile

scholarly journals A Mechanistic Evaluation of Antioxidant Nutraceuticals on Their Potential against Age-Associated Neurodegenerative Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1019 ◽  
Author(s):  
Nur Zuliani Ramli ◽  
Mohamad Fairuz Yahaya ◽  
Ikuo Tooyama ◽  
Hanafi Ahmad Damanhuri
Keyword(s):  
Oxidative Stress ◽  
Natural Antioxidants ◽  
Green Tea Polyphenols ◽  
Food Sources ◽  
Gene Expressions ◽  
Neuroprotective Effects ◽  
Antioxidative Effects

Nutraceuticals have been extensively studied worldwide due to its neuroprotective effects in in vivo and in vitro studies, attributed by the antioxidative properties. Alzheimer (AD) and Parkinson disease (PD) are the two main neurodegenerative disorders that are discussed in this review. Both AD and PD share the similar involvement of oxidative stress in their pathophysiology. Nutraceuticals exert their antioxidative effects via direct scavenging of free radicals, prevent damage to biomolecules, indirectly stimulate the endogenous antioxidative enzymes and gene expressions, inhibit activation of pro-oxidant enzymes, and chelate metals. In addition, nutraceuticals can act as modulators of pro-survival, pro-apoptotic, and inflammatory signaling pathways. They have been shown to be effective particularly in preclinical stages, due to their multiple mechanisms of action in attenuating oxidative stress underlying AD and PD. Natural antioxidants from food sources and natural products such as resveratrol, curcumin, green tea polyphenols, and vitamin E are promising therapeutic agents in oxidative stress-mediated neurodegenerative disease as they have fewer adverse effects, more tolerable, cheaper, and sustainable for long term consumption.

scholarly journals Neuroinflammation trajectories precede cognitive impairment after experimental meningitis—evidence from an in vivo PET study

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Vijayasree V. Giridharan ◽  
Allan Collodel ◽  
Jaqueline S. Generoso ◽  
Giselli Scaini ◽  
Rico Wassather ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Microglial Activation ◽  
Caspase 3 ◽  
Cns Infection ◽  
Control Group ◽  
Caspase 9 ◽  
Activation Markers

Abstract Background Bacterial meningitis is a devastating central nervous system (CNS) infection with acute and long-term neurological consequences, including cognitive impairment. The aim of this study was to understand the association between activated microglia-induced neuroinflammation and post-meningitis cognitive impairment. Method Meningitis was induced in male Wistar rats by injecting Streptococcus pneumoniae into the brain through the cisterna magna, and rats were then treated with ceftriaxone. Twenty-four hours and 10 days after meningitis induction, rats were imaged with positron emission tomography (PET) using [11C]PBR28, a specific translocator protein (TSPO) radiotracer, to determine in vivo microglial activation. Following imaging, the expression of TSPO, cardiolipin, and cytochrome c, inflammatory mediators, oxidative stress markers, and glial activation markers were evaluated in the prefrontal cortex and hippocampus. Ten days after meningitis induction, animals were subjected to behavioral tests, such as the open-field, step-down inhibitory avoidance, and novel object recognition tests. Results Both 24-h (acute) and 10-day (long-term) groups of rats demonstrated increased [11C]PBR28 uptake and microglial activation in the whole brain compared to levels in the control group. Although free from infection, 10-day group rats exhibited increased expression levels of cytokines and markers of oxidative stress, microglial activation (IBA-1), and astrocyte activation (GFAP) similar to those seen in the 24-h group. Acute meningitis induction also elevated TSPO, cytochrome c, and caspase-3 levels with no change in caspase-9 levels. Furthermore, upregulated levels of TSPO, cytochrome c, and caspase-3 and caspase-9 were observed in the rat hippocampus 10 days after meningitis induction with a simultaneous reduction in cardiolipin levels. Animals showed a cognitive decline in all tasks compared with the control group, and this impairment may be at least partially mediated by activating a glia-mediated immune response and upregulating TSPO. Conclusions TSPO-PET could potentially be used as an imaging biomarker for microglial activation and long-term cognitive impairment post-meningitis. Additionally, this study opens a new avenue for the potential use of TSPO ligands after infection-induced neurological sequelae.

scholarly journals FructationIn Vivo: Detrimental and Protective Effects of Fructose

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
H. M. Semchyshyn
Keyword(s):  
Oxidative Stress ◽  
Side Effects ◽  
Experimental Models ◽  
Oxygen Species ◽  
Protective Effects ◽  
Compelling Evidence ◽  
Animal Tissues

There is compelling evidence that long-term intake of excessive fructose can have deleterious side effects in different experimental models. However, the role of fructosein vivoremains controversial, since acute temporary application of fructose is found to protect yeast as well as animal tissues against exogenous oxidative stress. This review suggests the involvement of reactive carbonyl and oxygen species in both the cytotoxic and defensive effects of fructose. Potential mechanisms of the generation of reactive species by fructose in the nonenzymatic reactions, their implication in the detrimental and protective effects of fructose are discussed.

N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress

2003 ◽  
Vol 285 (4) ◽  
pp. E744-E753 ◽  
Author(s):  
C. Andrew Haber ◽  
Tony K. T. Lam ◽  
Zhiwen Yu ◽  
Neehar Gupta ◽  
Tracy Goh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
High Glucose ◽  
Muscle Protein ◽  
Fold Increase ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
High Concentrations

Exposure to high concentrations of glucose and insulin results in insulin resistance of metabolic target tissues, a characteristic feature of type 2 diabetes. High glucose has also been associated with oxidative stress, and increased levels of reactive oxygen species have been proposed to cause insulin resistance. To determine whether oxidative stress contributes to insulin resistance induced by hyperglycemia in vivo, nondiabetic rats were infused with glucose for 6 h to maintain a circulating glucose concentration of 15 mM with and without coinfusion of the antioxidant N-acetylcysteine (NAC), followed by a 2-h hyperinsulinemic-euglycemic clamp. High glucose (HG) induced a significant decrease in insulin-stimulated glucose uptake [tracer-determined disappearance rate (Rd), control 41.2 ± 1.7 vs. HG 32.4 ± 1.9 mg · kg–1 · min–1, P < 0.05], which was prevented by NAC (HG + NAC 45.9 ± 3.5 mg · kg–1 · min–1). Similar results were obtained with the antioxidant taurine. Neither NAC nor taurine alone altered Rd. HG caused a significant (5-fold) increase in soleus muscle protein carbonyl content, a marker of oxidative stress that was blocked by NAC, as well as elevated levels of malondialdehyde and 4-hydroxynonenal, markers of lipid peroxidation, which were reduced by taurine. In contrast to findings after long-term hyperglycemia, there was no membrane translocation of novel isoforms of protein kinase C in skeletal muscle after 6 h. These data support the concept that oxidative stress contributes to the pathogenesis of hyperglycemia-induced insulin resistance.

scholarly journals DNA damage after long-term repetitive hyperbaric oxygen exposure

2009 ◽  
Vol 106 (1) ◽  
pp. 311-315 ◽  
Author(s):  
Michael Gröger ◽  
Sükrü Öter ◽  
Vladislava Simkova ◽  
Markus Bolten ◽  
Andreas Koch ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Endurance Training ◽  
Hyperbaric Oxygen ◽  
Oxidative Dna Damage ◽  
Ex Vivo ◽  
Pure Oxygen ◽  
Repetitive Exposure

A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O2•−) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O2•− production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage.

scholarly journals Animal Models in Studies of Cardiotoxicity Side Effects from Antiblastic Drugs in Patients and Occupational Exposed Workers

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Monica Lamberti ◽  
Giancarlo Giovane ◽  
Elpidio M. Garzillo ◽  
Franca Avino ◽  
Antonia Feola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Animal Models ◽  
Cardiac Cells ◽  
Cytotoxic Drugs ◽  
Cyclopentenyl Cytosine ◽  
Exposed Workers ◽  
Immunologic Reactions

Cardiotoxicity is an important side effect of cytotoxic drugs and may be a risk factor of long-term morbidity for both patients during therapy and also for staff exposed during the phases of manipulation of antiblastic drugs. The mechanism of cardiotoxicity studied in vitro and in vivo essentially concerns the formation of free radicals leading to oxidative stress, with apoptosis of cardiac cells or immunologic reactions, but other mechanisms may play a role in antiblastic-induced cardiotoxicity. Actually, some new cytotoxic drugs like trastuzumab and cyclopentenyl cytosine show cardiotoxic effects. In this report we discuss the different mechanisms of cardiotoxicity induced by antiblastic drugs assessed using animal models.

scholarly journals Lead-Induced Motor Dysfunction Is Associated with Oxidative Stress, Proteome Modulation, and Neurodegeneration in Motor Cortex of Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Luana Ketlen Reis Leão ◽  
Leonardo Oliveira Bittencourt ◽  
Ana Carolina Alves Oliveira ◽  
Priscila Cunha Nascimento ◽  
Maria Karolina Martins Ferreira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Motor Cortex ◽  
Wistar Rats ◽  
Toxic Metal ◽  
Bioinformatic Analysis ◽  
Motor Dysfunction ◽  
Motor Deficits ◽  
Proteomic Profile ◽  
Adult Rats

Lead (Pb) is a toxic metal with great neurotoxic potential. The aim of this study was to investigate the effects of a long-term Pb intoxication on the global proteomic profile, oxidative biochemistry and neuronal density in motor cortex of adult rats, and the possible outcomes related to motor functions. For this, Wistar rats received for 55 days a dose of 50 mg/Kg of Pb acetate by intragastric gavage. Then, the motor abilities were evaluated by open field and inclined plane tests. To investigate the possible oxidative biochemistry modulation, the levels of pro-oxidant parameters as lipid peroxidation and nitrites were evaluated. The global proteomic profile was evaluated by ultraefficiency liquid chromatography system coupled with mass spectrometry (UPLC/MS) followed by bioinformatic analysis. Moreover, it was evaluated the mature neuron density by anti-NeuN immunostaining. The statistical analysis was performed through Student’s t -test, considering p < 0.05 . We observed oxidative stress triggering by the increase in malonaldehyde and nitrite levels in motor cortex. In the proteomic analysis, the motor cortex presented alterations in proteins associated with neural functioning, morphological organization, and neurodegenerative features. In addition, it was observed a decrease in the number of mature neurons. These findings, associated with previous evidences observed in spinal cord, cerebellum, and hippocampus under the same Pb administration protocol, corroborate with the motor deficits in the rats towards Pb. Thus, we conclude that the long-term administration to Pb in young Wistar rats triggers impairments at several organizational levels, such as biochemical and morphological, which resulted in poor motor performance.

scholarly journals Resveratrol Delivery from Implanted Cyclodextrin Polymers Provides Sustained Antioxidant Effect on Implanted Neural Probes

2020 ◽  
Vol 21 (10) ◽  
pp. 3579 ◽  
Author(s):  
Rebecca M. Haley ◽  
Sean T. Zuckerman ◽  
Hassan Dakhlallah ◽  
Jeffery R. Capadona ◽  
Horst A. von Recum ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neurological Diseases ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
The Novel ◽  
Systemic Delivery ◽  
Neuroprotective Effects

Intracortical microelectrodes are valuable tools used to study and treat neurological diseases. Due in large part to the oxidative stress and inflammatory response occurring after electrode implantation, the signal quality of these electrodes decreases over time. To alleviate this response, resveratrol, a natural antioxidant which elicits neuroprotective effects through reduction of oxidative stress, was utilized. This work compares traditional systemic delivery of resveratrol to the novel cyclodextrin polymer (pCD) local delivery approach presented herein, both in vitro and in vivo. The pCD displayed an extended resveratrol release for 100 days, as well as 60 days of free radical scavenging activity in vitro. In vivo results indicated that our pCD delivery system successfully delivered resveratrol to the brain with a sustained release for the entire short-duration study (up to 7 days). Interestingly, significantly greater concentrations of resveratrol metabolites were found at the intracortical probe implantation site compared to the systemic administration of resveratrol. Together, our pilot results provide support for the possibility of improving the delivery of resveratrol in an attempt to stabilize long-term neural interfacing applications.

scholarly journals Natural Product-Based Nanomedicine in Treatment of Inflammatory Bowel Disease

2020 ◽  
Vol 21 (11) ◽  
pp. 3956 ◽  
Author(s):  
Tripti Khare ◽  
Sushesh Srivatsa Palakurthi ◽  
Brijesh M. Shah ◽  
Srinath Palakurthi ◽  
Sharad Khare
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Bowel Disease ◽  
Natural Product ◽  
Bowel Disease ◽  
Synthetic Drugs ◽  
In Vivo Experiments ◽  
Inflammatory Bowel

Many synthetic drugs and monoclonal antibodies are currently in use to treat Inflammatory Bowel Disease (IBD). However, they all are implicated in causing severe side effects and long-term use results in many complications. Numerous in vitro and in vivo experiments demonstrate that phytochemicals and natural macromolecules from plants and animals reduce IBD-related complications with encouraging results. Additionally, many of them modify enzymatic activity, alleviate oxidative stress, and downregulate pro-inflammatory transcriptional factors and cytokine secretion. Translational significance of natural nanomedicine and strategies to investigate future natural product-based nanomedicine is discussed. Our focus in this review is to summarize the use of phytochemicals and macromolecules encapsulated in nanoparticles for the treatment of IBD and IBD-associated colorectal cancer.

FoxO Are Critical Mediators of Hematopoietic Stem Cell Resistance to Physiologic Oxidative Stress.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 439-439
Author(s):  
Zuzana Tothova ◽  
Ramya Kollipara ◽  
Brian J. Huntly ◽  
Benjamin H. Lee ◽  
Diego H. Castrillon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Bone Marrow Cells ◽  
Dynamic Balance ◽  
Normal Numbers ◽  
Hematopoietic Stem ◽  
The Impact

Abstract Hematopoietic development and long-term homeostasis are tightly regulated by a dynamic balance of stem cell self-renewal and differentiation. To understand the role of the FoxO family of transcription factors in these processes, we studied the impact of somatic deletion of all FoxO genes in the adult hematopoietic system of mice engineered with the interferon-inducible Mx-Cre transgene and various conditional FoxO alleles: FoxO1L/L; FoxO3 L/L; and/or FoxO4 L/L. Cre-mediated excision of FoxO1, FoxO3 and FoxO4 (FoxO1/O3/O4L/L), resulted in myeloid lineage expansion, lymphoid developmental abnormalities and a marked decrease of the lineage-negative, Sca-1+, c-Kit+ (LSK) compartment, containing the hematopoietic stem cell (HSC) population, but normal numbers of myeloid progenitors. Furthermore, FoxO1/O3/O4L/L null bone marrow cells were defective in competitive and noncompetitive repopulation assays. This FoxO deficient defect correlated with enhanced cell cycling and increased apoptosis of HSC cells. Notably, there was an HSC-restricted elevation in the level of reactive oxygen species (ROS) that was not observed in committed progenitors, and was associated with decreased catalase and MnSOD expression. Furthermore, in vivo treatment with the anti-oxidative agent N-acetyl-cysteine (NAC) resulted in complete reversion of the FoxO deficient HSC phenotype. Taken together, these results demonstrate that, in the HSC compartment, FoxO proteins are mediators of quiescence and enhanced survival and play essential regulatory roles in the response to physiologic oxidative stress, a function that may contribute to the long-term regenerative potential of the hematopoietic stem cell compartment.

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