scholarly journals Chronic Exposure to Fluoride Affects GSH Level and NOX4 Expression in Rat Model of This Element of Neurotoxicity

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 422 ◽  
Author(s):  
Karolina Dec ◽  
Agnieszka Łukomska ◽  
Karolina Skonieczna-Żydecka ◽  
Karolina Jakubczyk ◽  
Maciej Tarnowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Neuronal Loss ◽  
Brain Structures ◽  
Neural Cells ◽  
Nadph Oxidase 4 ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Total Antioxidant ◽  
Blood Brain Barrier Damage

Exposure of neural cells to harmful and toxic factors promotes oxidative stress, resulting in disorders of metabolism, cell differentiation, and maturation. The study examined the brains of rats pre- and postnatally exposed to sodium fluoride (NaF 50 mg/L) and activity of NADPH oxidase 4 (NOX4), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), concentration of glutathione (GSH), and total antioxidant capacity (TAC) in the cerebellum, prefrontal cortex, hippocampus, and striatum were measured. Additionally, NOX4 expression was determined by qRT–PCR. Rats exposed to fluorides (F-) showed an increase in NOX4 activity in the cerebellum and hippocampus, a decrease in its activity in the prefrontal cortex and hippocampus, and upregulation of NOX4 expression in hippocampus and its downregulation in other brain structures. Analysis also showed significant changes in the activity of all antioxidant enzymes and a decrease in TAC in brain structures. NOX4 induction and decreased antioxidant activity in central nervous system (CNS) cells may be central mechanisms of fluoride neurotoxicity. NOX4 contributes to blood–brain barrier damage, microglial activation, and neuronal loss, leading to impairment of brain function. Fluoride-induced oxidative stress involves increased reactive oxygen speciaes (ROS) production, which in turn increases the expression of genes encoding pro-inflammatory cytokines.

scholarly journals Global Regulatory Impact of ClpP Protease of Staphylococcus aureus on Regulons Involved in Virulence, Oxidative Stress Response, Autolysis, and DNA Repair

2006 ◽  
Vol 188 (16) ◽  
pp. 5783-5796 ◽  
Author(s):  
Antje Michel ◽  
Franziska Agerer ◽  
Christof R. Hauck ◽  
Mathias Herrmann ◽  
Joachim Ullrich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Dna Repair ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Transcriptional Analysis ◽  
Expression Of Genes ◽  
Wide Range ◽  
Genes Encoding ◽  
Regulatory Impact

ABSTRACT Staphylococcus aureus is an important pathogen, causing a wide range of infections including sepsis, wound infections, pneumonia, and catheter-related infections. In several pathogens ClpP proteases were identified by in vivo expression technologies to be important for virulence. Clp proteolytic complexes are responsible for adaptation to multiple stresses by degrading accumulated and misfolded proteins. In this report clpP, encoding the proteolytic subunit of the ATP-dependent Clp protease, was deleted, and gene expression of ΔclpP was determined by global transcriptional analysis using DNA-microarray technology. The transcriptional profile reveals a strong regulatory impact of ClpP on the expression of genes encoding proteins that are involved in the pathogenicity of S. aureus and adaptation of the pathogen to several stresses. Expression of the agr system and agr-dependent extracellular virulence factors was diminished. Moreover, the loss of clpP leads to a complete transcriptional derepression of genes of the CtsR- and HrcA-controlled heat shock regulon and a partial derepression of genes involved in oxidative stress response, metal homeostasis, and SOS DNA repair controlled by PerR, Fur, MntR, and LexA. The levels of transcription of genes encoding proteins involved in adaptation to anaerobic conditions potentially regulated by an Fnr-like regulator were decreased. Furthermore, the expression of genes whose products are involved in autolysis was deregulated, leading to enhanced autolysis in the mutant. Our results indicate a strong impact of ClpP proteolytic activity on virulence, stress response, and physiology in S. aureus.

scholarly journals Differential expression of glutamate transporters and monoaminergic genes in major depression and suicide

2019 ◽  
Author(s):  
Brian Powers ◽  
Joel E. Kleinman ◽  
Thomas M. Hyde ◽  
Olusola Ajilore ◽  
Alex Leow ◽  
...  
Keyword(s):  
Dorsolateral Prefrontal Cortex ◽  
Neuronal Loss ◽  
Severe Depression ◽  
Glutamate Transporters ◽  
Major Depressive ◽  
Expression Of Genes ◽  
Dorsolateral Prefrontal ◽  
Genes Encoding ◽  
Poor Treatment ◽  
Poor Treatment Response

AbstractAccumulating evidence indicates that the glutamate and monoamine systems contribute to the pathophysiology of major depressive disorder (MDD) and suicide. We have tested the expression of genes encoding glutamate transporters and monoaminergic proteins in the dorsolateral prefrontal cortex (DLPFC) of MDD subjects who died by suicide (MDD-S, n=51), MDD non-suicide subjects (MDD-NS, n=28), and non-psychiatric controls (CTRL, n=32). We analyzed glutamate transporters (EAAT1, EAAT2, VGLUT1, and VGLUT2) and monoaminergic genes (SERT, NET, DAT, PMAT, VMAT, TPH1 and TPH2). Females but not males with MDD showed higher expression of all glutamate transporters relative to CTRLs (P<0.05). MDD-S groups of both sexes had higher VGLUT2 expression (P<0.05). MDD-S females who were antidepressant positive (+) had lower EAAT1 expression (P=0.004), perhaps indicating poor treatment response. Analyses of monoaminergic genes revealed lower VMAT1 expression (P=0.002) in MDD males, and conversely higher VMAT2 in MDD females (P=0.004). MDD females also had higher VMAT2, TPH2 and NET expression (p<0.05), and in contrast, MDD males had lower VMAT1 and PMAT expression. Therefore, we report sex differences in the expression of glutamate transporters and some monoaminergic genes in the DLPFC in MDD. Most of these findings are novel, but lower EAAT1 expression in MDD-S replicates previous studies. Lower EAAT1 expression coupled with higher VGLUT2 expression in MDD-S may lead to increased synaptic glutamate, neuronal loss and glial loss in the DLPFC in MDD and suicide reported previously. These deficits may contribute to lower DLPFC activity, poor problem solving and impaired executive function exhibited in severe depression and suicide.

scholarly journals Methamphetamine-Triggered Neurotoxicity in Human Dorsolateral Prefrontal Cortex

2021 ◽  
Vol 10 ◽  
pp. 2016
Author(s):  
Ali Zare ◽  
Alireza Ghanbari ◽  
Mohammad Javad Hoseinpour ◽  
Mahdi Eskandarian Boroujeni ◽  
Alimohammad Alimohammadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Dorsolateral Prefrontal Cortex ◽  
Animal Studies ◽  
Molecular Mechanisms ◽  
Metabolic Activation ◽  
Neural Cells ◽  
Dorsolateral Prefrontal ◽  
The Central Nervous System ◽  
The Brain

Background: Methamphetamine (MA), is an extremely addictive stimulant that adversely affects the central nervous system. Accumulating evidence indicates that molecular mechanisms such as oxidative stress, apoptosis, and autophagy are involved in the toxicity of MA. Considering experimental animal studies exhibiting MA-induced neurotoxicity, the relevance of these findings needs to be evidently elucidated in human MA users. It is generally assumed that multiple chemical substances released in the brain following MA-induced metabolic activation are primary factors underlying damage of neural cells. Hence, this study aimed to investigate the role of autophagy and apoptosis as well as oxidative stress in the brain of postmortem MA-induced toxicity. Materials and Methods: In this study, we determine the gene expression of autophagy and apoptosis, including BECN1, MAP1ALC3, CASP8, TP53, and BAX genes in ten healthy controls and ten chronic users of MA postmortem dorsolateral prefrontal cortex (DLPFC) by real-time polymerase chain reaction. Also, we applied immunohistochemistry in formalin-fixed and paraffin-embedded human brain samples to analyze brain-derived neurotrophic factor (BDNF). Also, spectrophotometry was performed to measure glutathione (GSH) content. Results: The expression level of apoptotic and autophagic genes (BECN1, MAP1ALC3, CASP8, TP53, and BAX) were significantly elevated, while GSH content and BDNF showed substantial reductions in DLPFC of chronic MA users. Discussion: Our data showed that MA addiction provokes transduction pathways, namely apoptosis and autophagy, along with oxidative mechanisms in DLPFC. Also, MA induces multiple functional and structural perturbations in the brain, determining its toxicity and possibly contributing to neurotoxicity. [GMJ.2021;10:e2016]

scholarly journals PgRsp Is a Novel Redox-Sensing Transcription Regulator Essential for Porphyromonas gingivalis Virulence

2019 ◽  
Vol 7 (12) ◽  
pp. 623
Author(s):  
Michał Śmiga ◽  
Teresa Olczak
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Porphyromonas Gingivalis ◽  
Alternative Pathway ◽  
Redox Status ◽  
Oxidative Stress Response ◽  
Gene Encoding ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Redox Sensing

Porphyromonas gingivalis is one of the etiological agents of chronic periodontitis. Both heme and oxidative stress impact expression of genes responsible for its survival and virulence. Previously we showed that P. gingivalis ferric uptake regulator homolog affects expression of a gene encoding a putative Crp/Fnr superfamily member, termed P. gingivalis redox-sensing protein (PgRsp). Although PgRsp binds heme and shows the highest similarity to proteins assigned to the CooA family, it could be a member of a novel, separate family of proteins with unknown function. Expression of the pgrsp gene is autoregulated and iron/heme dependent. Genes encoding proteins engaged in the oxidative stress response were upregulated in the pgrsp mutant (TO11) strain compared with the wild-type strain. The TO11 strain showed higher biomass production, biofilm formation, and coaggregation ability with Tannerella forsythia and Prevotella intermedia. We suggest that PgRsp may regulate production of virulence factors, proteases, Hmu heme acquisition system, and FimA protein. Moreover, we observed growth retardation of the TO11 strain under oxidative conditions and decreased survival ability of the mutant cells inside macrophages. We conclude that PgRsp protein may play a role in the oxidative stress response using heme as a ligand for sensing changes in redox status, thus regulating the alternative pathway of the oxidative stress response alongside OxyR.

scholarly journals Anti-Amnesic and Neuroprotective Effects of Ziziphus Jujuba Aqueous Extract on Scopolamine-Induced Cognitive Impairments in Rats

2021 ◽  
Author(s):  
Etienne Djeuzong ◽  
Antoine Kandeda ◽  
Sefirin Djiogue ◽  
Danide Nguedia ◽  
Stephanie Lewale ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Aqueous Extract ◽  
Cognitive Impairments ◽  
Folk Medicine ◽  
Neuronal Loss ◽  
Neuroprotective Effects ◽  
Memory Impairments ◽  
Y Maze ◽  
Ziziphus Jujuba

Abstract Background: Alzheimer's disease is a neurological condition that affects more than 44 million people worldwide. The available treatments target the symptoms rather than underlying causes. Ziziphus jujuba (Rhamnaceae) is used in traditional Cameroonian medicine to treat many disorders including memory impairments. The study aimed to evaluate the anti-amnesic and neuroprotective effects of Z. jujuba aqueous extract on scopolamine-induced memory disorders in rats. Methods: Learning and memory impairments were induced in rats by scopolamine (1mg/kg, i.p.) for 15 days. Rats that developed cognitive impairments were divided as follows: two positive control groups received piracetam (200 mg/kg, p.o.) or tacrine (1 mg/kg, p.o.); three test groups received the extract (29, 57, and 114 mg/kg, p.o., respectively) daily for 15 days. At the end of treatments, memory impairments were assessed by Morris water maze and Y-maze tests. Thereafter, animals were sacrificed and some biochemical parameters (oxidative stress, inflammation, and apoptosis) were estimated in the hippocampus and prefrontal cortex.Results: Z. jujuba decreased the time to reach the platform and increased the time in the target quadrant. However, it failed to affect spontaneous alternation in the Y-maze. Furthermore, the extract reversed scopolamine-induced oxidative stress, inflammation, and apoptosis. This was confirmed with the prevention of neuronal loss in the hippocampus or prefrontal cortex. Conclusions: These findings suggest that Z. jujuba extract possesses ant-amnesic and neuroprotective effects. It seems that these effects are mediated in part by antioxidant, anti-inflammatory, and anti-apoptotic activities. This, therefore, justify its use to treat dementia and psychiatric disorders in Cameroon’s folk medicine.

scholarly journals Canavanine Increases the Content of Phenolic Compounds in Tomato (Solanum lycopersicum L.) Roots

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1595
Author(s):  
Pawel Staszek ◽  
Urszula Krasuska ◽  
Magdalena Bederska-Błaszczyk ◽  
Agnieszka Gniazdowska
Keyword(s):  
Oxidative Stress ◽  
Phenolic Compounds ◽  
Solanum Lycopersicum ◽  
Prolonged Treatment ◽  
Enzymatic Antioxidants ◽  
Root Tips ◽  
Polyphenol Oxidases ◽  
Solanum Lycopersicum L ◽  
Genes Encoding ◽  
Total Antioxidant

Canavanine (CAN) is a nonproteinogenic amino acid, and its toxicity comes from its utilization instead of arginine in many cellular processes. As presented in previous experiments, supplementation of tomato (Solanum lycopersicum L.) with CAN led to decreased nitric oxide (NO) level and induced secondary oxidative stress. CAN improved total antioxidant capacity in roots, with parallel inhibition of enzymatic antioxidants. The aim of this work was to determine how CAN-dependent limitation of NO emission and reactive oxygen species overproduction impact content, localization, and metabolism of phenolic compounds (PCs) in tomato roots. Tomato seedlings were fed with CAN (10 and 50 µM) for 24 or 72 h. Inhibition of root growth due to CAN supplementation correlated with increased concentration of total PCs; CAN (50 µM) led to the homogeneous accumulation of PCs all over the roots. CAN increased also flavonoids content in root tips. The activity of polyphenol oxidases and phenylalanine ammonia-lyase increased only after prolonged treatment with 50 µM CAN, while expressions of genes encoding these enzymes were modified variously, irrespectively of CAN dosage and duration of the culture. PCs act as the important elements of the cellular antioxidant system under oxidative stress induced by CAN.

scholarly journals Zinc and Copper Brain Levels and Expression of Neurotransmitter Receptors in Two Rat ASD Models

2021 ◽  
Vol 14 ◽  
Author(s):  
Elzbieta Zieminska ◽  
Anna Ruszczynska ◽  
Justyna Augustyniak ◽  
Beata Toczylowska ◽  
Jerzy W. Lazarewicz
Keyword(s):  
Cerebral Cortex ◽  
Copper Metabolism ◽  
Brain Structures ◽  
Brain Regions ◽  
Brain Diseases ◽  
Dopaminergic Receptors ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Pregnant Mothers ◽  
Serotoninergic Receptors

Zinc and copper are important trace elements necessary for the proper functioning of neurons. Impaired zinc and/or copper metabolism and signaling are implicated in many brain diseases, including autism (ASD). In our studies, autistic-like behavior in rat offsprings was induced by application to pregnant mothers valproic acid or thalidomide. Zinc and copper contents were measured in serum and brain structures: hippocampus, cerebral cortex, and cerebellum. Our research shows no interconnections in the particular metal concentrations measured in autistic animal brains and their sera. Based on patient researches, we studied 26 genes belonging to disturbed neurotransmitter pathways. In the same brain regions, we examined the expression of genes encoding proteins of cholinergic, adrenergic, serotonin, and dopamine receptors. In both rats’ ASD models, 17 out of the tested gene expression were decreased. In the cerebellum and cerebral cortex, expression of genes encoding cholinergic, adrenergic, and dopaminergic receptors decreased, whereas in the hippocampus only expression of serotoninergic receptors genes was downregulated. The changes in metals content observed in the rat brain can be secondary phenomena, perhaps elements of mechanisms that compensate for neurotransmission dysfunctions.

scholarly journals Salt stress in popcorn genotypes trigger changes of antioxidant enzymes

2019 ◽  
pp. 1607-1616
Author(s):  
Claudia Borsari Trevizan ◽  
Cristine Bonacina ◽  
Letícia Lourenceto ◽  
Tiago Benedito dos Santos ◽  
Silvia Graciele Hülse de Souza
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Salt Stress ◽  
Salt Concentration ◽  
Maximum Activity ◽  
Antioxidant Genes ◽  
Expression Of Genes ◽  
Differential Expression Pattern ◽  
Genes Encoding ◽  
Osmotic Activity

Salinity is a major problem in agriculture because it can alter the metabolism of plants and affect crop yield. This study aimed to evaluate the effect of NaCl on growth, key antioxidants and changes in the expression of genes encoding antioxidant enzymes. Two popcorn genotypes, IAC125 and UFMV2, experienced reduction in growth as the salt concentration increased. Increase in chlorophyll content and damage to the plasma membrane was observed. Consequently, changes in osmotic activity led to reduced water content in the leaves. Increased concentration of salt increased the activity of antioxidant enzymes like superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) in two popcorn genotypes but maximum activity was observed in the IAC125 genotype. Such enzymatic activities occur in order to maintain the levels of lipid peroxidation under salt stress, indicating that this genotype is tolerant to salinity conditions. The ZmAPX, ZmCAT, ZmSOD (Cu/Zn) and ZmSOD (Mn) genes increased their expression as salinity increased. The ZmSOD (Fe) gene was highly regulated in the IAC125 genotype under salt stress, but low regulation was observed in the UFM2 genotype, regardless of the salt concentration. The enhancement in tolerance against salt stress indicates that the genes involved in the antioxidative process are triggered by oxidative stress induced by abiotic stresses. These results showed that the popcorn varieties have different levels of salt tolerance due to the differential expression pattern of the antioxidant genes. The up-regulation of antioxidant enzymatic activity could lead to increased scavenging of excessive free radicals and reduce oxidative stress.

scholarly journals Pseudomonas syringae pv. tomato OxyR Is Required for Virulence in Tomato and Arabidopsis

2016 ◽  
Vol 29 (2) ◽  
pp. 119-131 ◽  
Author(s):  
Yasuhiro Ishiga ◽  
Yuki Ichinose
Keyword(s):  
Oxidative Stress ◽  
Pseudomonas Syringae ◽  
Molecular Mechanisms ◽  
Expression Profiles ◽  
High Sensitivity ◽  
Defense Responses ◽  
Bacterial Populations ◽  
Disease Symptoms ◽  
Expression Of Genes ◽  
Genes Encoding

Reactive oxygen species (ROS) have been shown to have a crucial role in plant defense responses and signaling pathways. In addition, ROS also have direct toxicity against pathogens. However, the molecular mechanisms of plant ROS in the direct effects against pathogens is still unclear. To investigate the function of plant ROS in the interactions of plant and bacterial pathogens, we focused on oxyR, encoding an oxidative stress-regulated transcription factor in Pseudomonas syringae pv. tomato DC3000 (DC3000), and generated an ΔoxyR mutant. The DC3000 ΔoxyR mutant showed high sensitivity to oxidative stress in comparison with wild type and the complemented line. The host plants of DC3000, including tomato and Arabidopsis inoculated with the ΔoxyR mutant, clearly showed reduced disease symptoms as well as reduced bacterial populations. Expression profiles of DC3000 genes revealed that OxyR could regulate the expression of genes encoding ROS-detoxifying enzymes, including catalases (KatB and KatG), in response to ROS. We also demonstrated that the expression of katB could be regulated by OxyR during the infection of DC3000 in Arabidopsis. These results suggest that OxyR has an important role in the virulence of DC3000 by regulating the expression of genes related to oxidative stress.

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