Oxidation Of Nucleic Acids Research Articles

Enhancement of salt tolerance of transgenic Arabidopsis thaliana by Zostera japonica DnaJ gene

Abstract Soil salt damage has become one of the main biological stresses affecting plant seed germination, crop growth and yield. Salt damage can lead to the accumulation of superoxide anion, hydrogen peroxide and hydroxyl free radicals in plants, and a large amount of accumulated reactive oxygen species will cause the oxidation of lipids, proteins and nucleic acids and then cause cell damage. In this experiment, the seedlings and adult plants of transgenic Arabidopsis with overexpression of Zostera japonica (Z. japonica) DnaJ gene ZjDjB1 were used as materials. Wild-type and transgenic ZjDjB1 Arabidopsis were treated with 100 mM and 200 mM NaCl and root length, fresh weight, leaf water content and dry weight, physiological indexes and antioxidant system enzyme activities were measured. The results showed that overexpression of Z. japonica DnaJ gene ZjDjB1 could significantly alleviate the damage caused by salt stress to transgenic ZjDjB1 Arabidopsis seedlings and adult plants. The results showed that overexpression of Z. japonica DnaJ gene ZjDjB1 could reduce the content of MDA and O2-, increase the content of proline and activate the enzyme activity of antioxidant system under salt stress, to reduce the damage of salt stress to plants.

Advanced glycation end products and their soluble receptor (sRAGE) in patients with Hashimoto's thyroiditis on levothyroxine substitution.

Advanced glycation end products (AGEs) are heterogenous group of irreversible chemical moieties originated from non-enzymatic glycation and oxidation of proteins, nucleic acids, and lipids. The engagement of AGEs with their chief cellular receptor (RAGE) activates a myriad of signaling pathways contributing to the progression of chronic diseases like autoimmune thyroiditis, type 2 diabetes mellitus and its complications. Soluble RAGE (sRAGE) prevents AGE-RAGE interaction in a competitive manner. We investigated the association between serum AGE, sRAGE and thyroid function in 73 Hashimoto thyroiditis patients (HT) on levothyroxine substitution, and in 83 age, BMI and gender-matched healthy controls. The serum AGEs levels were determined by autofluorescence on a multi-mode microplate reader, and the serum sRAGE levels by ELISA method. Mean AGE level was lower (10.71 vs 11.45 AU/µg protein; p=0.046), while mean sRAGE level was higher (923 vs 755 pg/mL; p<0.0005) in the serum of HT patients than the controls. AGE correlated with age, while sRAGE correlated negatively with BMI in both groups. We found negative correlation between AGE and fT3 levels (r=-0.32; p=0.006) and sRAGE and TSH levels (r=-0.27; p=0.022) in HT patients, while we failed to find association between AGE, sRAGE and parameters of thyroid function in the control group. Median AGE/sRAGE ratio was lower in HT patients than in controls (2.4, IQR 1.9 - 3.1 vs 3.3, IQR 2.3 - 4.1 AU/pg; p < 0.001). In HT patients, the AGE/sRAGE ratio correlated positively with BMI and correlated negatively with fT3. According to our results in HT patients lower TSH and higher fT3 levels within the reference range is accompanied by a favorable AGE/RAGE balance. Further investigations are needed to confirm these results.

A deep redox proteome profiling workflow and its application to skeletal muscle of a Duchenne Muscular Dystrophy model.

Perturbation to the redox state accompanies many diseases and its effects are viewed through oxidation of biomolecules, including proteins, lipids, and nucleic acids. The thiol groups of protein cysteine residues undergo an array of redox post-translational modifications (PTMs) that are important for regulation of protein and pathway function. To better understand what proteins are redox regulated following a perturbation, it is important to be able to comprehensively profile protein thiol oxidation at the proteome level. Herein, we report a deep redox proteome profiling workflow and demonstrate its application in measuring the changes in thiol oxidation along with global protein expression in skeletal muscle from mdx mice, a model of Duchenne Muscular Dystrophy (DMD). In-depth coverage of the thiol proteome was achieved with >18,000 Cys sites from 5,608 proteins in muscle being quantified. Compared to the control group, mdx mice exhibit markedly increased thiol oxidation, where a ∼2% shift in the median oxidation occupancy was observed. Pathway analysis for the redox data revealed that coagulation system and immune-related pathways were among the most susceptible to increased thiol oxidation in mdx mice, whereas protein abundance changes were more enriched in pathways associated with bioenergetics. This study illustrates the importance of deep redox profiling in gaining greater insight into oxidative stress regulation and pathways/processes that are perturbed in an oxidizing environment.

The role of oxidative stress in the development of Alzheimer's disease

Oxidative stress is one of the main mechanisms for the development of Alzheimer's disease (AD); it is closely related to other key mechanisms of neurodegeneration such as mitochondrial dysfunction, inflammation, dysregulation of metal homeostasis, and protein misfolding. We have considered the role of beta-amyloid plaques and neurofibrillary tau-glomeruli in the development of AD. We analyzed the role of the products of oxidation of proteins, lipids and nucleic acids in the pathogenesis of the disease, which can be considered as markers of an early stage of AD. The main mechanisms of mitochondrial dysfunction, the damaging effect of accumulating metals under oxidative stress, as well as the role of brain hypoperfusion in its occurrence are considered.

Vitamin B12 Attenuates Changes in Phospholipid Levels Related to Oxidative Stress in SH-SY5Y Cells.

Oxidative stress is closely linked to Alzheimer’s disease (AD), and is detected peripherally as well as in AD-vulnerable brain regions. Oxidative stress results from an imbalance between the generation and degradation of reactive oxidative species (ROS), leading to the oxidation of proteins, nucleic acids, and lipids. Extensive lipid changes have been found in post mortem AD brain tissue; these changes include the levels of total phospholipids, sphingomyelin, and ceramide, as well as plasmalogens, which are highly susceptible to oxidation because of their vinyl ether bond at the sn-1 position of the glycerol-backbone. Several lines of evidence indicate that a deficiency in the neurotropic vitamin B12 is linked with AD. In the present study, treatment of the neuroblastoma cell line SH-SY5Y with vitamin B12 resulted in elevated levels of phosphatidylcholine, phosphatidylethanolamine, sphingomyelin, and plasmalogens. Vitamin B12 also protected plasmalogens from hydrogen peroxide (H2O2)-induced oxidative stress due to an elevated expression of the ROS-degrading enzymes superoxide-dismutase (SOD) and catalase (CAT). Furthermore, vitamin B12 elevates plasmalogen synthesis by increasing the expression of alkylglycerone phosphate synthase (AGPS) and choline phosphotransferase 1 (CHPT1) in SH-SY5Y cells exposed to H2O2-induced oxidative stress.

Increased Oxidation From Glucose Limiting Conditions or SOD Deletions Result in Activation of No‐Go Decay and Subsequent P‐body Assembly

The budding yeast, Saccharomyces cerevisiaepreferentially metabolizes glucose anaerobically when it is abundant. However, as glucose becomes depleted, yeast will enter diauxic shift. Under this condition, growth will slow, and glucose becomes metabolized aerobically. Upregulation of aerobic glucose metabolism ultimately leads to the increase of intracellular reactive oxygen species (ROS). The increase of ROS can lead to oxidation of nucleic acids through formation of 8‐oxoguanine bases (8‐oxoG). In mRNA the presence of 8‐oxoG can elicit ribosome stalls, resulting in translational shutdown and the activation of the no‐go mRNA quality control pathway. No‐go decay is mediated by the proteins Hbs1p and Dom34p, which act to remove stalled ribosomes, and will promote cleavage of the mRNA at the stall site. The remaining 5’ fragment is subject to 3’‐5’ decay by the cytoplasmic exosome, while the 3’ fragment is degraded 5’‐3’ by exonuclease Xrn1p in P‐bodies, which are sites of mRNA degradation.Upon growing yeast into diauxic shift, an increase in P‐body assembly was observed. P‐bodies contain mRNA decay enzymes and are sites where nontranslating mRNA will localize to be degraded. This observed increase in P‐body assembly appears to be due to an upregulation of no‐go Decay, as P‐body assembly is reduced in strains lacking either Dom34p or Hbs1p. Upon exposure to the antioxidant quercetin during diauxic shift, P‐body assembly is abrogated showing that generation of ROS is responsible for the activation of no‐go decay and subsequent P‐body assembly. The same result is phenocopied by exposing yeast to glucose limiting conditions (0.5% glucose). As expected with the increased oxidation from glucose limiting conditions, global translation is also reduced. Interestingly, strains lacking either Sod1p or Sod2p, also show a reduction in global translation, along with an upregulation of no‐go decay and P‐body assembly. These data suggest that physiological stresses that lead to an increase in ROS, which can damage mRNA leading to activation of No‐Go Decay and subsequent P‐body assembly.

Effect of antioxidants in temporal lobe epilepsy

Epilepsy is a common neurological disorder that affects around 70 million people in the world, which represents approximately 1%of the world population. Seizures are transitory episodes produced by excessive neuronal discharges. They are characterized bytransient behavioral changes that are caused by abnormal and excessive neuronal synchronization in the brain. These episodes canbe triggered by genetic or acquired factors that alter normal brain function such as autoimmune diseases, genetic mutations,encephalopathies, head trauma, cerebrovascular accidents, febrile seizures or statusepilepticus. Temporal lobe epilepsy is a seriousneurological disorder, which represents 60% to 70% of drug-resistant epilepsy, and is an important form of epilepsy acquired byany of the factors mentioned. Seizures can generate recurrent cycles of excitotoxicity and oxidative stress that cause neuronaldamage and cell death. Oxidative stress is an imbalance between the endogenous antioxidant system and the overproduction ofreactive oxygen species (ROS), consequently, oxidation of proteins, lipids and nucleic acids occurs in the brain, resulting inapoptosis, proteopathies, mitochondrial dysfunction, glial cell activation and neuroinflammation. ROS are responsible for thegeneration of oxidative stress and could be involved in neuronal damage that contributes to the establishment of epileptogenesis andspontaneous seizures in patients and experimental models. The administration of agents with antioxidant and anti-inflammatoryproperties could represent a therapeutic alternative aimed at reducing oxidative stress during epileptogenesis or seizures to reducethe severity of the pathological processes involved, and thus attenuate the neurobiological consequences that occur in temporal lobeepilepsy.

Carrier-Free Deferoxamine Nanoparticles against Iron Overload in Brain

Carrier-Free Deferoxamine Nanoparticles against Iron Overload in Brain

The growth of Escherichia coli cultures under the influence of pheomelanin nanoparticles and a chelant agent in the presence of light.

Growing concern of antibiotic resistance has increased research efforts to find nonspecific treatments to inhibit pathogenic microorganisms. In this regard, photodynamic inactivation is a promising method. It is based on the excitation of a photosensitizer molecule (PS) with UV-Vis radiation to produce reactive oxygen species. The high reactivity of such species nearby the PS leads to oxidation of bacterial cell walls, lipid membranes (lipid peroxidation), enzymes, and nucleic acids, eventually producing cell death. In the last decade, many studies have been carried out with different photosensitizers to suppress the growth of bacteria, fungi, viruses, and malignant tumors. Here, our main motivation is to employ pheomelanin nanoparticles as sensitizers for inhibiting the growth of the Gram-negative bacteria E. coli, exposed to blue and UVA radiation. In order to perform our experiments, we synthesized pheomelanin nanoparticles from L-DOPA and L-cysteine through an oxidation process. We carried out experiments at different particle concentrations and different energy fluences. We found that cultures exposed to UVA at 166 μg/mL and 270 J/cm2, in conjunction with ethylenediaminetetraacetic acid (EDTA) as an enhancer, decreased in the viable count 5 log10. Different reactive oxygen species (singlet oxygen, hydroxyl radicals, and peroxynitrates) were detected using different procedures. Our results suggest that the method reported here is effective against E. coli, which could encourage further investigations in other type of bacteria.

Cerebral Ischemia Induces Iron Deposit, Ferritin Accumulation, Nuclear Receptor Coactivator 4-depletion, and Ferroptosis.

The neuronal death upon cerebral ischemia shares not only characteristics of necrosis, apoptosis, and autophagy but also exhibits biochemical and morphological characteristics of ferroptosis. Ferroptosis is a regulated form of cell death that is considered to be an oxidative iron-dependent process. It is now commonly accepted that iron and free radicals are considered to cause lipid peroxidation as well as the oxidation of proteins and nucleic acids, leading to increased membrane and enzymatic dysfunction and finally contributing to cell death. Although ferroptosis was first described in cancer cells, emerging evidence now links mechanisms of ferroptosis to many different diseases, including cerebral ischemia. The objective of this study was to identify the key players and underlying biochemical pathways of ferroptosis, leading to cell death upon focal cerebral ischemia in mice by using immunofluorescence, Western blotting, histochemistry, and densitometry. In this study, we demonstrated that cerebral ischemia induced iron-deposition, downregulated dramatically the expression of the glutathione peroxidase 4 (GPX4), decreased the expression of the nuclear receptor coactivator 4 (NCOA4), and induced inappropriate accumulation of ferritin in the ischemic brain. This supports the hypothesis that an ischemic insult may induce ferroptosis through inhibition of GPX4. We conclude that iron excess following cerebral ischemia leads to cell death despite activating compensatory mechanisms for iron homeostasis, as illustrated by the accumulation of ferritins. These data emphasized the presence of a cellular mechanism that allows neuronal cells to buffer iron levels.

Pathogenic Molecular Mechanisms in Periodontitis and Peri-Implantitis: Role of Advanced Glycation End Products.

Advanced Glycation End Products (AGEs), the products of the non-enzymatic oxidation of proteins, nucleic acids, and lipids, are accumulated in periodontal tissues under hyperglycemic conditions such as Diabetes Mellitus (DM) and are responsible for sustained periodontal destruction. AGEs mediate their intracellular effects either directly or indirectly through receptor binding (via RAGE) in all types of periodontal ligament cells (osteocytes, gingival fibroblasts, stem cells, epithelial cells), indicating an important target for intervention. In combination with lipopolysaccharides (LPS) from Porphyromonas gingivalis (Pg), the negative impact of AGEs on periodontal tissue is further enhanced and accentuated. In addition, AGE accumulation is evident in peri-implantitis, yet through different underlying molecular mechanisms. Novel therapeutic approaches targeting the effects of AGEs in periodontal ligament cells show beneficial effects in pre-clinical studies. Herein, we provide evidence on the detrimental role of AGE accumulation in oral cavity tissues and their associated signaling pathways in periodontitis and peri-implantitis to further highlight the significance of oral or topical use of AGE blockers or inhibitors along with dental biofilms’ removal and DM regulation in patients’ management.

Phthalate Exposure and Biomarkers of Oxidation of Nucleic Acids: Results on Couples Attending a Fertility Center.

Phthalates are substances used as plasticizing agents and solvents that can increase the risk of infertility and that appear to induce oxidative stress. The aim of the study was to show the possible relationship between urinary concentrations of phthalates metabolites, namely MEP, MBzP, MnBP, MEHP, MEHHP, and MnOP and biomarkers of nucleic acids oxidation, methylation, or protein nitroxidation. The oxidative stress biomarkers measured in human urine were 8-oxo-7,8-dihydroguanine, 8-oxo-7,8-dihydroguanosine, 8-oxo-7,8-dihydro-2′-deoxyguanosine, 3-nitrotyrosine, and 5-methylcytidine. Two hundred and seventy-four couples were enrolled, undergoing an assisted reproduction technology (ART) treatment, urine samples were analyzed in HPLC/MS-MS, and then two sub-groups with urinary concentration > 90th or <10th percentile were identified, reducing the sample size to 112 subjects. The levels of oxidative stress biomarkers were measured in both groups, reduced to 52 men and 60 women. A statistically significantly difference for 8-oxoGuo and 3-NO2Tyr between men and women, with higher levels in men, was found. The levels of oxidative stress biomarkers were directly correlated with some phthalate concentrations in both sexes.

On the Role of Paraoxonase-1 and Chemokine Ligand 2 (C-C motif) in Metabolic Alterations Linked to Inflammation and Disease. A 2021 Update.

Infectious and many non-infectious diseases share common molecular mechanisms. Among them, oxidative stress and the subsequent inflammatory reaction are of particular note. Metabolic disorders induced by external agents, be they bacterial or viral pathogens, excessive calorie intake, poor-quality nutrients, or environmental factors produce an imbalance between the production of free radicals and endogenous antioxidant systems; the consequence being the oxidation of lipids, proteins, and nucleic acids. Oxidation and inflammation are closely related, and whether oxidative stress and inflammation represent the causes or consequences of cellular pathology, both produce metabolic alterations that influence the pathogenesis of the disease. In this review, we highlight two key molecules in the regulation of these processes: Paraoxonase-1 (PON1) and chemokine (C-C motif) ligand 2 (CCL2). PON1 is an enzyme bound to high-density lipoproteins. It breaks down lipid peroxides in lipoproteins and cells, participates in the protection conferred by HDL against different infectious agents, and is considered part of the innate immune system. With PON1 deficiency, CCL2 production increases, inducing migration and infiltration of immune cells in target tissues and disturbing normal metabolic function. This disruption involves pathways controlling cellular homeostasis as well as metabolically-driven chronic inflammatory states. Hence, an understanding of these relationships would help improve treatments and, as well, identify new therapeutic targets.

ANTIOXIDANT ACTIVITY OF TARAXACUM OFFICINALE

Background. The oxygen is the ultimate electron acceptor in the electron flow system that produces energy. Problems appears when the electron flow becomes uncoupled thus, generating free radicals. While the majority of processes require oxygen, the last is a highly reactive molecule that can damage cells by producing reactive oxygen species, such as hydroxyl radical, superoxide radical, hydrogen peroxide and hypochlorous acid, all together defined as triggers of oxidative stress. The last is involved in many types of pathologies, such as cancer, atherosclerosis and rheumatic arthritis. Antioxidants can stop formation of free radical by giving hydrogen atoms or scavenging them. The antioxidant can be defined any molecule capable of preventing or blocking oxidation of lipids, proteins and nucleic acids. The reduced glutathione (GSH), as well enzymes, glutathione peroxidase (GPO), glutathione reductase (GR) and glutathione S-transferase (GST) represent antioxidants which prevent the formation of new free radicals, converting them into less harmful molecules. The present study was conducted to assess the antioxidant activity of Taraxacum officinale (TO) ethanolic extracts with different bioactive contents. This experiment was conducted with extracts prepared from dandelion (Taraxacum officinale F. H. Wigg) leaves. A series (10%, 20%, 25%, 40%, 50% and 80%) of ethanolic extracts were made. The influence of TO extracts on RBC’s GPO, GR, GST, glutathione (GSSG, GSH and total-GSH) and thiols (native and total) was evaluated by measuring absorbance spectrophotometrically. Conclusions. Taraxacum officinale ethanolic extracts exhibit a strong antioxidant activity. This plant is capable of preventing damage of cells during oxidative stress process, by using different targets of glutathione system. But, this activity depends of ethanol concentrations, maybe due to different bioactive content.

The Impact of Short-Wave UV Radiation on Peroxidase Activity in Soft Wheat Seeds

The effect of UV radiation on plants provokes oxidative stress, accompanied by the production of reactive oxygen species that can have a direct destructive effect on cellular structures and initiate free radical oxidation of proteins, lipids, and nucleic acids. There is an antioxidant defense system in plant cells that includes a complex of low and high molecular weight compounds. Antioxidants with high molecular weight are enzymes, the key of which is peroxidase [PO]. The paper studies changes in PO activity in soft spring wheat seedlings due to grain treatment with small and medium doses of short-wave UV radiation. A UV-dosed irradiation system (Bio-Link Vilber) with the exposure time 0–60 minutes in increments of 10 minutes was used for seed treatment. Pre-soaked wheat seeds were germinated in Petri dishes. PO activity was determined colorimetrically in three-day-old wheat seedlings, according to A. L. Boyarkin [3]. When the source was irradiated for up to 30 minutes, a clear dependence of the PO activity on the exposure time was not established. The maximum increase in peroxidase activity (by 25.9% relative to the control) was detected with 30-minute UV irradiation. A further increase in exposure time led to a significant decrease in enzyme activity. Moreover, vital feedback was revealed between the activity and exposure time in the range of 30–60 minutes.

Cumulative damage by nonthermal plasma (NTP) exceeds the defense barrier of multiple antibiotic-resistant Staphylococcus aureus: a key to achieve complete inactivation

Abstract Objectives The aim of this study was to provide a comprehensive understanding of the nonthermal plasma (NTP)-induced inactivated behaviors on a multiple antibiotic–resistant (MAR) Staphylococcus aureus (S. aureus). Materials and Methods A dielectric barrier discharge (DBD) NTP system was employed for the inactivation of a MAR S. aureus under various applied powers of 35, 45, and 55 W, and gas distances of 4, 6, and 8 mm. The inactivation kinetics of S. aureus were estimated with linear and nonlinear predictive models. In addition, degradation of carotenoid pigment, peroxidation of fatty acids, oxidation of nucleic acids and proteins, and alteration in gene expression were analyzed after NTP treatment. Results and Discussion The computationally simulated results indicated that the densities of various reactive species increased with enhanced applied powers and decreased discharge distances. These species were further transformed into reactive oxidative and nitrogen species in the gas–liquid interphase and liquid phase. The oxidative and nitrosative stress of NTP resulted in severe damage to cellular components and the morphological structure of S. aureus. On the other hand, the plasma reactive species could also induce the sublethal injury of S. aureus through upregulating the general stress response, antioxidative and antinitrosative defensive systems. Once the cumulative damages overrode the stress tolerance of S. aureus, the completed cell death was finally achieved by NTP. Conclusions This work infers the possible risk of inducing the repair and resistant capacity of pathogens when the applied NTP parameters are inappropriate, which helps the optimization of NTP process to achieve sufficient inactivation.

New Promises from an Old Friend: Iodine-Rich Compounds as Prospective Energetic Biocidal Agents.

For a very long time, frequent occurrences of biocrises have wreaked havoc on human beings, animals, and the environment. As a result, it is necessary to develop biocidal agents to destroy or neutralize active agents by releasing large amounts of strong biocides which are obtained upon detonation. Iodine is an efficient biocidal agent for bacteria, fungi, yeasts, viruses, spores, and protozoan parasites, and it is the sole element in the periodic table that can destroy microbes without contaminating the environment. Based on chemical biology, the mechanism of iodine as a bactericide may arise from oxidation and iodination reactions of cellular proteins and nucleic acids. However, because of the high vapor pressure causing elemental iodine to sublime readily at room temperature, it is inconvenient to use this material in its normal solid state directly as a biocidal agent under ambient conditions. Iodine-rich compounds where iodine is firmly bonded in molecules as a C-I or I-O moiety have been observed to be among the most promising energetic biocidal compounds. Gaseous products comprised of large amounts of iodine or iodine-containing components as strong biocides are released in the decomposition or explosion of iodine-rich compounds. Because of the detonation pressure, the iodine species are distributed over a large area greatly improving the efficacy of the system and requiring considerably less effort compared to traditional biocidal methods. The commercially available tetraiodomethane and tetraiodoethene, which possess superb iodine content also have the disadvantages of volatility, light sensitivity, and chemically reactivity, and therefore, are not suitable for use directly as biocidal agents. It is absolutely critical to synthesize new iodine-rich compounds with good thermal and chemical stabilities.In this Account, we describe our strategies for the syntheses of energetic iodine-rich compounds while maintaining the maximum iodine content with concomitant stability and routes for the synthesis of oxygen-containing iodine-rich compounds to improve the oxygen balance and achieve both high-energy and high-iodine content. In the other work, which involves cocrystals, iodine-containing polymers were also summarized. It is hoped that this Account will provide guidelines for the design and syntheses of new iodine-rich compounds and a route for the development of inexpensive, more efficient, and safer iodine-rich antibiological warfare agents of the future.

Electrophile Modulation of Inflammation: A Two-Hit Approach.

Electrophilic small molecules have gained significant attention over the last decade in the field of covalent drug discovery. Long recognized as mediators of the inflammatory process, recent evidence suggests that electrophiles may modulate the immune response through the regulation of metabolic networks. These molecules function as pleiotropic signaling mediators capable of reversibly reacting with nucleophilic biomolecules, most notably at reactive cysteines. More specifically, electrophiles target critical cysteines in redox regulatory proteins to activate protective pathways such as the nuclear factor erythroid 2-related factor 2-Kelch-like ECH-associated protein 1 (Nrf2-Keap1) antioxidant signaling pathway while also inhibiting Nuclear Factor κB (NF-κB). During inflammatory states, reactive species broadly alter cell signaling through the oxidation of lipids, amino acids, and nucleic acids, effectively propagating the inflammatory sequence. Subsequent changes in metabolic signaling inform immune cell maturation and effector function. Therapeutic strategies targeting inflammatory pathologies leverage electrophilic drug compounds, in part, because of their documented effect on the redox balance of the cell. With mounting evidence demonstrating the link between redox signaling and metabolism, electrophiles represent ideal therapeutic candidates for the treatment of inflammatory conditions. Through their pleiotropic signaling activity, electrophiles may be used strategically to both directly and indirectly target immune cell metabolism.

Targeting mitochondrial oxidative stress with MitoQ reduces NET formation and kidney disease in lupus-prone MRL-lpr mice

ObjectivesRecent investigations in humans and mouse models with lupus have revealed evidence of mitochondrial dysfunction and production of mitochondrial reactive oxygen species (mROS) in T cells and neutrophils. This can...

Role of Oxidative Stress and Antioxidant Defense Biomarkers in Neurodegenerative Diseases.

Oxidative stress is caused by an imbalance in a redox system. It may involve either excessive production of reactive oxygen species or dysfunction of the antioxidant defense system. Unlike other viscera, the brain is especially highly susceptible to oxidative damage because of it requires a high oxygen level and contains an abundance of peroxida-tion-susceptible lipid cells. Oxidative stress is among the common etiological factors involved in neurodegeneration. To measure The extent of oxidative stress is measured with several indicators or biomarkers that are known to arise from oxidation of major biomolecules, including lipids, proteins, carbohydrates, and nucleic acids. In this review, we will discuss oxidative stress biomarkers associated with neurodegenerative diseases, for instance, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. We will also highlight the biomarkers of antioxidant defense mechanisms that are impaired in these diseases.