Oxidative Response Research Articles

Antioxidant effects of resveratrol in granulocytes from multiple sclerosis patients

Aim: Neuroinflammation is a characteristic of multiple sclerosis (MS). Resveratrol (RSV) has potent antioxidant properties and has emerged as a promising therapeutic agent for various inflammatory diseases. This study investigated the effects of RSV on inflammatory responses via reactive oxygen species (ROS) production and leukocyte cytokine secretion in patients with MS and healthy controls. Methods: The effects of RSV on ROS production in resting and stimulated granulocytes (in the presence of opsonized particles) were assessed using luminol-dependent chemiluminescence. The cytokines interleukin (IL)-10, IL-1β, IL-6, and high mobility group box 1 (HMGB1) in the supernatant of peripheral blood mononuclear cells (PBMNCs) were quantified using enzyme-linked immunosorbent assay (ELISA). Results: RSV significantly downregulated ROS production in resting and stimulated granulocytes in patients with MS and healthy controls. In the control group, RSV reduced IL-6 levels by 49% in the PBMNC supernatant, whereas IL-6 levels remained unchanged in the MS group. Interestingly, higher levels of IL-10 were detected in PBMNC supernatants from patients with MS than in controls. No significant changes were observed in IL-1β and HMGB1 levels in the PBMNC supernatant. Conclusions: Controlling ROS production is a key target for treating inflammatory diseases. Our findings suggest that RSV can effectively modulate ROS production in MS, highlighting its potential as a promising adjunct therapy for controlling oxidative innate immune responses in MS.

Mitochondrial DNA is a sensitive surrogate and oxidative stress target in oral cancer cells.

Cellular oxidative stress mediated by intrinsic and/or extrinsic reactive oxygen species (ROS) is associated with disease pathogenesis. Oxidative DNA damage can naturally be substituted by mitochondrial DNA (mtDNA), leading to base lesion/strand break formation, copy number changes, and mutations. In this study, we devised a single test for the sensitive quantification of acute mtDNA damage, repair, and copy number changes using supercoiling-sensitive quantitative PCR (ss-qPCR) and examined how oxidative stress-related mtDNA damage responses occur in oral cancer cells. We observed that exogenous hydrogen peroxide (H2O2) induced dynamic mtDNA damage responses, as reflected by early structural DNA damage, followed by DNA repair if damage did not exceed a particular threshold. However, high oxidative stress levels induced persistent mtDNA damage and caused a 5-30-fold depletion in mtDNA copy numbers over late responses. This dramatic depletion was associated with significant growth arrest and apoptosis, suggesting persistent functional consequences. Moreover, oral cancer cells responded differentially to oxidative injury when compared with normal cells, and different ROS species triggered different biological consequences under stress conditions. In conclusion, we developed a new method for the sensitive detection of mtDNA damage and copy number changes, with exogenous H2O2 inducing dynamic mtDNA damage responses associated with functional changes in stressed cancer cells. Finally, our method can help characterize oxidative DNA damage in cancer and other human diseases.

Cellular responses following ex vivo lung exposure to the nerve agent VX – Potential for additional treatment targets?

Following inhalation exposure to organophosphorus nerve agents, symptoms rapidly develop and severe respiratory symptoms, such as bronchorrhea and bronchoconstriction are the leading causes of lethality. Nerve agent-induced lung injury is little investigated and the standard treatment for symptomatic relief targets the enzyme acetylcholinesterase and muscarinic acetylcholine and GABAergic receptors. In the present study, cellular responses in lung tissue during the acute (40 min) and extended phase (24 h) following severe exposure to the nerve agent VX have been investigated using an ex vivo rat precision-cut lung slice model including electrostimulation to induce a cholinergic response. Changes in protein amount, cell viability, together with, inflammatory and oxidative stress markers have been determined in both the lung tissue and incubation medium.During the acute phase, VX caused significantly increased airway contraction and decreased airway relaxation. Five micromolar of VX did not affect the sample protein levels and cell viability in lung tissue. Among seven markers of cellular responses investigated in the lung tissue, increased levels of heme oxygenase-1 and matrix metalloproteinase-9 together with decreased levels of glutathione in the incubation medium were observed in the acute phase following VX-exposure compared to electrostimulation only. No difference in cellular response was observed following VX-exposure for 24 h compared to the air control. In comparison, LPS-exposure resulted in time-dependent changes in all markers of inflammation and oxidative response.In conclusion, the present study demonstrated VX-specific patterns of oxidative responses in the lung, as well as, signs of inflammatory response and remodelling of extracellular matrix. These potential mechanisms of tissue injury should be further investigated for their potential as additional therapeutic targets during the acute phase of intoxication.

Exploring the potential of cold plasma in Optimising quality and boosting antioxidant defence in fresh‐cut bamboo shoots

SummaryCold plasma (CP) is a promising technology for fresh‐cut fruits and vegetables. In this study, the effects of CP on postharvest senescence, especially from the perspective of oxidative response of fresh‐cut bamboo shoots were examined, including the colour, firmness, lignin content, reactive oxygen species (ROS) accumulation and antioxidant enzymatic activities. CP treatments delayed the browning of bamboo shoots indicating by the increase of L* and b* values and decrease of a* value. The browning inhibition coincided with the reduction of PPO activities up to 62% by CP at 20 kV. Cellulose and lignin accumulated during storage. CP at 30 kV accelerated lignification, whereas CP at 10 and 20 kV inhibited the increase. These results were also reflected by PAL, CAD and POD activities that were enhanced by CP at 30 kV and inhibited by CP at 10 and 20 kV. The content of O2− and H2O2 was significantly increased at the first 3 days and decreased afterwards, with a similar trend of antioxidant enzymes SOD and CAT. As smaller increases in H2O2 and O2− production in CP treated samples than in control were probably attributed to elevated CP‐induced SOD activity. In addition, there was a delay effect observed in the internal parts of bamboo shoots compared with the surface (<5 mm thick). CP extended the shelf‐life of bamboo shoots by triggering the antioxidant defence. CP at 20 kV exhibited the best preservative effect on fresh‐cut bamboo shoots.

Machine learning and single-cell analysis identify the mitophagy-associated gene TOMM22 as a potential diagnostic biomarker for intervertebral disc degeneration

BackgroundMitophagy selectively eliminates potentially cytotoxic and damaged mitochondria and effectively prevents excessive cytotoxicity from damaged mitochondria, thereby attenuating inflammatory and oxidative responses. However, the potential role of mitophagy in intervertebral disc degeneration remains to be elucidated. MethodsThe GSVA method, two machine learning methods (SVM-RFE algorithm and random forest), the CIBERSORT and MCPcounter methods, as well as the consensus clustering method and the WGCNA algorithm were used to analyze the involvement of mitophagy in intervertebral disc degeneration, the diagnostic value of mitophagy-associated genes in intervertebral disc degeneration, and the infiltration of immune cells, and identify the gene modules that were closely related to mitophagy. Single-cell analysis was used to detect mitophagy scores and TOMM22 expression, and pseudo-temporal analysis was used to explore the function of TOMM22 in nucleus pulposus cells. In addition, TOMM22 expression was compared between human normal and degenerated intervertebral disc tissue samples by immunohistochemistry and PCR. ResultsThis study identified that the mitophagy pathway score was elevated in intervertebral disc degeneration compared with the normal condition. A strong link was present between mitophagy genes and immune cells, which may be used to typify intervertebral disc degeneration. The single-cell level showed that mitophagy-associated gene TOMM22 was highly expressed in medullary cells of the disease group. Further investigations indicated the upregulation of TOMM22 expression in late-stage nucleus pulposus cells and its role in cellular communication. In addition, human intervertebral disc tissue samples established that TOMM22 levels were higher in disc degeneration samples than in normal samples. ConclusionsOur findings revealed that mitophagy may be used in the diagnosis of intervertebral disc degeneration and its typing, and TOMM22 is a molecule in this regard and may act as a potential diagnostic marker in intervertebral disc degeneration.

The Role and Mechanism of Vascular Aging in Geriatric Vascular Diseases.

Vascular aging is the pathological basis for the aging of various organ systems in the human body and is a common pathogenesis leading to the development of atherosclerosis, Alzheimer's disease, and other conditions among older adults. Aging is characterized by accelerated pulse wave velocity, thickening of the carotid artery intima-media, and decreased vascular dilation function. Signaling pathways such as mTOR, AMPK, NF-κB, Klotho, SIRT, and other key proteins are likely involved in these processes. The detection of biomarkers related to vascular aging, including senescence-associated β-galactosidase, endothelial progenitor cells, circulating endothelial microparticles, and exosomal miRNAs, aids in assessing vascular status and prognosis. Repairing endothelial injury, reducing oxidative stress-inflammatory responses, and restoring mitochondrial and telomere functions are reliable measures to counter vascular aging. In summary, research on vascular aging is the driving force that will provide rational strategies to intervene in geriatric vascular diseases and achieve the long-term goal of healthy aging.

WITHDRAWN: Grape defense against gray mold involves VvBZR1-mediated autophagy

Brassinosteroids (BRs) are a class of polyhydroxylated steroidal phytohormones that effectively affect the disease resistance in grape. However, the molecular mechanism of BR signaling networks responsible for activation of host defense against gray mold infection remained to be elucidated. The induced resistance mechanism of eBR treatment on table grapes (Vitis vinifera L. cv. Thompson Seedless) was conducted by an artificial inoculation trial. Grape berries were soaked in 0.5 mg L-1 24-epibrassinolide solution, and Botrytis cinerea suspension was injected after 6 hours. We reported a novel defense mechanism that BR-regulated autophagy in grape berry against B. cinerea. Exogenous application of 24-epibrassinolide (eBR) enhanced the grape disease resistance. The eBR-treated berries activated an oxidation-reduction (redox), polyamines metabolism, and autophagy during Botrytis infection. Transcript of BR signaling pathway genes were up-regulated within 12 h. In addition, transcriptome analysis in EBR-treated grapes infected with gray mold showed that the differentially expressed genes (DEGs) were enriched in the metabolic pathway of BR signaling pathway and autophagy. Meanwhile, the endogenous BR, SA and JA accumulated transiently. Overexpressing and silencing VvBZR1 in grape significantly affected oxidation, autophagy, and defense response. DNA affinity purification sequencing (Dap-seq), Yeast one-hybrid assay (Y1H) and dual luciferase assays (LUC) verified VvBZR1 transcriptionally regulated the autophagy related gene VvATG18a. Overexpressing VvATG18a improved the resistance of grapes to gray mold. Overall, this study sheds light on the immune mechanisms underlying the involvement of the BR signal transduction pathway in grape innate immunity, highlighting the pivotal role of VvBZR1-mediated autophagy in enhancing disease resistance.

Impact of singular versus combinatorial environmental stress on RONS generation in Drosophila melanogaster larvae.

We investigated environmentally correlated abiotic stressor desiccation (D), heat (H), and starvation (S) in the generation of reactive oxygen and nitrogen species (RONS) using Drosophila melanogaster larvae as an experimental model, subjected to either individual stressors or exposed to a combinatorial form of stressors (D + H, H + S, and D + S). The study was also extended to find synergistic endpoints where the impacts of all three stressors (D + H + S) were exerted simultaneously. We estimated the lethal time (LT20) at specific doses using regression and probit analyses based on the larval survival. LT20 values were used as the base-level parameter for further oxidative stress experimental analysis work. First, all stressors led to the activation of a typical common oxidative stress-mediated response irrespective of the mode of exposure. As envisaged, D. melanogaster larvae exhibited a homeostatic stress tolerance mechanism, triggering an antioxidant defense mechanism, indicated by an elevated level of total antioxidant capacity and enhanced activities of superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase. In all types of stress-exposed regimes, we found a negative impact of stressors on the activity of mitochondrial enzyme aconitase. Elevated levels of other oxidative stress markers, viz., lipid peroxidation, protein carbonyl content, and advanced oxidative protein products, were obvious although the increment was treatment-specific. Desiccation stress proved to be the most dominant stressor compared to heat and starvation. Among the combination of stressors, rather than a single stressor, D + H impacted more than other binary stress exposures. Focusing on the impact of singular versus combinatorial stress exposure on RONS generation, we observed an increase in the RONS level in both singular and combinatorial forms of stress exposure although the magnitude of the increment varied with the nature of stressors and their combinations. The present study indicated an "additive" effect when all three stressors (D + H + S) operate simultaneously, rather than a "synergistic" effect.

Ameliorative effect of α-tocopherol and curcumin against the deleterious effects of hydrogenated (thermally oxidized) rice bran oil in rats

Rice bran oil (RBO) is known for its health benefits due to its high content of natural antioxidants like tocotrienols, tocopherols, and oryzanols, which combat oxidative stress and inflammation. However, repeated heating of RBO above 110°C leads to degradation, forming harmful oxidative components and reducing its antioxidant content. This study aimed to investigate the effects of long-term consumption of thermally oxidized RBO on rats and the potential protective effects of curcumin and α-tocopherol supplementation. RBO was subjected to oxidative degradation through repeated frying cycles at temperatures ranging from 100°C to 180°C for 45 days. Physicochemical and phytochemical parameters of the oxidized RBO were analyzed. In vivo experiments evaluated serum biochemical, hematological, and histopathological parameters, along with oxidative and inflammatory responses in rats fed with oxidized RBO for 45 days. Results showed that thermal oxidation at 180°C significantly altered the chemical composition of RBO, increasing oxidative markers and reducing nutritional components. Consumption of oxidized RBO led to decreased body weight gain, elevated levels of various biochemical markers indicating liver and kidney dysfunction, hyperlipidemia, and increased oxidative and inflammatory damage in rats. However, supplementation with curcumin and α-tocopherol effectively mitigated these harmful effects. In conclusion, long-term consumption of thermally oxidized RBO negatively affects health parameters in rats, but fortification with curcumin and α-tocopherol helps alleviate these adverse effects

On the microscale deformation of the oxide layer formed on a Zr-2.5 Nb alloy: A micropillar compression study

Oxides are prone to brittle failure, leading to passivity loss and exposing the underlying metal during service. Thus, understanding the mechanical response of oxides is crucial for evaluating metal passivity. The present study examines the oxide layer on a Zr-2.5 Nb alloy used in CANDU® reactors after different exposure times. Micropillar compression tests on the oxide layer revealed that the mean failure stress and strain remain unchanged (are within the error) for both samples. Post-deformation characterization confirms that the failure of the oxide layer is brittle and could be pseudo-shear, which is consistent with the critical failure mode for brittle materials.

Premature senescence is regulated by crosstalk among TFEB, the autophagy lysosomal pathway and ROS derived from damaged mitochondria in NaAsO2-exposed auditory cells

Age-related hearing loss (ARHL) is one of the most prevalent types of sensory decline in a superaging society. Although various studies have focused on the effect of oxidative stress on the inner ear as an inducer of ARHL, there are no effective preventive approaches for ARHL. Recent studies have suggested that oxidative stress-induced DNA damage responses (oxidative DDRs) drive cochlear cell senescence and contribute to accelerated ARHL, and autophagy could function as a defense mechanism against cellular senescence in auditory cells. However, the underlying mechanism remains unclear. Sodium arsenite (NaAsO2) is a unique oxidative stress inducer associated with reactive oxygen species (ROS) that causes high-tone hearing loss similar to ARHL. Transcription factor EB (TFEB) functions as a master regulator of the autophagy‒lysosome pathway (ALP), which is a potential target during aging and the pathogenesis of various age-related diseases. Here, we focused on the function of TFEB and the impact of intracellular ROS as a potential target for ARHL treatment in a NaAsO2-induced auditory premature senescence model. Our results suggested that short exposure to NaAsO2 leads to DNA damage, lysosomal damage and mitochondrial damage in auditory cells, triggering temporary signals for TFEB transport into the nucleus and, as a result, causing insufficient autophagic flux and declines in lysosomal function and biogenesis and mitochondrial quality. Then, intracellular ROS derived from damaged mitochondria play a role as a second messenger to induce premature senescence in auditory cells. These findings suggest that TFEB activation via transport into the nucleus contributes to anti-senescence activity in auditory cells and represents a new therapeutic target for ARHL. We have revealed the potential function of TFEB as a master regulator of the induction of oxidative stress-induced premature senescence and the senescence-associated secretion phenotype (SASP) in auditory cells, which regulates ALP and controls mitochondrial quality through ROS production.

The ototoxicity of chlorinated paraffins via inducing apoptosis, oxidative stress and endoplasmic reticulum stress in cochlea hair cells

Hearing loss is a common chronic sensory deficit that affects millions of people worldwide and has emerged as a significant public health concern. The association between environmental exposure to chemicals and the prevalence of hearing impairment has recently attracted increased attention. Chlorinated paraffins (CPs) are a type of chemical compound that has been widely used and commonly detected in samples of both environmental and human origin. The knowledge of the toxicological effects of CPs, particularly its ototoxicity, remains limited at present. In this study, six commercial CPs were selected and evaluated using cochlea hair HEI-OC1 cells for their cytotoxicity, apoptosis, DNA damage, reactive oxygen species (ROS) accumulation and oxidative response. The cytotoxicity was observed after CPs exposure at high concentrations except for C-40 and was positively related to the chlorine content (Cl-content) in both CCK-8 and trypan blue assays. All 6 CPs induced cells apoptosis through caspase-dependent apoptotic pathway. CPs exposure induced DNA damage and stimulated ROS overproduction. Antioxidant N-acetyl-L-cysteine (NAC) could reverse the cytotoxicity and ROS accumulation caused by CPs exposure. The overexpression of ATF4 and CHOP indicated that endoplasmic reticulum (ER) stress was involved in the CPs induced cytotoxicity. Thus, CPs induced cytotoxicity and apoptosis via ROS accumulation, ER stress and DNA damage and positively related to the Cl-content and our findings indicate that CPs may pose a risk of ototoxicity at environmental relevant exposure levels.

Enhanced removal of antibiotic-resistant bacteria and resistance genes by three-dimensional electrochemical process using MgFe2O4-loaded biochar as both particle electrode and catalyst for peroxymonosulfate activation

In this study, MgFe2O4-loaded biochar (MFBC) was used as a three-dimensional particle electrode to active peroxymonosulfate (EC/MFBC/PMS) for the removal of antibiotic-resistant bacteria (ARB) and antibiotic resistance genes (ARGs). The results demonstrated that, under the conditions of 1.0 mM PMS concentration, 0.4 g/L material dosage, 5 V voltage intensity, and MFBC preparation temperature of 600 °C, the EC/MFBC600/PMS system achieved complete inactivation of E. coli DH5α within 5 min and the intracellular sul1 was reduced by 81.5 % after 30 min of the treatment. Compared to EC and PMS alone treatments, the conjugation transfer frequency of sul1 rapidly declined by 92.9 % within 2 min. The cell membrane, proteins, lipids, as well as intracellular and extracellular ARGs in E. coli DH5α were severely damaged by free radicals in solution and intracellular reactive oxygen species (ROS). Furthermore, up-regulation was observed in genes associated with oxidative stress, SOS response and cell membrane permeability in E. coli DH5α, however, no significant changes were observed in functional genes related to gene conjugation and transfer mechanisms. This study would contribute to the underlying of PMS activation by three-dimensional particle electrode, and provide novel insights into the mechanism of ARB inactivation and ARGs degradation under PMS advanced oxidation treatment.

Tissues response and bone-forming capacity of zinc oxide–eugenol sealer following the addition of nanohydroxyapatite-tyrosine amino acid: An in vivo animal study

Abstract Introduction: The zinc oxide–eugenol (ZOE) sealer is used till now in many private dental clinics although many sealers have been developed. The current study aimed to compare the biocompatibility and remineralizing capacity of ZOE sealer following the addition of nanohydroxyapatite-tyrosine amino acid. Materials and Methods: Twenty rabbits were used in this investigation, and they were divided into four groups based on the test observation period (3, 7, 21, and 28 days) following surgical implantation. General anesthesia was given for each rabbit with a subcutaneous incision of about 1 cm ± 0.5 cm made along the symphyseal area of the mandible of each rabbit. Each rabbit had four bone cavities generated in the interdental space of the lower jaw between the central and molar teeth, with one longitudinal subcutaneous incision. The ZOE sealers were mixed and directly inserted within the cavities as follows: ZOE alone on the central area of the right side of the jaw (Group A), 10% nHAp and Tyrosine mixed ZOE at the molar area (Group B), empty cavity (−ve control) located at the central area of the left side of the jaw (Group C) and 20%/nHAp and Tyrosine mixed ZOE located at the molar area on the left side of the jaw (Group D). Animals were scarified and bone biopsy samples from the tested parts were collected. Histological analysis was performed using a low-power light microscope and immunohistochemistry using runt-related transcription factor 2 (Runx2) antibody. Data were statistically analyzed utilizing the SPSS software. One-way analysis of variance was used and the post hoc test Duncan’s test was utilized to measure the significance among various groups at P ≤ 0.01. Results: The inflammatory process decreased over time for all experimental groups, associated with an increase in granulation tissue formation which was gradually decreasing over time to permit an increase in new blood vessels and new bone formation for all experimental groups that increased with time. Group D displayed the highest levels of new bone formation. Runx2 antibody expression declined progressively, particularly in Group D on 28 days. Conclusion: Superior new bone formation and biocompatible properties were demonstrated by the 20% nHAp and tyrosine mixed ZOE sealer.

Facile fabrication of bismuth oxide anchored graphene oxide for the effective electrochemical sensing of diuron

BackgroundDiuron (DU), a weed controller widely used in the agricultural industry, prolonged conception of this agrochemical residue contaminated with environmental water bodies and soil sources could cause an acute impact on the human health system. This work utilized the electrochemical determination technique due to their rapid detection, outstanding sensitivity, and economical purpose. MethodsThe electrochemical behavior of DU at the γ-Bi2O3 microplates interconnected with sheet-like graphene oxide (GO) as a surface-modified electrode was scrutinized by cyclic voltammetry (CV) and differential pulse voltammetry (DPV). The surface-modified γ-Bi2O3/GO/GCE elucidates superior electrocatalytic performance towards the irreversible oxidation response of diuron than the other surface-modified electrode in the phosphate buffer solution of 0.1 M. Significant findingsThe γ-Bi2O3/GO/GCE electrode displayed an extensive detection range of 0.1–631 µM with a 0.751 µM lower detection limit furthermore, noticeable 0.0280 µA µM-1 cm-2 sensitivity for diuron determination. In addition, the DPV experiment exposed that the γ-Bi2O3/GO/GCE electrode achieves stupendous selectivity, durability, and acceptable feasibility of the real-time samples.

Inflammatory and Oxidant Responses to Arduous Military Training: Associations with Stress, Sleep, and Performance.

Arduous military training frequently consists of prolonged physical activity, sleep disturbance, and stress that increases musculoskeletal injury risk and performance decrements. Inflammatory and oxidative stress responses have been reported in response to arduous training, but with inconsistencies across markers and with under-representation of women. The purpose of the current report was to measure circulating inflammation and oxidative stress responses to military training and to correlate biomarkers with subjective measures of stress and sleep quality as well as military fitness test performance. Candidates undergoing the 10-week Marine Corps Officer Candidate School (OCS; 101 men; 62 women) were monitored, with demographic and questionnaire data collected, and blood drawn before and after OCS. Blood was analyzed for six markers of inflammation and three markers of oxidative stress. Associations between biomarkers and questionnaire and fitness test performance were tested. All measured inflammatory markers as well as plasma antioxidant capacity were elevated following OCS. The inflammatory increase was higher in women for several markers. Sleep disturbance and stress perception were associated with IL-6, IL-10 and CRP concentrations, suggesting that low sleep disturbance and stress perception were associated with low inflammatory load. Additionally, those with the highest inflammation at each time point performed worse on fitness tests than those with low inflammation. Following arduous military training, the circulating environment in a significant portion of officer candidates resembled chronic low-grade inflammation. This circulating inflammatory environment appeared worse with poor sleep, high stress perception, and poor fitness test performance, with utility observed for CRP, IL-6, and IL-10 as biomarkers of these responses. Since inflammation may contribute to musculoskeletal injury and performance decrements, minimizing chronic inflammation during military training should be explored.

Molecular Hydrogen and Extracorporeal Gas Exchange: A Match Made in Heaven? An In Vitro Pilot Study

Extracorporeal circulation (ECC) is frequently implemented in a vast array of modalities such as hemodialysis, cardiopulmonary bypass, extracorporeal membrane oxygenation (ECMO), and others. Patients receiving any such therapy are frequently encumbered with chronic inflammation, which is inherently accompanied by oxidative stress. However, ECC treatments themselves are also responsible for sustaining or promoting inflammation. On these grounds, an in vitro study was designed to investigate the therapeutic potential of molecular hydrogen (H2) against pro-inflammatory agents in ECC settings. Five miniature ECMO circuits and a small vial (Control) were primed with heparinized blood from healthy adult donors (n = 7). Three of the ECMO systems were injected with lipopolysaccharide (LPS), out of which one was additionally treated with an H2 gas mixture. After 6 h, samples were drawn for the assessment of specific biomarkers (MCP-1, MPO, MDA-a, TRX1, and IL-6). Preliminary results indicate a progressive oxidative and inflammatory response between the six systems. Circulation has triggered inflammation and blood trauma, but the staggering influence of LPS in this outcome is indisputable. Accordingly, hydrogen’s remedial potential becomes immediately apparent as biomarker concentrations tend to be lower in the H2-handled circuit. Future research should have distinct objectives (e.g., dosage/duration/cycle of hydrogen administration) in order to ascertain the optimal protocol for patient treatment.

Oxidative response to cadmium and lead accumulations in the tissues of blue swimming crabs Portunus pelagicus from the Trang Province coastline, Southern Thailand.

Metals have been reported to alter the oxidative status of both redox-active and redox-inactive metals accompanying oxidative stress induction. In aquatic ecosystems, metal contamination is regarded as serious pollutants and bioaccumulation, especially when aquatic seafood products are involved, which results in human risk. The blue swimming crab Portunus pelagicus is a highly popular crab species for consumption as seafood in Thailand. The meat parts and the hepatopancreas (HP) together with gonad are consumed and in high demand. Therefore, the present study aimed to investigate bioaccumulation of cadmium (Cd) and lead (Pb) along with tissue oxidative responses in P. pelagicus. Sixty-seven samples of P. pelagicus were obtained from small-scale fishers along the coastline of Trang Province. Bioaccumulation of Cd and Pb and oxidative response in gill, muscle, and HP + gonad were evaluated. Cadmium and Pb accumulation levels were highest in the HP and gonad, followed by the gill and then muscle, indicating that Cd and Pb have a high affinity to be concentrated in the HP and gonad. An organ-specific oxidative response to Cd and Pb accumulation was demonstrated in which Cd significantly activated superoxide dismutase (SOD) activity in the gills and muscle tissue, while Pb significantly activated the SOD activity only in the HP and gonad. Only Cd accumulation in gill tissue represented a significant activation of lipid peroxidation, as indicated by the malondialdehyde level. This study implied that P. pelagicus exhibits an "adaptive stage" in the oxidative response of tissue due to metal accumulation. Additionally, the data presented here further indicate that the consumption of only the meat parts and removal of the HP and gonad would reduce human exposure to metal toxicity.

Chikungunya and Mayaro Viruses Induce Chronic Skeletal Muscle Atrophy Triggered by Pro-Inflammatory and Oxidative Response.

Chikungunya (CHIKV) and Mayaro (MAYV) viruses are arthritogenic alphaviruses that promote an incapacitating and long-lasting inflammatory muscle-articular disease. Despite studies pointing out the importance of skeletal muscle (SkM) in viral pathogenesis, the long-term consequences on its physiology and the mechanism of persistence of symptoms are still poorly understood. Combining molecular, morphological, nuclear magnetic resonance imaging, and histological analysis, we conduct a temporal investigation of CHIKV and MAYV replication in a wild-type mice model, focusing on the impact on SkM composition, structure, and repair in the acute and late phases of infection. We found that viral replication and induced inflammation promote a rapid loss of muscle mass and reduction in fiber cross-sectional area by upregulation of muscle-specific E3 ubiquitin ligases MuRF1 and Atrogin-1 expression, both key regulators of SkM fibers atrophy. Despite a reduction in inflammation and clearance of infectious viral particles, SkM atrophy persists until 30 days post-infection. The genomic CHIKV and MAYV RNAs were still detected in SkM in the late phase, along with the upregulation of chemokines and anti-inflammatory cytokine expression. In agreement with the involvement of inflammatory mediators on induced atrophy, the neutralization of TNF and a reduction in oxidative stress using monomethyl fumarate, an agonist of Nrf2, decreases atrogen expression and atrophic fibers while increasing weight gain in treated mice. These data indicate that arthritogenic alphavirus infection could chronically impact body SkM composition and also harm repair machinery, contributing to a better understanding of mechanisms of arthritogenic alphavirus pathogenesis and with a description of potentially new targets of therapeutic intervention.

Shenling Baizhu powder attenuates lard diet in a fatigued state-induced diarrhea via targeting microbial metabolites short chain fatty acids-mediated lipid metabolism.

Shenling Baizhu Powder (SLBZP), a traditional Chinese medicine (TCM) prescription renowned for its efficacy, is specifically recognized for its therapeutic effects in managing diarrhea associated with spleen qi deficiency. Our previous research has demonstrated that a lard diet in a fatigued state induced diarrhea belonging to spleen qi deficiency in TCM. Through a comprehensive investigation, we aimed to provide insights into the intricate relationship between SLBZP and the modulation of gut microbiota in alleviating symptoms associated with spleen qi deficiency-induced diarrhea. We induced diarrhea in mice by subjecting them to continuous standing on a multiple-platform apparatus while administering lard through intragastric administration for 14days. Subsequently, we conducted gavage administration of SLBZP at a concentration of 0.637g/ml for seven days. We observed a therapeutic effect of SLBZP on diarrhea induced by a lard diet in a fatigued state. SLBZP mitigated disorders in lipid metabolism and diminished hepatic oxidative responses. Additionally, SLBZP reversed gut microbiota dysbiosis of diarrheic mice and notably increased the production of short-chain fatty acids (SCFAs), primarily acetic acid, butyric acid, and valeric acid. Through correlation analysis, we additionally identified Lactobacillus reuteri and Lactobacillus intestinalisas potentially pivotal species associated with the therapeutic effects of SLBZP. We demonstrated that SLBZP exerts therapeutic effects on diarrhea caused by a lard diet in a fatigued state by repairing the intestinal mucosal barrier, improving lipid metabolism disorders, and regulating gut microbiota and metabolites SCFAs.