Oxidative Imbalance Research Articles

Ginsenoside Rg1 attenuates chronic inflammation-induced renal fibrosis in mice by inhibiting AIM2 inflammasome in an Nrf2-dependent manner

Chronic kidney disease (CKD) is a growing global public health issue. Ginsenoside Rg1 (Rg1) has favorable nephroprotective effects, but its role and mechanism in CKD need further investigation. Therefore, we observed the effect of Rg1 on the mouse kidneys after 21 days of low-dose lipopolysaccharide (LPS) exposure. Meanwhile, we investigated the protective mechanism of Rg1 in LPS-induced mesangial cells using the Nrf2 inhibitor ML385. We found that chronic exposure to LPS caused fibrosis in mouse kidneys, accompanied by AIM2 activation and oxidative stress imbalance; however, Rg1 restored the anomalies, accompanied by activation of Nrf2/HO-1 signaling. Finally, our in vitro studies revealed that Rg1′s nephroprotective effects could be inhibited by ML385, and Rg1 can bind Nrf2, suggesting that the protective effects of Rg1 may involve Nrf2 activation and then inhibition of the AIM2. Our study has significant implications for the prevention and treatment of kidney diseases, particularly those related to inflammation.

Analysis of oxidative status, inflammatory cytokines, and Ascaris lumbricoides infection in women at a health district in Bamenda, Northwest, Cameroon

BackgroundClinical outcomes of ascariasis, one of the most common parasitic infections, are remarkably variable ranging from asymptomatic infection to death. Ascariasis can pair absorption of fats, vitamin A, iodine, and lactose digestion and destroys the villi, with significant consequences in pregnancy outcomes, leading to growth retardation, and cognitive impairment, decreased work capacity, and adverse pregnancy outcomes. One of the crucial factors driving the clinical outcomes of ascariasis is the immune response and associated oxidative stress. This study therefore examined the prevalence of ascariasis and associated immune response dysfunction by measuring four inflammatory cytokines alongside with the oxidant and antioxidant biomarkers in women of reproductive age in a health center in Cameroon.ResultsThree-hundred and fifty-five women (pregnant and non-pregnant) were examined for the parasite. Because some participants did not donate blood and due to low volume of blood available, only 127 individuals (62 non-pregnant women and 65 pregnant women) were included for analysis of oxidative biomarkers, and 90 samples were used for the evaluation of inflammatory biomarkers (40 non-pregnant and 50 pregnant). The prevalence of Ascaris lumbricoides was of 13.23%. Ascariasis was associated with high levels in inflammatory cytokines (IL-1β, IL-12, IL-10, and TNF-α) and oxidative markers (TOS, OSI, MDA, and CAT) in both pregnant and non-pregnant women, while high level of NO was only seen in pregnant women. A significant relation was observed between some cytokines and oxidant markers: IL-10 and OSI and IL-12 and NO and between IL-1β and MDA in pregnant women, while in non-pregnant, significant relation was found between Il-10 and NO as well as IL-1β and OSI and NO. Principal component analysis (PCA) underlined a pro-inflammatory cytokine signature (with strongest contributions from IL-1β, IL-10, TNF-α). PCA also highlighted an oxidative stress with strongest contributions from TOS, OSI, SOD, NO, and CAT in pregnant and from OSI, TOS, NO, CAT, and TAC in non-pregnant.ConclusionThese findings demonstrate elevated cytokines (IL-1β, IL-12, IL-10, and TNF-α) and high oxidative stress imbalance, adding further evidence for the role of a pro-inflammatory cytokine signature of oxidative stress in women with A. lumbricoides.

Association of impulsive behavior and cerebrospinal fluid/plasma oxidation and antioxidation ratio in Chinese men

ObjectivesImpulsive behavior is the precursor of many psychiatric and neurological conditions. High levels of impulsive behavior will increase health risk behavior and related injuries. Impulsive behavior is produced and regulated by central and peripheral biological factors, and oxidative stress (OS) can aggravate it. However, previous studies only showed that impulsive behavior was related to the level of the peripheral OS. Therefore, this study aims to clarify the relationship between OS and impulsive behavior in the brain and peripheral blood. MethodsWe recruited 64 Chinese men. We measured superoxide dismutase (SOD) (including copper, zinc and manganese) and nitric oxide synthase (NOS) (including total, inducible and constitutive) in cerebrospinal fluid (CSF) and plasma. The Barratt Impulsiveness Scale version 11 (BIS-11) was used to evaluate impulsive behavior. The relationship between OS and impulsive behavior was evaluated by partial correlation analysis and stepwise multiple regression analysis. ResultsPartial correlation analysis showed that the ratio of total NOS-to-MnSOD and iNOS-to-MnSOD in CSF were negatively correlated with the BIS-11 motor scores (r = −0.431, p = −0.001; r = −0.434, p = −0.001). Stepwise multiple regression analysis showed that the ratio of CSF iNOS-to-MnSOD was the most influential variable on the BIS-11 motor scores(β = −0.434, t = −3.433, 95 %CI(−0.374, −0.098), p = 0.001). Conclusions and RelevanceThe imbalance of central oxidation and antioxidation is related to impulsive behavior, which broadens our understanding of the correlation between impulsive behavior and OS.

Glycyl-l-histidyl-l-lysine prevents copper- and zinc-induced protein aggregation and central nervous system cell death in vitro.

Common features of neurodegenerative diseases are oxidative and inflammatory imbalances as well as the misfolding of proteins. An excess of free metal ions can be pathological and contribute to cell death, but only copper and zinc strongly promote protein aggregation. Herein we demonstrate that the endogenous copper-binding tripeptide glycyl-l-histidyl-l-lysine (GHK) has the ability to bind to and reduce copper redox activity and to prevent copper- and zinc-induced cell death in vitro. In addition, GHK prevents copper- and zinc-induced bovine serum albumin aggregation and reverses aggregation through resolubilizing the protein. We further demonstrate the enhanced toxicity of copper during inflammation and the ability of GHK to attenuate this toxicity. Finally, we investigated the effects of copper on enhancing paraquat toxicity and report a protective effect of GHK. We therefore conclude that GHK has potential as a cytoprotective compound with regard to copper and zinc toxicity, with positive effects on protein solubility and aggregation that warrant further investigation in the treatment of neurodegenerative diseases.

Single-cell and spatial RNA sequencing reveal the spatiotemporal trajectories of fruit senescence

The senescence of fruit is a complex physiological process, with various cell types within the pericarp, making it highly challenging to elucidate their individual roles in fruit senescence. In this study, a single-cell expression atlas of the pericarp of pitaya (Hylocereus undatus) is constructed, revealing exocarp and mesocarp cells undergoing the most significant changes during the fruit senescence process. Pseudotime analysis establishes cellular differentiation and gene expression trajectories during senescence. Early-stage oxidative stress imbalance is followed by the activation of resistance in exocarp cells, subsequently senescence-associated proteins accumulate in the mesocarp cells at late-stage senescence. The central role of the early response factor HuCMB1 is unveiled in the senescence regulatory network. This study provides a spatiotemporal perspective for a deeper understanding of the dynamic senescence process in plants.

Cellular and Mitochondrial Pathways Contribute to SGLT2 Inhibitors-mediated Tissue Protection: Experimental and Clinical Data.

In metabolic syndrome and diabetes, compromised mitochondrial function emerges as a critical driver of cardiovascular disease, fueling its development and persistence, culminating in cardiac remodeling and adverse events. In this context, angiotensin II - the main interlocutor of the renin-angiotensin-aldosterone system - promotes local and systemic oxidative inflammatory processes. To highlight, the low activity/expression of proteins called sirtuins negatively participates in these processes, allowing more significant oxidative imbalance, which impacts cellular and tissue responses, causing tissue damage, inflammation, and cardiac and vascular remodeling. The reduction in energy production of mitochondria has been widely described as a significant element in all types of metabolic disorders. Additionally, high sirtuin levels and AMPK signaling stimulate hypoxia- inducible factor 1 beta and promote ketonemia. Consequently, enhanced autophagy and mitophagy advance through cardiac cells, sweeping away debris and silencing the orchestra of oxidative stress and inflammation, ultimately protecting vulnerable tissue from damage. To highlight and of particular interest, SGLT2 inhibitors (SGLT2i) profoundly influence all these mechanisms. Randomized clinical trials have evidenced a compelling picture of SGLT2i emerging as game-changers, wielding their power to demonstrably improve cardiac function and slash the rates of cardiovascular and renal events. Furthermore, driven by recent evidence, SGLT2i emerge as cellular supermolecules, exerting their beneficial actions to increase mitochondrial efficiency, alleviate oxidative stress, and curb severe inflammation. Its actions strengthen tissues and create a resilient defense against disease. In conclusion, like a treasure chest brimming with untold riches, the influence of SGLT2i on mitochondrial function holds untold potential for cardiovascular health. Unlocking these secrets, like a map guiding adventurers to hidden riches, promises to pave the way for even more potent therapeutic strategies.

Analyzing mechanisms of Qing Fei Bao Yuan Decoction granules in treating COPD based on LC-MS, network pharmacology and in vivo methods

Background and aimThe current therapeutic interventions of chronic obstructive pulmonary disease offer only partial alleviation of symptoms, leaving the majority of patients with persistent and significant clinical manifestations. This investigation seeks to elucidate the underlying pharmacological mechanisms of Qing Fei Bao Yuan Decoction (QFBYD) employing a multidisciplinary approach that includes network pharmacology and molecular docking techniques. Experimental procedureThe QFBYD formulation were subjected to mass spectrometry analysis, while critical compounds and biological targets were subsequently identified through the TCMSP database. Disease- and drug-specific targets were collated from a plethora of databases, including Batman-TCM, Stitch, Swiss Target Prediction and GeneCards. GO and KEGG pathways were analyzed for the collected targets. A PPI network was constructed using STRING database to isolate core targets. Molecular docking was executed using Auto Dock Tools and PyMOL software, and an animal model of COPD was developed for experimental validation. Results and conclusionsSeven salient compounds and five core biological targets were ascertained through our analysis. Additionally, four compounds demonstrated high-affinity binding to the identified targets. Pathways involving bacterial endotoxin response, oxidative stress regulation, and endothelial cell migration were significantly enriched according to the KEGG database. Animal models substantiated that QFBYD ameliorated pathological hallmarks, enhanced respiratory functionality, mitigated overexpression of pro-inflammatory cytokines, augmented the antioxidant defense mechanism, and suppressed the hyperactivity of the five core targets. The efficacy of QFBYD in COPD treatment may be primarily attributed to its role in moderating inflammatory responses and rectifying oxidative imbalances.

Targeting Vascular Impairment, Neuroinflammation, and Oxidative Stress Dynamics with Whole-Body Cryotherapy in Multiple Sclerosis Treatment.

Multiple sclerosis (MS), traditionally perceived as a neurodegenerative disease, exhibits significant vascular alternations, including blood-brain barrier (BBB) disruption, which may predispose patients to increased cardiovascular risks. This vascular dysfunction is intricately linked with the infiltration of immune cells into the central nervous system (CNS), which plays a significant role in perpetuating neuroinflammation. Additionally, oxidative stress serves not only as a byproduct of inflammatory processes but also as an active contributor to neural damage. The synthesis of these multifaceted aspects highlights the importance of understanding their cumulative impact on MS progression. This review reveals that the triad of vascular damage, chronic inflammation, and oxidative imbalance may be considered interdependent processes that exacerbate each other, underscoring the need for holistic and multi-targeted therapeutic approaches in MS management. There is a necessity for reevaluating MS treatment strategies to encompass these overlapping pathologies, offering insights for future research and potential therapeutic interventions. Whole-body cryotherapy (WBCT) emerges as one of the potential avenues for holistic MS management approaches which may alleviate the triad of MS progression factors in multiple ways.

The Association of Redox Regulatory Drug Target Genes with Psychiatric Disorders: A Mendelian Randomization Study.

Redox regulatory drug (RRD) targets may be considered potential novel drug targets of psychosis due to the fact that the brain is highly susceptible to oxidative stress imbalance. The aim of the present study is to identify potential associations between RRD targets' perturbation and the risk of psychoses; to achieve this, Mendelian randomization analyses were conducted. The expression quantitative trait loci (eQTL) and protein QTL data were used to derive the genetic instrumental variables. We obtained the latest summary data of genome-wide association studies on seven psychoses as outcomes, including schizophrenia (SCZ), bipolar disorder (BD), major depressive disorder (MDD), attention-deficit/hyperactivity disorder, autism, obsessive-compulsive disorder and anorexia nervosa. In total, 95 unique targets were included in the eQTL panel, and 48 targets in the pQTL one. Genetic variations in the vitamin C target (OGFOD2, OR = 0.784, p = 2.14 × 10-7) and melatonin target (RORB, OR = 1.263, p = 8.80 × 10-9) were significantly related to the risk of SCZ. Genetic variation in the vitamin E (PRKCB, OR = 0.248, p = 1.24 × 10-5) target was related to an increased risk of BD. Genetic variation in the vitamin C target (P4HTM: cerebellum, OR = 1.071, p = 4.64 × 10-7; cerebellar hemisphere, OR = 1.092, p = 1.98 × 10-6) was related to an increased risk of MDD. Cognitive function mediated the effects on causal associations. In conclusion, this study provides supportive evidence for a causal association between RRD targets and risk of SCZ, BD or MDD, which were partially mediated by cognition.

Compound Z526 alleviates chemotherapy-induced cachectic muscle loss by ameliorating oxidative stress-driven protein metabolic imbalance and apoptosis

Chemotherapy is one of the primary and indispensable intervention against cancers though it is always accompanied by severe side effects especially cachexia. Cachexia is a fatal metabolic disorder syndrome, mainly characterized by muscle loss. Oxidative stress is the key factor that trigger cachectic muscle loss by inducing imbalance in protein metabolism and apoptosis. Here, we showed an oral compound (Z526) exhibited potent alleviating effects on C2C12 myotube atrophy induced by various chemotherapeutic agents in vitro as well as mice muscle loss and impaired grip force induced by oxaliplatin in vivo. Furthermore, Z526 also could ameliorate C2C12 myotube atrophy induced by the combination of chemotherapeutic agents with conditioned medium of various tumor cells in vitro as well as mice muscle atrophy of C26 tumor-bearing mice treated with oxaliplatin. The pharmacological effects of Z526 were based on its potency in reducing oxidative stress in cachectic myocytes and muscle tissues, which inhibited the activation of NF-κB and STAT3 to decrease Atrogin-1-mediated protein degradation, activated the AKT/mTOR signaling pathway to promote protein synthesis, regulated Bcl-2/BAX ratio to reduce Caspase-3-triggered apoptosis. Our work suggested Z526 to be an optional strategy for ameliorating cachexia muscle atrophy in the multimodality treatment of cancers.

The silent threat: Nanopolystyrene and chrysene pollutants disrupt the intestinal mucosal barrier, new insights from juvenile Siniperca chuatsi

The intestinal mucosal barrier—comprising microbial, mechanical, chemical, and immunological barriers—is critical to protection against pathogens and maintenance of host health; however, it remains unclear whether it is affected by environmental contaminants. Therefore, the present study assessed whether exposure to ambient concentrations of nanopolystyrene (NP) and chrysene (CHR)—two ubiquitous environmental pollutants in the aquatic environment—affect the intestinal mucosal barrier in juvenile Siniperca chuatsi. After exposure for 21 days, S. chuatsi exhibited intestinal oxidative stress and imbalance of intestinal microbial homeostasis. NP and/or CHR exposure also disrupted the intestinal mechanical barrier, as evidenced by the altered intestinal epithelial cell morphology, disrupted structure of intercellular tight junctions, and decreased expression of tight junction proteins. Damage to the intestinal chemical barrier manifested as thinning of the mucus layer owing to the loss and damage of goblet cells. Furthermore, the intestinal immunological barrier was impaired as indicated by the loss of intestinal intraepithelial lymphocytes and increase in pro-inflammatory cytokines, chemokines, and immunoglobulins. These findings collectively suggest that the intestinal mucosal barrier was damaged. This study is, to the best of our knowledge, the first to report that exposure to NP and/or CHR at environmentally relevant concentrations disrupts the intestinal mucosal barrier in organisms and highlight the significance of nanoplastic/CHR pollution for intestinal health.

Oxidative Stress: Insights into Nutrition, Psychological Stress, Environmental Exposure, and Antioxidants Roles

This comprehensive review describes the intricate realms of oxidative stress, examining its origins in nutrition, psychological stress, environmental exposures, and the vital roles of antioxidants. Nutritional factors, particularly macronutrients and dietary elements, play a dual role in either inducing or preventing oxidative stress, with implications for inflammation, metabolic disorders, and carcinogenesis. The exploration extends to the profound impact of psychological stress, highlighting oxidative imbalance as a "new stress" linked to various diseases, including psychiatric disorders. Environmental exposures, encompassing pollutants and UV radiation, contribute significantly to oxidative stress, emphasizing the need for a comprehensive understanding of these mechanisms. The role of endogenous and exogenous antioxidants is crucial in neutralizing free radicals and maintaining redox homeostasis. This thorough analysis provides insights into potential interventions and underscores the complex relationships between oxidative stress, antioxidants, and human health.

Cyperus esculentus extract mitigates sertraline-induced behavioral and histopathological changes in the brain of rats

ABSTRACT Chronic use of sertraline (SRT) for depression treatment can elevate oxidative stress, potentially leading to neuropathy. Cyperus esculentus extract (CEE) has demonstrated neuroprotective properties against oxidative imbalance, memory impairment, and neural degeneration. Adult male albino rats (40 rats) were placed into four groups: control (GI), CEE (200 mg/kg/day, orally) (GII), SRT (20 mg/kg/day, intraperitoneal) (GIII), and SRT+CEE (GIV). The rats’ spatial learning was assessed using a multiple T-maze after four weeks. Subsequently, rats were euthanized, and brain tissue samples were collected to assess oxidative stress indicators, monoamine oxidase, and dopamine. Brain tissue samples were also examined histologically and immunohistochemically for synaptophysin. SRT significantly increased monoamine oxidase activity, leading to oxidative stress, reduced dopamine levels, and neuronal degeneration in the brain. Treatment with SRT resulted in a decrease in the expression of synaptophysin in the cerebral cortex, dentate gyrus of the hippocampus, and cornu ammonis. These changes, in turn, led to impaired spatial learning. Co-treatment with CEE ameliorated changes in the levels of monoamine oxidase, dopamine, and synaptophysin, restored the redox balance, and improved spatial learning. CEE demonstrated a protective effect against sertraline-induced oxidative damage, preserving neurons, synaptogenesis, and spatial learning. These findings suggest CEE’s potential positive impact on sertraline-related neurodegeneration.

Oxidative potential apportionment of atmospheric PM1: a new approach combining high-sensitive online analysers for chemical composition and offline OP measurement technique

Abstract. Source apportionment models were widely used to successfully assign highly time-resolved aerosol data to specific emissions and/or atmospheric chemical processes. These techniques are necessary for targeting the sources affecting air quality and for designing effective mitigation strategies. Moreover, evaluation of the toxicity of airborne particulate matter is important since the classically measured particulate matter (PM) concentrations appear insufficient for characterizing the impact on human health. Oxidative potential (OP) measurement has recently been developed to quantify the capability of PM to induce an oxidative imbalance in the lungs. As a result, this measurement unit could be a better proxy than PM mass concentration to represent PM toxicity. In the present study, two source apportionment analyses were performed using positive matrix factorization (PMF) from organic aerosol (OA) mass spectra measured at a 15 min time resolution using a time-of-flight aerosol chemical speciation monitor (ToF-ACSM) and from 19 trace elements measured on an hourly basis using an online metal analyser (Xact 625i). The field measurements were carried out in summer 2018. While it is common to perform PMF studies individually on ACSMs and more recently on Xact datasets, here we used a two-step methodology leading to a complete PM1 source apportionment. The outputs from both OA PMF and Xact PMF, the inorganic species concentrations from the ACSM, and the black carbon (BC) fractions (fossil fuel and wood burning) measured using an Aethalometer (AE33) were gathered into a single dataset and subjected to a combined PMF analysis. Overall, eight factors were identified, each of them corresponding to a more precise source than performing single PMF analyses. The results show that besides the high contribution of secondary ammonium sulfate (28 %) and organic nitrate (19 %), about 50 % of PM1 originated from distinct combustion sources, including emissions from traffic, shipping, industrial activities, cooking, and biomass burning. Simultaneously, PM1 filters were collected during the experimental period on a 4 h sampling basis. On these filters, two acellular OP assays were performed (dithiothreitol; OPDTT and ascorbic acid; OPAA) and an inversion method was applied on factors issued from all PMFs to assess the contribution of the PM sources to the OP. This work highlights the sensitivity of OPAA to industrial and dust resuspension sources and those of OPDTT to secondary ammonium sulfate, shipping, and biomass burning.

Putative Molecular Mechanisms Underpinning the Inverse Roles of Mitochondrial Respiration and Heme Function in Lung Cancer and Alzheimer's Disease.

Mitochondria are the powerhouse of the cell. Mitochondria serve as the major source of oxidative stress. Impaired mitochondria produce less adenosine triphosphate (ATP) but generate more reactive oxygen species (ROS), which could be a major factor in the oxidative imbalance observed in Alzheimer's disease (AD). Well-balanced mitochondrial respiration is important for the proper functioning of cells and human health. Indeed, recent research has shown that elevated mitochondrial respiration underlies the development and therapy resistance of many types of cancer, whereas diminished mitochondrial respiration is linked to the pathogenesis of AD. Mitochondria govern several activities that are known to be changed in lung cancer, the largest cause of cancer-related mortality worldwide. Because of the significant dependence of lung cancer cells on mitochondrial respiration, numerous studies demonstrated that blocking mitochondrial activity is a potent strategy to treat lung cancer. Heme is a central factor in mitochondrial respiration/oxidative phosphorylation (OXPHOS), and its association with cancer is the subject of increased research in recent years. In neural cells, heme is a key component in mitochondrial respiration and the production of ATP. Here, we review the role of impaired heme metabolism in the etiology of AD. We discuss the numerous mitochondrial effects that may contribute to AD and cancer. In addition to emphasizing the significance of heme in the development of both AD and cancer, this review also identifies some possible biological connections between the development of the two diseases. This review explores shared biological mechanisms (Pin1, Wnt, and p53 signaling) in cancer and AD. In cancer, these mechanisms drive cell proliferation and tumorigenic functions, while in AD, they lead to cell death. Understanding these mechanisms may help advance treatments for both conditions. This review discusses precise information regarding common risk factors, such as aging, obesity, diabetes, and tobacco usage.

Quantifying effect of faradaic imbalance and crossover on capacity fade of vanadium redox flow battery

In this work, we aimed to reveal two main contributors to the capacity fade of a vanadium redox flow battery (VRFB). These contributors are the oxidative imbalance caused by the hydrogen evolution reaction (HER) competing with V3+ reduction during charging, and crossover, particularly the net transfer of vanadium ions from negolyte to posolyte. To investigate this, we performed VRFB cycling under various operation conditions with sequential monitoring of the electrolytes composition. We discovered that shortly after cycling starts, the crossover makes the negolyte capacity-limiting. This leads to high polarization of the negative electrode inducing HER and increasing average oxidation state (AOS) of the electrolyte. Our examination shows that the magnitude of the oxidative imbalance correlates with that of the crossover, both being dependent on the state-of-charge (SoC). Therefore, by changing operation conditions, we can slightly influence the crossover, while dramatically affect the oxidative imbalance. We also found that the resulting magnitude of the capacity fade is a trade-off between these two side-processes. This necessitates careful optimization of the battery and electrolyte composition, along with its cycling regime. From the data obtained, we conclude that the only proper approach to achieve lower capacity fade is by ensuring that the negolyte is capacity-limiting over long-term cycling. We hope that the data on the capacity fade mechanisms presented here will facilitate development of more stable and cost-effective VRFBs.

Changes in the blood redox status of horses subjected to combat training

Combat training of police horses, involving physical activity in the presence of environmental stressors, poses a risk of oxidative stress. This study compared the oxidative imbalance after combat training in horses in the regular police service and in horses that had just been schooled. Blood collection was performed immediately after training and after 16 h rest. The activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and total antioxidant status (TAS) were determined as the markers of enzymatic antioxidant defence. At the same time, lipid peroxidation (TBARS) and protein carbonylation (Carb) were assessed as oxidation biomarkers. Additionally, oxidative imbalance indexes such as SOD/CAT, SOD/GPx, TBARS/TAS and TBARS/GPx were calculated. Animals during schooling had significantly lower SOD activity in erythrocytes than those experienced. CAT activity in erythrocytes was insignificantly higher immediately after training than during recovery. The SOD/GPx ratio was higher in experienced animals, which may reflect the intra-erythrocyte imbalance between enzymes producing and degrading hydrogen peroxide towards the first one. The concentration of carbonyl groups was significantly higher after the combat training compared to the recovery period in all horses. In inexperienced animals slight increase in TBARS/TAS and TBARS/GPx indexes were observed during the recovery time after exercises, contrary to experienced horses, in which these markers decreased slightly. These results suggest that the oxidative imbalance in inexperienced horses, although less pronounced just after combat training, was more prolonged as compared to horses in regular service.

Disruption of intestinal epithelial permeability in the Co-culture system of Caco-2/HT29-MTX cells exposed individually or simultaneously to acrylamide and ochratoxin A

Mycotoxins and thermal processing hazards are common contaminants in various foods and cause severe problems in terms of food safety and health. Combined use of acrylamide (AA) and ochratoxin A (OTA) would result in more significant intestinal toxicity than either toxin alone, but the underlying mechanisms behind this poor outcome remain unclear. Herein, we established the co-culture system of Caco-2/HT29-MTX cells for simulating a real intestinal environment that is more sensitive to AA and OTA, and showed that the combination of AA and OTA could up-regulate permeability of the intestine via increasing LY permeabilization, and decreasing TEER, then induce oxidative stress imbalance (GSH, SOD, MDA, and ROS) and inflammatory system disorder (TNF-α, IL-1β, IL-10, and IL-6), thereby leading a rapid decline in cell viability. Western blot, PAS- and AB-staining revealed that AA and OTA showed a synergistic effect on the intestine mainly through the disruption of tight junctions (TJs) and a mucus layer. Furthermore, based on correlation analysis, oxidative stress was more relevant to the mucus layer and TJs. Therefore, our findings provide a better evaluation model and a potential mechanism for further determining or preventing the combined toxicity caused by AA and OTA.

Oxidative Stress in Sepsis: A Focus on Cardiac Pathology.

This study aims to analyze post-mortem human cardiac specimens, to verify and evaluate the existence or extent of oxidative stress in subjects whose cause of death has been traced to sepsis, through immunohistological oxidative/nitrosative stress markers. Indeed, in the present study, i-NOS, NOX2, and nitrotyrosine markers were higher expressed in the septic death group when compared to the control group, associated with also a significant increase in 8-OHdG, highlighting the pivotal role of oxidative stress in septic etiopathogenesis. In particular, 70% of cardiomyocyte nuclei from septic death specimens showed positivity for 8-OHdG. Furthermore, intense and massive NOX2-positive myocyte immunoreaction was noticed in the septic group, as nitrotyrosine immunostaining intense reaction was found in the cardiac cells. These results demonstrated a correlation between oxidative and nitrosative stress imbalance and the pathophysiology of cardiac dysfunction documented in cases of sepsis. Therefore, subsequent studies will focus on the expression of oxidative stress markers in other organs and tissues, as well as on the involvement of the intracellular pattern of apoptosis, to better clarify the complex pathogenesis of multi-organ failure, leading to support the rationale for including therapies targeting redox abnormalities in the management of septic patients.

Avoidance of Inhaled Pollutants and Irritants in Asthma from a Salutogenic Perspective.

Much is known about the role of aeroallergens in asthma, but little is described about the damage caused by inhaled pollutants and irritants to the respiratory epithelium. In this context, the most frequent pollutants and irritants inhaled in the home environment were identified, describing the possible repercussions that may occur in the respiratory tract of the pediatric population with asthma and highlighting the role of the caregiver in environmental control through a salutogenic perspective. Searches were carried out in the MEDLINE/PubMed, Web of Science, Lilacs and Scopus databases for articles considered relevant for the theoretical foundation of this integrative review, in which interactions between exposure to pollutants and inhaled irritants and lung involvement. Articles published in the last 10 years that used the following descriptors were considered: air pollution; tobacco; particulate matter; disinfectants; hydrocarbons, fluorinated; odorants; chloramines; pesticide; asthma; and beyond Antonovsky's sense of coherence. Exposure to smoke and some substances found in cleaning products, such as benzalkonium chloride, ethylenediaminetetraacetic acid and monoethanolamine, offer potential risks for sensitization and exacerbation of asthma. The vast majority of the seven main inhaled products investigated provoke irritative inflammatory reactions and oxidative imbalance in the respiratory epithelium. In turn, the caregiver's role is essential in health promotion and the clinical control of paediatric asthma. From a salutogenic point of view, pollutants and irritants inhaled at home should be carefully investigated in the clinical history so that strategies to remove or reduce exposures can be used by caregivers of children and adolescents with asthma.