Changes In Oxidative Stress Markers Research Articles

Respiratory Symptoms and Changes of Oxidative Stress Markers among Motorbike Drivers Chronically Exposed to Fine and Ultrafine Air Particles: A Case Study of Douala and Dschang, Cameroon.

Recent studies revealed that the high production of reactive oxidative species due to exposure to fine or ultrafine particles are involved in many chronic respiratory disorders. However, the poor standard of clinical data in sub-Saharan countries makes the assessment of our knowledge on the health impacts of air pollution in urban cities very difficult. Objective: The aim of this study was to evaluate the distribution of respiratory disorders associated with exposure to fine and ultrafine air particles through the changes of some oxidative stress biomarkers among motorbike drivers from two cities of Cameroon. Methods: A cross-sectional survey using a standardized questionnaire was conducted in 2019 on 191 motorcycle drivers (MDs) working in Douala and Dschang. Then, the activities of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) were measured using colorimetric methods. The data of participants, after being clustered in Microsoft Excel, were analyzed and statistically compared using SPSS 20 software. Results: The motorbike drivers recruited from both cities were from 21 to 40 years old, with a mean age of 29.93 (±0.82). The distribution of respiratory disorders, such as a runny nose, cold, dry cough, chest discomfort, and breathlessness, was significantly increased among MDs in Douala. According to the results of biological assays, SOD and MDA were significantly greater among the MDs recruited in Douala compared to those of Dschang. The change in these oxidative stress markers was significantly positively correlated with the mobilization of monocytes and negatively correlated with neutrophils, showing the onset and progression of subjacent inflammatory reactions, and it seemed to be significantly influenced by the location MDs lived in. Conclusions: Through this study, we have confirmed the evidence supporting that the onset and progression of oxidative stress is caused by the long-term exposure to fine or ultrafine air particles among working people living in urban cities. Further studies should be conducted to provide evidence for the cellular damage and dysfunction related to the chronic exposure to fine particulate matter (PM) in the air among working people in the metropolitan sub-Saharan Africa context.

Genomic instability and oxidative stress markers in pregnant women presenting fetal malformation

ObjectivesTo evaluated the oxidative stress and genomic instability in the peripheral blood of pregnant women with fetal malformation (PWFM), pregnant women (PW) and non-pregnant women (NPW). MethodsProtein carbonyl test (CP), thiobarbituric acid reactive substances test (TBARS), catalase enzyme activity (CAT), micronucleus assay with blocking cell cytokinesis - cytome (CBMN - cyt) and myeloperoxidase (MPO) assay were performed. Fetal karyotype and alpha-fetoprotein (AFP) in combination with ultrasound, were assessed to allow the diagnosis of fetal malformation. ResultsAn increase in CP, CAT and micronucleus was observed in the third trimester of pregnancy of PW compared to NPW. PWFM presented similar parameter analysis to PW, as well as in the comparison of the second trimesters of this groups. PWFM in the third gestational trimester showed a reduction in CP, nucleoplasmic bridge (NPB) and CAT compared to the same gestational period of PW. Considering the complete sample, participants who usually drank coffee daily had an increased frequency of nuclear buds (NBUD); CAT was decreased in whites compared to other ethnic groups. ConclusionsPregnancy is a physiological process that can lead to changes in oxidative stress markers and genomic instability through its course and compared to non-pregnant women.

Surfactant protein-D, diabetes mellitus, oxidative stress, infections and inflammation on the crossroad: A Systematic review.

To review the association of surfactant protein-D with type 2 diabetes mellitus, infections, oxidative stress and inflammation, and the changes in oxidative stress markers in type 2 diabetes mellitus. The systematic review was conducted from April to September 2022, and comprised search on PubMed, Web of Sciences, Scopus, Science Direct and Google Scholar databases for relevant studies published in English language between January 1, 2000, and June 30, 2022. The search was updated in September 2022. After transferring literature to Mendeley, relevant data was extracted from the included studies. Quality assessment for eligible studies was done using Joanna Briggs Institute Critical Appraisal Checklist. Quality of evidences was assessed by using Grading of Recommendations Assessment, Development and Evaluation tool. Of the 203 studies identified, 18(8.9%) were analysed; 16(89%) with humans and 2(11%) with animals as subjects There were 5 (31.25%) studies for SP-D, of which 4 (80%) studies reported lower surfactant protein-D in type 2 diabetes mellitus cases than controls. Its significant negative association with glycated haemoglobin was reported by 1(20%) study and 2(40%) studies with fasting blood glucose levels. Higher surfactant protein-D in type 2 diabetes mellitus cases and its positive association with glycated haemoglobin was reported by 1(20%) study. Recurrent infections were frequent in type 2 diabetes mellitus patients. Malondialdehyde level was higher and superoxide dismutase activity was lower in type 2 diabetes mellitus cases, reflecting oxidative stress. Animal studies also showed that reactive oxygen species generating from hypochlorous acid during oxidative stress promoted the formation of non-disulfide linkages in surfactant protein-D structure, resulting in its decreased functionality. Surfactant protein-D, oxidative stress, inflammation and infections were found to be linked to each other for pathogenesis of infections in type 2 diabetes mellitus.

Effects of prenatal dexamethasone exposure on adult C57BL/6J mouse metabolism and oxidative stress.

Prenatal glucocorticoid exposure has been shown to alter hypothalamic-pituitary-adrenal axis function resulting in altered fetal development that can persist through adulthood. Fetal exposure to excess dexamethasone, a synthetic glucocorticoid, has been shown to alter adult behaviour and metabolism. This study investigated the effects prenatal dexamethasone exposure had on adult offspring cardiac and liver metabolism and oxidative stress. Pregnant C57BL/6 mice received a dose of 0.4 mg/kg dexamethasone on gestational days 15-17. Once pups were approximately 7 months old, glucose uptake was determined using positron emission tomography and insulin resistance (IR) was determined by homeostatic model assessment (HOMA) IR calculation. Oxidative stress was assessed by measuring 4-hydroxynonenal protein adduct formation and total reactive oxygen species. Female dexamethasone group had significantly increased glucose uptake when insulin stimulated compared to vehicle-treated mice. HOMA IR revealed no evidence of IR in either male or female offspring. There was also no change in oxidative stress markers in either cardiac or liver tissues of male or female offspring. These data suggest that prenatal dexamethasone exposure in male mice does not alter oxidative stress or metabolism. However, prenatal dexamethasone exposure increased glucocorticoids, cardiac glucose uptake, and pAkt signaling in female heart tissues in adult mice, suggesting there are sex differences in prenatal dexamethasone exposure.

Modulation by Withania somnifera of stress-induced anxiogenesis and airway inflammation in rats.

Stress is an aversive stimulus which disrupts the biological milieu of the organism and a variety of emotional and environmental stressors are known to influence allergic and immunological disorders like bronchial asthma but the pharmacological basis of such interactions is not clearly defined. Withania somnifera (ashwagandha) is a potent anti-stress agent used widely in Indian traditional medicine and the present experimental study evaluated the effects of W.somnifera extract (WSE) on chronic stress-induced neurobehavioral and immunological responses in an experimental model of allergic asthma in rats. Wistar rats (200-250 g) were immunized and challenged with ovalbumin (OVA) and exposed to restraint stress (RS) and WSE treatments for 15days. Following this, anxiety behavior was assessed by the elevated plus maze (EPM) test, and blood and BAL fluid samples were collected for measuring of inflammatory/immune markers by ELISA and biochemical assay. The data of the various treatment groups were analyzed by ANOVA and Tukey's test. Restraint stress (RS) induced anxiogenic behavior in the (EPM) test in OVA immunized rats, and this was attenuated by WSE (200 and 400 mg/kg), in a dose related manner. Examination of blood and BAL fluid in these RS exposed rats also resulted in elevations in IgE, TNF-α andIL-4 levels, which were also attenuated by WSE pretreatments. Further, WSE pretreatment neutralized the such RS induced changes in oxidative stress markers viz. elevated MDA and reduced GSH levels. The data pharmacologically validates role of stress in asthma and suggests that adaptogens like WSE could be a potential complementary agent for reducing anxiety as well as airway inflammation by a multi-targeted and holistic approach. The study also highlights the significance of integration of traditional and modern medical concepts in such chronic disorders.

Orientin Modulates Nrf2-ARE, PI3K/Akt, JNK-ERK1/2, and TLR4/NF-kB Pathways to Produce Neuroprotective Benefits in Parkinson's Disease.

Parkinson's disease (PD) is characterized by oxidative stress and neuroinflammation as key pathological features. Emerging evidence suggests that nuclear factor erythroid 2 related factor 2-antioxidant response element (Nrf2-ARE), phosphatidylinositol 3‑kinase-protein kinase B (PI3K-Akt), c-Jun N-terminal kinase-extracellular signal-regulated kinase 1/2 (JNK-ERK1/2), and toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-kB) pathways play pivotal roles in PD pathogenesis. Orientin, a phenolic phytoconstituent, has demonstrated modulatory potential on these pathways in various experimental conditions other than PD. In this study, we aimed to evaluate the neuroprotective effects of Orientin against rotenone-induced neurodegeneration in SH-SY5Y cell lines and the Swiss albino mice model of PD. Orientin was administered at doses 10 and 20µM in cell lines and 10 and 20mg/kg in mice, and its effects on rotenone-induced neurodegeneration were investigated. Oxidative stress markers including mitochondrial membrane potential (ΔΨm), reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as inflammatory markers including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), were measured. The expression levels of genes related to Nrf2-ARE (Nrf2), PI3K/Akt (Akt), JNK-ERK1/2 (TNF-α), and TLR4/NF-kB (TNF-α) pathways were measured to understand the modulatory effect of Orientin on these pathways. Additionally, behavioral studies assessing locomotor activity, muscle coordination, and muscle rigidity were conducted with mice. Our results indicate that Orientin dose-dependently attenuated rotenone-induced changes in oxidative stress markers, inflammatory markers, gene expression levels, and behavioral parameters. Therefore, our study concludes that Orientin exhibits significant neuroprotective benefits against rotenone-induced PD by modulating Nrf2-ARE, PI3K-Akt, JNK-ERK1/2, and TLR4/NF-kB pathways.

The changes of oxidative stress markers and Vitamin E in patients with diabetes using SGLT2 inhibitors

The changes of oxidative stress markers and Vitamin E in patients with diabetes using SGLT2 inhibitors

Rehabilitation training enhanced the therapeutic effect of calycosin on neurological function recovery of rats following spinal cord injury

BackgroundCalycosin (CA), a flavonoids component, has demonstrated potential neuroprotection effects by inhibiting oxidative stress in spinal cord injury (SCI) models. This study aims to investigate the impact of combined rehabilitation training (RT) and calycosin therapy on neurological function following SCI, primarily by assessing changes in motor function recovery, neuronal survival, neuronal oxidative stress levels, and neural proliferation, in order to provide novel insights for the treatment of SCI. Materials and MethodsThe SCI model was constructed by compressing the spinal cord using vascular clamps. Calycosin was injected intraperitoneally into the SCI model rats, and a group of 5 rats underwent RT. The motor function of rats after SCI was evaluated using the Basso Beattle Bresnaha (BBB) score and the inclined plate test. Histopathological changes were evaluated by NeuN immunohistochemistry, HE and Nissl staining. Apoptosis was detected by TUNEL staining. The antioxidant effect of combined treatment was assessed by measuring changes in oxidative stress markers after SCI. Western blot analysis was conducted to examine changes in Hsp90-Akt/ASK1-p38 pathway-related proteins. Finally, cell proliferation was detected by BrdU and Ki67 assays. ResultsRT significantly improved the BBB score and angle of incline promoted by calycosin, resulting in enhanced motor function recovery in rats with SCI. Combining rehabilitation training with calycosin has a positive effect on morphological recovery. Similarly, combined RT enhanced the Nissl and NeuN staining signals of spinal cord neurons increased by calycosin, thereby increasing the number of neurons. TUNEL staining results indicated that calycosin treatment reduced the apoptosis signal in SCI, and the addition of RT further reduced the apoptosis. Moreover, RT combined with calycosin reduced oxidative stress by increasing SOD and GSH levels, while decreasing MDA, NO, ROS, and LDH expressions compared to the calycosin alone. RT slightly enhanced the effect of calycosin in activating Hsp90 and Akt and inhibiting the activation of ASK1 and p38, leading to enhanced inhibition of oxidative stress by calycosin. Additionally, the proliferation indexes (Ki67 and BrdU) assays showed that calycosin treatment alone increased both, whereas the combination treatment further promoted cell proliferation. ConclusionOur research findings demonstrate that rehabilitation training enhances the ability of calycosin to reduce oxidative stress, resulting in a decrease in neuronal apoptosis and an increase in proliferation, ultimately promoting neuronal survival.

Dose-response effect of L-citrulline on skeletal muscle damage after acute eccentric exercise: an in vivo study in mice.

Eccentric exercise may trigger mechanical stress, resulting in muscle damage that may decrease athletic performance. L-citrulline potentially prevents skeletal muscle damage after acute eccentric exercise. This study aimed to assess the dose-response effect of L-citrulline as a preventive therapy for skeletal muscle damage in mice after acute eccentric exercise. This is a controlled laboratory in vivo study with a post-test-only design. Male mice (BALB/c, n=25) were randomized into the following groups: a normal control (C1) (n=5); a negative control (C2) with downhill running and placebo intervention (n=5); treatment groups: T1 (n=5), T2 (n=5), and T3 (n=5), were subjected to downhill running and 250, 500, and 1,000mg/kg of L-citrulline, respectively, for seven days. Blood plasma was used to determine the levels of TNNI2 and gastrocnemius muscle tissue NOX2, IL-6, and caspase 3 using ELISA. NF-κB and HSP-70 expressions were determined by immunohistochemistry. Skeletal muscle damage (plasma TNNI2 levels) in mice after eccentric exercise was lower after 250 and 500 mg/kg of L-citrulline. Further, changes in oxidative stress markers, NOX2, were reduced after a 1,000mg/kg dose. However, a lower level of change has been observed in levels of cellular response markers (NF-κB, HSP-70, IL-6, and caspase 3) after administration of L-citrulline doses of 250, 500, and 1,000 mg/kg. L-citrulline may prevent skeletal muscle damage in mice after acute eccentric exercise through antioxidant effects as well as inflammatory and apoptotic pathways. In relation to dose-related effects, it was found that L-citrulline doses of 250, 500, and 1,000 mg/kg significantly influenced the expression of NF-κB and HSP-70, as well as the levels of IL-6 and caspase 3. Meanwhile, only doses of 250 and 500mg/kg had an impact on TNNI2 levels, and the 1,000 mg/kg dose affected NOX2 levels.

Long-term behavioral and neurochemical paradoxical alterations elicited following intranasal application of a chlorpyrifos formulation in mice

The intranasal (IN) administration route represents a pathway for xenobiotics to reach the brain. The present study aimed to address the long-term consequences of IN administration of a chlorpyrifos (CPF) commercial formulation (fCPF) in mice. For this purpose, adult male CF-1 mice were intranasally administered with fCPF (10 mg/kg/day) three days a week, for 2 and 4 weeks, respectively. Behavioral and biochemical analyses were conducted 3–7, and 7.5 months after the last IN fCPF administration, respectively. Following a 6-month fCPF-free washout period, fur appearance and body injuries scores improved in the fCPF-treated groups. Notably, spatial learning and memory enhancement was observed 4 and 7 months after the last IN fCPF administration. Changes in oxidative stress markers and the activities of enzymes involved in cholinergic and glutamatergic pathways were observed in different brain areas from fCPF-treated mice, still after 7.5 months from fCPF application. Altogether, these neurochemical disturbances could be responsible for the described behavioral observations.

The deleterious effects of cadmium on oxidative stress markers, drug-metabolizing, and antioxidant enzyme activities: Role of Silymarin and Garlic as Antioxidants.

Exposure to cadmium has been related to liver and kidney diseases such as polycystic and nephrotic syndrome. It is still unclear how cadmium contributes to these diseases. It is believed that the induction of oxidative stress resulting from the inhibition of antioxidant enzyme activities and changes in drug-metabolizing enzymes in the liver could explain the role of cadmium in the development of different diseases in the kidney and probably other organs. Changes in oxidative stress markers, antioxidant enzymes, and drug-metabolizing enzyme activities were assessed in the liver of male rats exposed to cadmium chloride. Additionally, the protective effects of silymarin and garlic extract against cadmium toxicosis were evaluated. Rats were randomly divided into eight groups as follows, groups 1, 2, 3, 4, and 5, received orally saline, CdCl2 (1mg/kg), garlic extract [800mg/kg], silymarin (25mg/kg) and silymarin plus garlic extract respectively for 28 consecutive days. Rats in groups 6, 7, and 8 were pretreated with the same doses of garlic, silymarin, and garlic plus silymarin, respectively for two hours before cadmium administration. The Western immunoblotting technique was used to investigate the protein expression of cytochrome P450 isozymes. Spectrophotometric methods were used to assess the activity of both antioxidant- and drug-metabolizing enzymes. Free radical levels [measured as thiobarbituric acid reactive substances (TBARS)], catalase, superoxide dismutase, and glutathione peroxidase activities increased whereas the levels of glutathione and the activities of glutathione S-transferase, glutathione reductase, and glutamyl transferase, cytochrome P450, aryl hydrocarbon dehydrogenase (AHH), dimethylnitrosamine-N-demethylase I (DMN-dI), 7-ethoxycoumarine-O-deethylase (ECOD), cytochrome b5 and NADPH-Cytochrome-c-reductase enzyme activities decreased after cadmium treatment. Furthermore, Western immunoblotting data revealed that glutathione peroxidase protein expression increased following cadmium exposure, but cytochrome P450 2E1 and 3A4 expressions were downregulated. However, pretreatment of rats with silymarin or garlic extract or both before cadmium administration was found to restore the protein expression of cytochrome P450 2E1 and 3A4, the level of free radicals, antioxidant enzymes, drug-metabolizing enzyme activities to their normal levels. Similarly, histological studies revealed that silymarin and/or garlic extract reduced the liver damage caused by cadmium. Silymarin and/or garlic extract reduced the adverse effects of cadmium on the activity of both drug-metabolizing and antioxidant enzymes activity. These antioxidants could be provided to those who work in cadmium-based sectors to help them cope with the adverse effects of cadmium on their kidneys. In addition, Inhibiting drug-metabolizing enzyme activity should be considered when administering therapeutic medications to persons exposed to cadmium because most therapeutic drugs and many endogenous substances are largely metabolized by these enzymes.

The correlation between oxidative stress markers and increasing intracranial pressure: a study of Malondialdehyde (MDA), Superoxide Dismutase (MnSOD), Nicotinamide Adenine Dinucleotide Phosphate Hydrogen (NADPH), and catalase

Link of Video Abstract: https://youtu.be/nINFPi4uVow Background: Abnormalities in the neurosurgical field concerning cranial structure are almost always followed by increased intracranial pressure (ICP), which causes cerebral hypoxia and disrupts the whole cellular system. This study analyzes the correlation between ICP changes and oxidative stress markers, in subjects with various anatomical pathology abnormalities who underwent surgery. Methods: This was a cross sectional study of 24 subjects with ICP conducted in the Department of Neurosurgery, Cipto Mangunkusumo Hospital, Jakarta, from November to December 2009. In this study, ANOVA analysis has been done to measure the mean difference oxidative stress (MnSOD, NADPH, MDA, and catalase) in subjects with various changes in ICP who have undergone surgery and Spearman analysis to measure the correlation between each oxidative stress markers. Oxidative stress markers were measured from normal brain tissue taken intra-operatively, cerebrospinal fluid (CSF) taken while doing ventriculostomy, and peripheral blood taken from a central vein catheter (CVC). Results: The results showed that MDA concentrations in blood were significantly correlated with MDA in brain tissue (P = 0.029) in all of the ICP groups, CSF MnSOD concentration and CSF NADPH concentrations correlated with brain tissue NAPDH (p= 0.000) in congenital group and CSF catalase concentration correlated with brain tissue catalase (p = 0.00) in congenital group. Conclusion: Increased ICP caused by various pathological conditions causes changes in oxidative stress markers in brain cells, CSF and blood. Oxidative stress markers in blood and CSF are correlated strongly with the brain. It is suggested that it could be used to predict intracranial high pressure in all cases with intracranial abnormalities.

Protective and antioxidant effects of chia oil and canola oil on testicular injury induced by lead in rats

Environmental pollution is a global problem that needs more efforts to overcome the increase of environmental pollution rates and the threat of ecosystem stability. Due to the increase of human activities in the field of industry and agriculture, heavy metals are increasingly spreaded and accumulated in water, air and soil, which pose a great risk to living organisms. Medicinal plants and natural products constitute an important source for relieving and treating many diseases in a safe manner, as it is characterized by low cost and fewer side effects compared to industrial chemical drugs. The present study was aimed to evaluate the ameliorative influence of chia oil and canola oil on testicular injury induced by lead (Pb) in rats. To evaluate the role of chia oil and canola oil against Pb toxicity, sixty Wistar male rats were taken and divided into six groups. Group 1 was kept as control, group 2 received Pb solution (150 mg/kg BW), group 3 was treated with chia oil at (600 mg/kg BW) and exposed to Pb (150 mg/kg BW), group 4 was treated with canola oil (600 mg/kg BW) and exposed to Pb (150 mg/kg BW), groups 5 and 6 were treated with chia oil (600 mg/kg BW) and canola oil (600 mg/kg BW) respectively. In rats of group 2, the level of serum GSH, SOD and CAT were significantly decreased, while the level of MDA was increased. Histopathological examination of testicular tissues in rats of group 2 showed severe alterations. Treatment of rats with chai oil (group 3) and canola oil (group 4) reduced the changes of oxidative stress markers (GSH, SOD, CAT and MDA) accompanied with normal structure of testicular tissues. The results of this conclude that chia oil and canola oil have shown protection against Pb induced testicular injury due to their antioxidant roles.

Effect of Sofosbuvir on rats' ovaries and the possible protective role of vitamin E: biochemical and immunohistochemical study.

Hepatitis C virus (HCV) infection is a major health problem worldwide and its eradication is mandatory. Direct acting HCV polymerase inhibitors, such as Sofosbuvir (SOF), is an effective regimen. However, it has some side effects like mutagenesis, carcinogenesis, and the impairment of testicular function. It is important to evaluate the safety of SOF on the ovary, as there are no studies yet. Increasing the production of Reactive Oxygen Species (ROS), causes oxidative stress, which affects ovulation process, female reproduction, and fertility. Accumulation of SOF in the cells was demonstrated to promote ROS generation. Vitamin E (Vit E) is an antioxidant agent that has an essential role in the female reproductive system, its deficiency can cause infertility. We explored the effect of SOF treatment alone and co-treated with Vit E on ovarian ROS level and ovarian morphology experimentally using biochemical and immunohistochemical studies. Significant changes in oxidative stress markers; nitric oxide and malondialdehyde lipid peroxidation, antioxidant enzymes; catalase, super oxide dismutase, and reduced glutathione, proliferating markers; proliferation cell nuclear antigen and Ki-67 antigen and caspase 3 apoptotic marker were demonstrated. It was shown that where SOF induced oxidative stress, it also aggravated ovarian dysfunction. The essential role of Vit E as an antioxidant agent in protecting the ovarian tissue from the effect of oxidative stress markers and preserving its function was also displayed. This could be guidance to add Vit E supplements to SOF regimens to limit its injurious effect on ovarian function.

Antioxidant activity enhancement and oxidative damage inhibition by Lagenaria breviflora fruit and Xanthosoma sagittifolium corm in hypertensive Wistar rats.

Cardiovascular diseases are the leading causes of mortality in the world today with hypertension being the major clinical presentation of these diseases. This study assessed the anti-hypertensive effects of Lagenaria breviflora whole fruit and Xanthsoma sagittifolium corms in experimentally inudced hypertensive Wistar rats. The ability of the plants to ameliorate oxidative damage accompanying hypertension was evaluated using changes in oxidative stress markers as well as monitoring of cardiovascular parameters. Hypertension was induced by intraperitoneal injection of DOCA salt twice weekly and daily inclusion of NaCl (1%) in drinking water. Methanol extracts of L.breviflora or X. sagittifolium was administered to hypertensive rats for 35 days and the outcome was compared to hypertensive rats administred with lisinopril or hydrochlorothiazide and a group of normotensive rats (control). Systolic, diastolic and mean arterial pressures were determined on day 34 and blood sample collected on day 35. The rats were thereafter humanely sacrificed, and organs were harvested. This study showed that the extracts lowered blood pressure, free protein thiols but increased toal protein, gluthathione peroxidase, reduced glutathione, glutathione S-transferase, catalase and nitric oxide in the heart, kidney and liver compared to untreated hypertensive rats. However, malondialdehyde levels and hydrogen peroxide activities were reduced. L. breviflora fruit and X. sagittifloium corm exhibited antihypertensive properties and ameliorate oxidative damage associated with hypertension by enhancing the antioxidant defense sysyem and inhibiting generation of free radicals.

Measures of Oxidative Status Markers in Relation to Age, Sex, and Season in Sick and Healthy Captive Asian Elephants in Thailand.

Oxidative stress is a pathological condition that can have adverse effects on animal health, although little research has been conducted on wildlife species. In this study, blood was collected from captive Asian elephants for the assessment of five serum oxidative status markers (reactive oxygen species (ROS) concentrations; malondialdehyde, MDA; albumin; glutathione peroxidase, GPx; and catalase) in healthy (n = 137) and sick (n = 20) animals. Health problems consisted of weakness, puncture wounds, gastrointestinal distress, eye and musculoskeletal problems, and elephant endotheliotropic herpesvirus hemorrhagic disease (EEHV-HD). Fecal samples were also collected to assess glucocorticoid metabolites (fGCMs) as a measure of stress. All data were analyzed in relation to age, sex, sampling season, and their interactions using generalized linear models, and a correlation matrix was constructed. ROS and serum albumin concentrations exhibited the highest concentrations in aged elephants (>45 years). No sex differences were found for any biomarker. Interactions were observed for age groups and seasons for ROS and catalase, while GPx displayed a significant interaction between sex and season. In pairwise comparisons, significant increases in ROS and catalase were observed in summer, with higher ROS concentrations observed only in the adult female group. Lower catalase activity was exhibited in juvenile males, subadult males, adult females, and aged females compared to subadult and adult elephants (males and females) in winter and the rainy season. There was a positive association between catalase activity and fGCMs (r = 0.23, p < 0.05), and a number of red blood cell parameters were positively associated with several of these biomarkers, suggesting high oxidative and antioxidative activity covary in red cells (p < 0.05). According to health status, elephants with EEHV-HD showed the most significant changes in oxidative stress markers, with MDA, GPx, and catalase being higher and albumin being lower than in healthy elephants. This study provides an analysis of understudied health biomarkers in Asian elephants, which can be used as additional tools for assessing the health condition of this species and suggests age and season may be important factors in data interpretation.

Biochemical and behavioral effects of zinc oxide nanorods on the freshwater mussel Potomida littoralis

ABSTRACT Our study aimed to investigate the impact of nano-zinc oxide (nZnO), a widely used pollutant in industry, pharmaceuticals, and personal care products, on the behavior and oxidative stress of freshwater mussels (Potomida littoralis) an indicator species and also a model non-target organism in ecotoxicology. To this end mussels were exposed to nZnO (50 and 100 µg/L) and Zn2+ from ZnSO4 (50 and 100 µg/L) for 7 days. ZnSO4 was used for comparison purposes and to determine if the toxicity of nZnO was due to the release of ions into the aquatic environment. We evaluated changes in oxidative stress markers, including catalase (CAT), glutathione-S-transferase (GST), acetylcholinesterase (AChE), and malondialdehyde (MDA) levels, on the mussel gills and digestive glands. Additionally, the effect of nZnO on the filtration rate of bivalves was studied. The findings showed that the mussel tissue’s different parameters were significantly affected by exposure to various concentrations of nZnO, causing changes in their behavior that led to a decrease in filtration rate. Additionally, noteworthy increments were observed in CAT activity, AChE activity, and MDA levels, whereas GST activity displayed a decreasing trend, implying that oxidative stress contributes to the toxicity of nZnO. The purpose of this review is to present a framework for comprehending the toxicological impacts of nanoparticles from an environmental standpoint. Additionally, it includes novel information about the connections between nanoparticles (NPs) and bivalve species.

Loss of Ncoa7 leads to oxidative stress in kidney intercalated cells

Oxidative stress (OS) results from excessive production of reactive oxygen species, relative to endogenous antioxidant defenses, leading to cellular damage. The metabolically active kidney is vulnerable to OS, which is a key step in the progression of many renal pathologies. Furthermore, many non-renal pathologies are characterized by OS. Therefore, although our work focuses on kidney epithelial cells, it has significant implications for understanding how OS is regulated at a molecular level in many organs and cell types.The V-ATPase, or proton pump, is required for the acidification of intracellular compartments. Recently, we identified a family of V-ATPase interacting proteins defined by their TLDc domain (Ncoa7, Oxr1, Tbc1d24, Tldc1, and Tldc2). TLDc proteins are protective against OS in the nervous system and mutations cause human neurological pathologies. However, little is known about the molecular mechanisms that provide these protective properties. The V-ATPase, like TLDc proteins, also protects against OS. Therefore, we hypothesize that TLDc proteins play a V-ATPase-dependent protective role against OS. This is supported by our previous findings that mutating an amino acid in Ncoa7 that is protective against OS abolishes the interaction with the V-ATPase, and Ncoa7 knockout (KO) decreases V-ATPase-dependent urinary acidification in mice.To test this, we focused on Ncoa7 because it showed the most robust protective effect against OS in previous studies and is highly expressed in the kidney where it is enriched in epithelial intercalated cells (ICs). RNA sequencing of isolated ICs from Ncoa7 KO mice revealed significant downregulation of antioxidant enzymes including glutathione peroxidase-3 (Gpx3) and carbonyl reductase-2 (Cbr2). Immunofluorescence (IF) showed Cbr2 enrichment in medullary ICs from control mouse kidneys and a decrease in Cbr2 fluorescent signal intensity in ICs from Ncoa7 KO mice. Furthermore, Cbr2 localizes to the mitochondria of ICs, a significant source of cellular OS.To investigate whether the loss of Ncoa7 promotes OS in ICs we examined changes in OS markers by IF. We monitored the expression of Advanced Glycation End products (AGEs) and malondialdehyde (MDA) in fixed kidney sections using specific antibodies. AGEs are generated by glycation events accompanying OS and their formation can be suppressed by Gpx3. MDA is a product of lipid oxidation due to OS and can be reduced by Cbr2. ICs in Ncoa7 KO mice exhibited a striking accumulation of both AGEs and MDA, often found in large V-ATPase-bound intracellular compartments. Furthermore, knockdown of Ncoa7 in cultured kidney cells increased expression of AGEs, supporting loss of Ncoa7 as the mechanism behind the increased accumulation of intracellular AGEs.Based on these data we conclude that loss of Ncoa7 promotes OS in renal intercalated cells potentially through a regulatory interaction with the V-ATPase, which leads to decreased expression of antioxidant enzymes. NIH/NIDDK T32DK007540-33 and NIH/NIDDK R01DK121848 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Combined Treatment of Glutathione Sodium Salt and Ascorbic Acid for Preventing Contrast-Associated Acute Kidney Injury in ST-Elevation Myocardial Infarction Patients Undergoing Primary PCI: A Hypothesis to Be Validated.

The occurrence of Contrast-Associated Acute Kidney Injury (CA-AKI) in patients with ST-Elevation Myocardial Infarction (STEMI) has a negative impact on the length of hospital stay and mortality. Reactive Oxygen Species (ROS) release, along with vasoconstriction and hypoperfusion, play a key role in its development. To date, there is still no validated prophylactic therapy for this disease. The use of antioxidants, based on experimental and clinical studies, looks promising. Taking into consideration previous literature, we speculate that an early, combined and prolonged intravenous administration of both Glutathione (GSH) and ascorbic acid in STEMI patients undergoing primary Percutaneous Coronary Intervention (pPCI) may be of value in counteracting the occurrence of CA-AKI. We aimed at evaluating this hypothesis by applying a multicenter research protocol, using a double-blind randomized, placebo-controlled trial design. The primary endpoint will be to test the efficacy of this combined antioxidant therapy in reducing the occurrence of renal damage, in patients with acute myocardial infarction treated with pPCI. Furthermore, we will investigate the effect of the study compounds on changes in oxidative stress markers and platelet activation levels through bio-humoral analyses.

Changes in oxidative stress markers in pediatric burn injury over a 1-week period

Abstract The importance of oxidative stress in the pathogenesis of burn injuries has been shown in various studies. Glutathione (GSH) and thiols have important roles in antioxidant protection and detoxification. The study aimed to investigate the relationship between pediatric burn trauma and GSH and thiol homeostasis. Twenty-nine children with thermal-burn injuries and 29 healthy peers are included in this prospective randomized study. Children with burn wounds of 15–25% of total body surface area (TBSA) were included in the patient group. The control group was created from healthy peers of both sexes. All children were 1–10 years of age. Serum GSH, oxidized glutathione (GSSG), redox ratio (GSH/GSSG), and thiol–disulfide (SS) tests were conducted in both groups, and the changes between admission and day 7 were analyzed in patients with burn injuries. The mean age was 4.09 ± 2.54 years for the patient group and 4.28 ± 2.55 years for the controls (p &gt; 0.05). Total thiol (TT), native thiol (SH), and SS levels were significantly lower in the patient group than in the controls (TT = 291.69 ± 7.93 vs 346.79 ± 18.89 μmol/L, SH = 259.39 ± 7.90 vs 297.64 ± 12.81 μmol/L, SS = 16.15 ± 4.68 vs 24.58 ± 5.76 μmol/L; p &lt; 0.001). SH/TT ratio was higher in the patient group (89.05 ± 3.00 vs 85.93 ± 3.01 μmol/L; p &lt; 0.001). The SS/SH and SS/TT ratios were significantly lower in the patient group, while the SH/TT ratio was significantly higher (p &lt; 0.001). The patients had significantly decreased GSH levels (26.12 ± 2.42 vs 34.80 ± 2.26) and GSH/GSSG ratios (1.69 ± 0.12 vs 3.05 ± 0.29) and increased GSSG levels (16.09 ± 0.34 vs 11.48 ± 1.17, p &lt; 0.001 for all). The GSSG level and GSSG/SH and GSSG/TT ratios were higher in the patient group than in the controls while the SH, TT, and SS levels, and SS/SH and SS/TT ratios were lower in the patient group. Analysis of serum GSSG levels, and ratios with SH and TT homeostasis, might be useful in order to determine burn damage in children.