Low Levels Of Oxidative Stress Research Articles

Organic photovoltaic biomaterial with fullerene derivatives for near-infrared light sensing in neural cells.

Retinal degenerative diseases, which can lead to photoreceptor cell apoptosis, have now become the leading irreversible cause of blindness worldwide. In this study, we developed an organic photovoltaic biomaterial for artificial retinas, enabling neural cells to detect photoelectric stimulation. The biomaterial was prepared using a conjugated polymer donor, PCE-10, and a non-fullerene receptor, Y6, both known for their strong near-infrared light absorption capabilities. Additionally, a fullerene receptor, PC61BM, was incorporated, which possesses the ability to absorb reactive oxygen species. We conducted a comprehensive investigation into the microstructure, photovoltaic properties, and photothermal effects of this three-component photovoltaic biomaterial. Furthermore, we employed Rat adrenal pheochromocytoma cells (PC-12) as a standard neural cell model to evaluate the in vitro photoelectric stimulation effect of this photovoltaic biomaterial. The results demonstrate that the photovoltaic biomaterial, enriched with fullerene derivatives, can induce intracellular calcium influx in PC-12 cells under 630 nm (red light) and 780 nm (near-infrared) laser irradiation. Moreover, there were lower levels of oxidative stress and higher levels of mitochondrial activity compared to the non-PC61BM group. This photovoltaic biomaterial proves to be an ideal substrate for near-infrared photoelectrical stimulation of neural cells and holds promise for restoring visual function in patients with photoreceptor apoptosis.

The toxic effects induced by benzethonium chloride on Daphnia carinata over two generations: Resistance and higher sublethal toxicity

With the widespread utilization of the sanitizing product benzethonium chloride (BEC) throughout the coronavirus pandemic, concerns have emerged regarding its potential hazards. Nevertheless, the long-term and multigenerational toxic effects of BEC on aquatic organisms remains unexplored. This study investigates acute and chronic toxicity, oxidative stress, mitochondrial membrane potential, ATP concentrations, and gene expression using Daphnia carinata as the model organism. Meanwhile, hierarchical clustering analysis was utilized to investigate phenotypic effects among different treatment groups. The integrated biomarker response index version 2 (IBRv2) was employed to estimate the deviation in toxic effects over two generations. These results indicated that D. carinata in the second generation exhibited higher survival rate and lower levels of oxidative stress than the first generation. However, the higher sublethal effects were found in the second generation as follows, the weakened growth performance, mitochondrial membrane potential depolarization, reduced ATP concentrations, and down-regulated gene expression. The mitochondrial toxicity induced by BEC may account for the distinct toxic effects exhibited in two generations. The findings here can assist with the evaluation of potential risk for BEC on aquatic organisms, and provide new insight into the cross-generational toxicity mechanisms of pollutants in aquatic ecosystems.

NOX2 and NOX4 expression in monocytes and macrophages-extracellular vesicles in signalling and therapeutics.

Extracellular vesicles (EVs) are a type of cytoplasmic vesicles secreted by a variety of cells. EVs originating from cells have been known to participate in cell communication, antigen presentation, immune cell activation, tolerance induction, etc. These EVs can also carry the active form of Nicotinamide Adenine Dinucleotide Phosphate Oxidase Hydrogen (NADPH) oxidase, which is very essential for the production of reactive oxygen species (ROS) and that can then modulate processes such as cell regeneration. The aim of this study is to characterize the EVs isolated from U-937 and THP-1 cells, identify the NADPH oxidase (NOX) isoforms, and to determine whether EVs can modulate NOX4 and NOX2 in monocytes and macrophages. In our study, isolated EVs of U-937 were characterized using dynamic light scattering (DLS) spectroscopy and immunoblotting. The results showed that the exogenous addition of differentiation agents (either phorbol 12-myristate 13-acetate (PMA) or ascorbic acid) or the supplementation of EVs used in the study did not cause any stress leading to alterations in cell proliferation and viability. In cells co-cultured with EVs for 72h, strong suppression of NOX4 and NOX2 is evident when monocytes transform into macrophagic cells. We also observed lower levels of oxidative stress measured using immunoblotting and electron paramagnetic resonance spectroscopy under the EVs co-cultured condition, which also indicates that EVs might contribute significantly by acting as an antioxidant source, which agrees with previous studies that hypothesized the role of EVs in therapeutics. Therefore, our results provide evidence for NOX regulation by EVs in addition to its role as an antioxidant cargo.

POSSIBLE ROLES OF ANTIOXIDANTS IN ROTATOR CUFF TENDINOPATHY

The rotator cuff tendinopathy is one of the most common shoulder problems leading to full-thickness rotator cuff tendon tear and, eventually, to degenerative arthritis. Recent research on rotator cuff tendon degeneration has focused on its relationship to cell death. The types of cell death known to be associated with rotator cuff tendon degeneration are apoptosis, necrosis, and autophagic cell death. The increased incidence of cell death in degenerative tendon tissue may affect the rates of collagen synthesis and repair, possibly weakening tendon tissue and increasing the risk of tendon rupture. The biomolecular mechanisms of the degenerative changes leading to apoptotic cell death in rotator cuff tenofibroblasts have been identified as oxidative-stress-related cascade mechanisms. Furthermore, apoptosis, necrosis, and autophagic cell death are all known to be mediated by oxidative stress, a condition in which ROS (reactive oxygen species) are overproduced. Lower levels of oxidative stress trigger apoptosis; higher levels mediate necrosis. Although the signaltransduction pathway leading to autophagy has not yet been fully established, ROS are known to be essential to autophagy. A neuronal theory regarding rotator cuff degeneration has been developed from the findings that glutamate, a neural transmitter, is present in increased concentrations in tendon tissues with tendinopathy and that it induces rat supraspinatus tendon cell death. Recent studies have reported that hypoxia involved in rotator cuff tendon degeneration. Because antioxidants are known to scavenge for intracellular ROS, some studies have been conducted to determine whether antioxidants can reduce cell death in rotator cuff tendon-origin fibroblasts. The first study reported that an antioxidant has the ability to reduce apoptosis in oxidative-stressed rotator cuff tenofibroblasts. The second study reported that antioxidants have both antiapoptotic effects and antinecrotic effects on rotator cuff tendon-origin fibroblasts exposed to an oxidative stimulus. The third study reported that an antioxidant has antiautophagic-cell-death effects on rotator cuff tendon-origin fibroblasts exposed to an oxidative stimulus. The fourth study reported that glutamate markedly increases cell death in rotator cuff tendonorigin fibroblasts. The glutamate-induced cytotoxic effects were reduced by an antioxidant, demonstrating its cytoprotective effects against glutamate-induced tenofibroblast cell death. The fifth study reported that hypoxia significantly increases intracellular ROS and apoptosis. The hypoxia-induced cytotoxic effects were markedly attenuated by antioxidants, demonstrating their cytoprotective effects against hypoxia-induced tenofibroblast cell death. In conclusion, antioxidants have cytoprotective effects on tenofibroblasts exposed in vitro to an oxidative stressor, a neurotransmitter, or hypoxia. These cytoprotective effects result from antiapoptotic, antinecrotic, and antiautophagic actions involving the inhibition of ROS formation. These findings suggest that antioxidants may have therapeutic potential for rotator cuff tendinopathy. Further studies must be conducted in order to apply these in vitro findings to clinical situations.

Does dietary total antioxidant capacity relate to oxidative stress levels in water immersion during labor? A case-control study.

The aim of this study was to investigate the effect of water immersion during the first stage of labor on maternal and neonatal oxidative stress and the association between serum and dietary total antioxidant capacity. Women were divided into two groups: those immersed in water during the first stage of labor (n=30) and those who had conventional birth (n=33). Total oxidative stress and total antioxidant status levels were examined in antepartum and postpartum maternal serum and neonatal cord blood samples. Dietary total antioxidant capacity was determined by the food frequency questionnaire. Vitamin C and dietary total antioxidant capacity consumption were found to be higher in the water immersion group (106.92 mg/day and 18.94 mmol/gün, respectively) than the conventional birth group (92.69 mg/day and 15.99 mmol/gün, respectively) (p<0.05). Women immersed in water during the first stage of labor had lower total oxidative stress levels in antepartum and postpartum maternal serum and neonatal cord blood samples than those who had conventional birth (5.43±2.42 mmol/L and 5.59±3.35 mmol/L vs. 8.58±5.53 mmol/L and 12.68±16.58 mmol/L; p<0.05). Dietary total antioxidant capacity was found to be negatively correlated with total oxidative stress levels in antepartum and postpartum maternal serum and neonatal cord blood samples (p=0.012, p=0.047, p=0.035, and p<0.05). Women immersed in water during the first stage of labor had lower total oxidative stress levels in their postnatal maternal serum and neonatal cord blood samples and dietary total antioxidant capacity was also a factor associated with low total oxidative stress levels.

Empagliflozin alone and in combination with metformin ameliorate diabetes type 2-oxidative stress

Currently, one of the major public health concerns is diabetes mellitus, which is known as a silent killer due to the failure to diagnose it at an early stage. A growing body of research indicates that metformin and empagliflozin have antioxidant properties in addition to their hypoglycemic properties. Our research looked into the potential antioxidant effects of metformin and empagliflozin on diabetic rats by decreasing oxidative stress. For eight weeks, 42 adult male Sprague Dawley rats were divided into six groups: normal control, diabetic control group, diabetic group received dimethyl sulfoxide as a vehicle(solvent) of the empagliflozin, 250 mg/kg metformin only, 10 mg/kg empagliflozin only and a combination of both. A single injection of 40 mg/kg streptozocin administered intraperitoneally was after administering 10% fructose in drinking water for two weeks to cause type 2 diabetes in rats. The evaluation of oxidative stress involved the quantification of serum malondialdehyde (MDA) and superoxide dismutase (SOD) levels upon completion of the experimental period. Additionally, blood glucose levels were determined using blood samples from the tail, and body weight was monitored on a weekly basis. Our findings showed that compared to the diabetic group, the therapy groups had considerably lower blood glucose, and serum MDA levels, while higher levels of SOD, and less decrease in body weight. Furthermore, even better results were obtained when empagliflozin and metformin were administered together. As a result of our findings, diabetic rats treated with empagliflozin and metformin had lower levels of oxidative stress.

Satellite III (1q12) Copy Number Variation in Cultured Human Skin Fibroblasts from Schizophrenic Patients and Healthy Controls.

The chromosome 1q12 region harbors the genome's largest pericentromeric heterochromatin domain that includes tandemly repeated satellite III DNA [SatIII (1)]. Increased SatIII (1) copy numbers have been found in cultured human skin fibroblasts (HSFs) during replicative senescence. The aim of this study was to analyze the variation in SatIII (1) abundance in cultured HSFs at early passages depending on the levels of endogenous and exogenous stress. We studied 10 HSF cell lines with either high (HSFs from schizophrenic cases, n = 5) or low (HSFs from healthy controls, n = 5) levels of oxidative stress. The levels of endogenous stress were estimated by the amounts of reactive oxygen species, DNA damage markers (8-hydroxy-2'-deoxyguanosine, gamma-H2A histone family member X), pro- and antioxidant proteins (NADPH oxidase 4, superoxide dismutase 1, nuclear factor erythroid 2-related factor 2), and proteins that regulate apoptosis and autophagy (B-cell lymphoma 2 [Bcl-2], Bcl-2-associated X protein, light chain 3). SatIII (1) copy numbers were measured using the nonradioactive quantitative hybridization technique. For comparison, the contents of telomeric and ribosomal RNA gene repeats were determined. RNASATIII (1 and 9) were quantified using quantitative Polymerase Chain Reaction (PCR). Increased SatIII (1) contents in DNA from confluent HSFs were positively correlated with increased oxidative stress. Confluent cell cultivation without medium replacement and heat shock induced a decrease of SatIII (1) in DNA in parallel with a decrease in RNASATIII (1) and an increase in RNASATIII (9). During HSF cultivation, cells with increased SatIII (1) content accumulated in the cell pool under conditions of exaggerated oxidative stress. This fraction of cells decreased after the additional impact of exogenous stress. The process seems to be oscillatory.

Identification of Compounds Protecting Pancreatic Islets against Oxidative Stress using a 3D Pseudoislet Screening Platform.

Oxidative stress leads to a lower success rate of clinical islet transplantation. Here, FDA-approved compounds are screened for their potential to decrease oxidative stress and to protect or enhance pancreatic islet viability and function. Studies are performed on in vitro "pseudoislet" spheroids, which are pre-incubated with 1280 different compounds and subjected to oxidative stress. Cell viability and oxidative stress levels are determined using a high-throughput fluorescence microscopy pipeline. Initial screening on cell viability results in 59 candidates. The top ten candidates are subsequently screened for their potential to decrease induced oxidative stress, and eight compounds efficient reduction of induced oxidative stress in both alpha and beta cells by 25-50%. After further characterization, the compound sulfisoxazole is found to be the most capable of reducing oxidative stress, also at short pre-incubation times, which is validated in primary human islets, where low oxidative stress levels and islet function are maintained. This study shows an effective screening strategy with 3D cell aggregates based on cell viability and oxidative stress, which leads to the discovery of several compounds with antioxidant capacity. The top candidate, sulfisoxazole is effective after a 30 min pre-incubation, maintains baseline islet function, and may help alleviate oxidative stress in pancreatic islets.

Identifying oxidative stress-related biomarkers in idiopathic pulmonary fibrosis in the context of predictive, preventive, and personalized medicine using integrative omics approaches and machine-learning strategies.

Idiopathic pulmonary fibrosis (IPF) is a rare interstitial lung disease with a poor prognosis that currently lacks effective treatment methods. Preventing the acute exacerbation of IPF, identifying the molecular subtypes of patients, providing personalized treatment, and developing individualized drugs are guidelines for predictive, preventive, and personalized medicine (PPPM/3PM) to promote the development of IPF. Oxidative stress (OS) is an important pathological process of IPF. However, the relationship between the expression levels of oxidative stress-related genes (OSRGs) and clinical indices in patients with IPF is unclear; therefore, it is still a challenge to identify potential beneficiaries of antioxidant therapy. Because PPPM aims to recognize and manage diseases by integrating multiple methods, patient stratification and analysis based on OSRGs and identifying biomarkers can help achieve the above goals. Transcriptome data from 250 IPF patients were divided into training and validation sets. Core OSRGs were identified in the training set and subsequently clustered to identify oxidative stress-related subtypes. The oxidative stress scores, clinical characteristics, and expression levels of senescence-associated secretory phenotypes (SASPs) of different subtypes were compared to identify patients who were sensitive to antioxidant therapy to conduct differential gene functional enrichment analysis and predict potential therapeutic drugs. Diagnostic markers between subtypes were obtained by integrating multiple machine learning methods, their expression levels were tested in rat models with different degrees of pulmonary fibrosis and validation sets, and nomogram models were constructed. CIBERSORT, single-cell RNA sequencing, and immunofluorescence staining were used to explore the effects of OSRGs on the immune microenvironment. Core OSRGs classified IPF into two subtypes. Patients classified into subtypes with low oxidative stress levels had better clinical scores, less severe fibrosis, and lower expression of SASP-related molecules. A reliable nomogram model based on five diagnostic markers was constructed, and these markers' expression stability was verified in animal experiments. The number of neutrophils in the immune microenvironment was significantly different between the two subtypes and was closely related to the degree of fibrosis. Within the framework of PPPM, this work comprehensively explored the role of OSRGs and their mediated cellular senescence and immune processes in the progress of IPF and assessed their capabilities aspredictors of high oxidative stress and disease progression,targets of the vicious loop between regulated pulmonary fibrosis and OS for targeted secondary and tertiary prevention, andreferences for personalized antioxidant and antifibrotic therapies. The online version contains supplementary material available at 10.1007/s13167-023-00334-4.

Oxidative Stress and Performance after Training in Professional Soccer (European Football) Players.

Vitamins, hormones, free radicals, and antioxidant substances significantly influence athletic performance. The aim of this study was to evaluate whether these biological mediators changed during the season and if this was associated with the rate of improvement in performance after training, assessed by means of a standardized test. Professional male soccer players took part in the study. Two evaluations were performed: the first in the pre-season period and the second at the mid-point of the official season, after about 6 months of intensive training and weekly matches. Blood levels of vitamins D, B12, and folic acid, testosterone and cortisol, free radicals, and antioxidant substances were measured. Two hours after breakfast, a Yo-Yo test was performed. The relationships between the biological mediators and the rate of improvement after training (i.e., the increase in meters run in the Yo-Yo test between the pre-season and mid-season periods) were evaluated by means of a linear mixed models analysis. Results: Eighty-two paired tests were performed. The athletes showed better performance after training, with an increase in the meters run of about 20%. No significant relationships between the vitamin and hormone values and the gain in the performance test were observed. Plasmatic levels of free radicals increased significantly, as did the blood antioxidant potential. An indirect relationship between oxidative stress and the improvement in performance was observed (free radicals β ± SE: = -0.33 ± 0.10; p-value = 0.001), with lower levels of oxidative stress being associated with higher levels of performance in the Yo-Yo test. Monitoring the measures of oxidative stress could be a useful additional tool for coaches in training and/or recovery programs tailored to each player.

The Interplay of Exogenous and Endogenous Hydrogen Sulfide (H2S) in Maintaining Redox Homeostasis in Individuals with Low Ferritin Levels

The primary objective of this study was to investigate the influence of living near a thermal spring and being exposed to hydrogen sulfide (H2S) gas, which lingers in the surrounding atmosphere, on the redox and lipid peroxidation status of individuals with low ferritin levels. Participants in the study were divided into two groups based on their H2S exposure frequency and ferritin levels. Within Group A, individuals who did not experience occasional H2S exposure (2–3 h, 2–3 times per year) and had an average of normal ferritin levels of 87.5 ng/mL exhibited lower levels of oxidative stress and lipid peroxidation compared to those with low ferritin levels (average of 6.57 ng/mL) in the same group. Additionally, individuals with normal ferritin levels showed higher levels of thiol, H2S, and antioxidant capacity. However, it was observed that individuals with low ferritin levels had significantly lower levels of endogenous H2S and thiol and higher levels of oxidative stress and lipid peroxidation. In Group B, individuals who experienced occasional H2S exposure (2–3 h, 10–12 times per year) and had an average of normal ferritin levels of 91.65 ng/mL showed lower oxidative stress and lipid peroxidation, as well as higher thiol, H2S, and antioxidant capacity. Surprisingly, individuals in Group B with low ferritin levels (average of 6.18 ng/mL) showed increased endogenous levels of H2S, which resulted in lower oxidative stress, and lipid peroxidation. These findings suggest that inhaling environmental H2S emitted from thermal springs may serve as an adaptive and protective mechanism for individuals with low ferritin levels by enhancing antioxidant capacity and reducing oxidative stress and lipid peroxidation modification, thus mitigating the harmful effects of reactive oxygen species.

Analysis of Radiation Toxicity in Mammalian Cells Stably Transduced with Mitochondrial Stat3.

A coordinated action between nuclear and mitochondrial activities is essential for a proper cellular response to genotoxic stress. Several nuclear transcription factors, including STAT3, translocate to mitochondria to exert mitochondrial function regulation; however, the role of mitochondrial STAT3 (mitoSTAT3) under stressed conditions is still poorly understood. In this study, we examined whether the stable expression of mitoSTAT3 wild-type or mutated at the conserved serine residue (Ser727), which is involved in the mitochondrial function of STAT3, can affect the DNA damage response to UVC radiation. To address this issue, we generated mammalian cells (NIH-3T3 and HCT-116 cells) stably transduced to express the mitochondrial-targeted Stat3 gene in its wild-type or Ser727 mutated forms. Our results show that cell proliferation is enhanced in mitoStat3-transduced cells under both non-stressed and stressed conditions. Once irradiated with UVC, cells expressing wild-type mitoSTAT3 showed the highest cell survival, which was associated with a significant decrease in cell death. Low levels of oxidative stress were detected in UVC-irradiated NIH-3T3 cells expressing mitoSTAT3 wild-type or serine-related dominant active form (Ser727D), confirming a role of mitochondrial STAT3 in minimizing oxidant cellular stress that provides an advantage for cell survival.

Deoxyshikonin inhibited rotavirus replication by regulating autophagy and oxidative stress through SIRT1/FoxO1/Rab7 axis

BackgroundRotavirus (RV) is a double-stranded RNA virus. RV prevention and treatment remain a major public health problem due to the lack of clinically specific drugs. Deoxyshikonin is a natural compound isolated from the root of Lithospermum erythrorhizon and one of the shikonin derivatives which owns remarkable therapeutic effects on multiple diseases. The purpose of this research was to inquire Deoxyshikonin's role and mechanism in RV infection. MethodsDeoxyshikonin's function in RV was estimated using Cell Counting Kit-8 analysis, cytopathic effect inhibition assay, virus titer determination, quantitative real-time PCR, enzyme linked-immunosorbent assay, Western blot, immunofluorescence, and glutathione levels detection. Also, Deoxyshikonin's mechanism in RV was appraised with Western blot, virus titer determination, and glutathione levels detection. Moreover, Deoxyshikonin's function in RV in vivo was determined using animal models, and diarrhea score analysis. ResultsDeoxyshikonin owned anti-RV activity and repressed RV replication in Caco-2 cells. Furthermore, Deoxyshikonin reduced autophagy and oxidative stress caused by RV. Mechanistically, Deoxyshikonin induced low protein levels of SIRT1, ac-Foxo1, Rab7, VP6, low levels of RV titers, low autophagy and oxidative stress. SIRT1 overexpression abolished the effects of Deoxyshikonin on RV-treated Caco-2 cells. Meanwhile, in vivo research affirmed that Deoxyshikonin also possessed anti-RV function, and this was reflected in increased survival rate, body weight, GSH levels, and decreased diarrhea score, RV virus antigen, LC-3II/LC3-I. ConclusionDeoxyshikonin reduced RV replication through mediating autophagy and oxidative stress via SIRT1/FoxO1/Rab7 pathway.

Stress Activated MAP Kinases and Cyclin-Dependent Kinase 5 Mediate Nuclear Translocation of Nrf2 via Hsp90α-Pin1-Dynein Motor Transport Machinery

Non-lethal low levels of oxidative stress leads to rapid activation of the transcription factor nuclear factor-E2-related factor 2 (Nrf2), which upregulates the expression of genes important for detoxification, glutathione synthesis, and defense against oxidative damage. Stress-activated MAP kinases p38, ERK, and JNK cooperate in the efficient nuclear accumulation of Nrf2 in a cell-type-dependent manner. Activation of p38 induces membrane trafficking of a glutathione sensor neutral sphingomyelinase 2, which generates ceramide upon depletion of cellular glutathione. We previously proposed that caveolin-1 in lipid rafts provides a signaling hub for the phosphorylation of Nrf2 by ceramide-activated PKCζ and casein kinase 2 to stabilize Nrf2 and mask a nuclear export signal. We further propose a mechanism of facilitated Nrf2 nuclear translocation by ERK and JNK. ERK and JNK phosphorylation of Nrf2 induces the association of prolyl cis/trans isomerase Pin1, which specifically recognizes phosphorylated serine or threonine immediately preceding a proline residue. Pin1-induced structural changes allow importin-α5 to associate with Nrf2. Pin1 is a co-chaperone of Hsp90α and mediates the association of the Nrf2-Pin1-Hsp90α complex with the dynein motor complex, which is involved in transporting the signaling complex to the nucleus along microtubules. In addition to ERK and JNK, cyclin-dependent kinase 5 could phosphorylate Nrf2 and mediate the transport of Nrf2 to the nucleus via the Pin1-Hsp90α system. Some other ERK target proteins, such as pyruvate kinase M2 and hypoxia-inducible transcription factor-1, are also transported to the nucleus via the Pin1-Hsp90α system to modulate gene expression and energy metabolism. Notably, as malignant tumors often express enhanced Pin1-Hsp90α signaling pathways, this provides a potential therapeutic target for tumors.

The co-occurrent microplastics and nano-CuO showed antagonistic inhibitory effects on bacterial denitrification: Interaction of pollutants and regulations on functional genes

The wide occurrence of microplastics (MPs) and nanoparticles resulted in their inevitable coexistence in environment. However, the joint effects of these two types of particulate emerging contaminants on denitrification have seldomly been investigated. Herein, non-biodegradable polyvinyl chloride, polypropylene, polyethylene and biodegradable polyhydroxyalkanoate (PHA) MPs were chosen to perform the co-occurrent effects with nano copper oxide (nano-CuO). Both the nano-CuO and MPs inhibited the denitrification process, and biodegradable PHA-MPs showed severer inhibition than non-biodegradable MPs. However, the presence of MPs significantly alleviated the inhibition of nano-CuO, suggesting an antagonistic effect. Other than MPs decreasing copper ion release from nano-CuO, MPs and nano-CuO formed agglomerations and induced lower levels of oxidative stress compared to individual exposure. Transcriptome analysis indicated that the co-occurrent MPs and nano-CuO induced different regulation on denitrifying genes (e. g. nar and nor) compared to individual ones. Also, the expressions of genes involved in denitrification-associated metabolic pathways, including glycolysis and NADH electron transfer, were down-regulated by nano-CuO or MPs, but exhibiting recovery under the co-occurrent conditions. This study firstly discloses the antagonistic effect of nano-CuO and MPs on environmental process, and these findings will benefit the systematic evaluation of MPs environmental behavior and co-occurrent risk with other pollutants.

Risk reduction and prevention of cardiovascular diseases: biological mechanisms of lycopene

Background and aims: The conservational effects of dietary interventions as advantageous instruments in the primary and secondary prevention of cardiovascular disease (CVD) have gotten more attention in recent years. Numerous nutritional epidemiological studies have highlighted the ability of diets to decrease costly care and treatments as well as adverse side effects from standard treatments. Lycopene is a non-pro-vitamin A carotenoid that is present in tomatoes, processed tomato products, and different fruits like watermelon, autumn olive, gac, pink grapefruit, pink guava, papaya, sea buckthorn, and wolfberry. As one of the most powerful antioxidants among dietary tetraterpenoids, lycopene can also assist in lowering the risk of early death and extending life in patients with heart disease. By reducing the destructive effects of free radicals along with total and “bad” LDL cholesterol levels while increasing “good” HDL cholesterol, lycopene holds the power to reduce the risk factors of heart disease. Several studies have investigated a reduction of oxidized-LDL (oxLDL) cholesterol levels following lycopene consumption which supports these claims and suggests the conceivable function of lycopene in the blockage of oxidative stress-associated CVD. A negative correlation between serum lycopene concentration and mortality of people with metabolic syndrome was found. Over 10 years, researchers observed a 39% decreased chance of premature death in individuals with the metabolic disease who had the highest blood concentrations of lycopene. Lycopene’s protective impacts are especially beneficial in those with low blood antioxidant levels or high levels of oxidative stress. This includes older adults, smokers, and diabetic individuals or other vascular disorders. Lycopene intake has been thought to reduce the risk of obesity, insulin resistance, and diabetes mellitus.Lycopene acts as an antihypertensive agent by impeding the angiotensin-converting enzyme and improving the production of nitric oxide (NO) in the endothelium. The purpose of this review is to summarize the possible mechanisms of lycopene in the prevention of CVD. Keywords: Lycopene, Risk factors of heart disease, Antioxidants, Carotenoids, Cardio-metabolic, Insulin resistance

Oxidative stress in workers in indoor and outdoor environments

Background and aim: Occupational exposure to particles can raises important health issues for exposed workers. High concentrations of these particles can be found in a variety of occupational and environmental contexts, depending on the type of scenario, whether indoors or outdoors working environments. The aim of this study was to investigate the role that indoor and outdoor environments play in altering oxidative stress levels in workers in relation to the exposure to particles. Methods: 162 subjects were recruited; 62 were subjects working in indoor environments (13 employed in the handling of waste, 49 not exposed to this task), 100 subjects working in outdoor environments (65 employed in sweeping of the streets, 35 not exposed to this task). Oxidative stress was assessed by analysing 15-F2t-isoprostane concentrations in urine samples of all the recruited subjects. In addition, a questionnaire was administered to each to obtain information among which gender, age, BMI, smoking habits. Statistical analyses were done using SPSS and 15-F2t-Isoprostane concentrations were compared each other using the Kruskal-Wallis test. Results: The analyses showed a higher level of 15-F2t-Isoprostane in workers working in indoor environment when compared to workers working in outdoor environments (P&amp;#x3c;0.01). Furthermore, the employed in the handling of waste in indoors show the highest level of 15-F2t-isoprostane (P&amp;#x3c;0.05) while, subjects not exposed to this task in indoors, place themselves at intermediate 15-F2t-isoprostane levels. Conclusions: This study shows that higher levels of oxidative stress were found in both exposed and unexposed workers in indoor environments. Analysing the responses to the questionnaire, we also controlled tobacco smoke exposure because it may have a role in the redox imbalance recorded in workers. These results hypothesise that particle dilution in outdoor environments may be directly associated with lower levels of oxidative stress in the workers. Keywords: occupational exposure, environmental exposure, particle emissions.

Differential effects of high-altitude exposure on markers of oxidative stress, antioxidant capacity, and iron profiles.

High-altitude (HA) exposure may stimulate significant physiological and molecular changes, resulting in HA-related illnesses. HA may impact oxidative stress, antioxidant capacity, and iron homeostasis, yet it is unclear how both repeated exposure and HA acclimatization may modulate such effects. Therefore, we assessed the effects of weeklong repeated daily HA exposure (2,900-5,050 m) in altitude-naïve individuals (n = 21 individuals, 13 females, mean ± SD, 25.3 ± 3.7 yr) to mirror the working schedule of HA workers (n = 19 individuals, all males, 41.1 ± 9.4 yr) at the Atacama Large Millimeter Array (ALMA) Observatory (San Pedro de Atacama, Chile). Markers of oxidative stress, antioxidant capacity, and iron homeostasis were measured in blood plasma. Levels of protein oxidation (P < 0.001) and catalase activity (P = 0.023) increased and serum iron (P < 0.001), serum ferritin (P < 0.001), and transferrin saturation (P < 0.001) levels decreased with HA exposure in both groups. HA workers had lower levels of oxidative stress, and higher levels of antioxidant capacity, iron supply, and hemoglobin concentration as compared with altitude-naïve individuals. On a second week of daily HA exposure, changes in levels of protein oxidation, glutathione peroxidase, and nitric oxide metabolites were lower as compared with the first week in altitude-naïve individuals. These results indicate that repeated exposure to HA may significantly alter oxidative stress and iron homeostasis, and the degree of such changes may be dependent on if HA is visited naïvely or routinely. Further studies are required to fully elucidate differences in HA-induced changes in oxidative stress and iron homeostasis profiles among visitors of HA.

TISSUE-SPECIFIC RESPONSES IN SOYBEAN PLANTS EXPOSED TO CADMIUM

Cadmium seriously affects plant growth, development, homeostasis and yield production. The effect of two doses of cadmium (10 and 100 mg.kg-1 Cd2+) on plants of sensitive soybean variety (Glycine max L. cv. Kyivska 98) were studied after short treatment in a pot experiment. Several parameters were determined in roots and leaves, including cell viability, the content of malondialdehyde and proline, and activity of defense proteins (catalases, guaiacol peroxidases, ascorbate peroxidases, superoxide dismutases, chitinases, β-1,3-glucanases). Changes caused by cadmium depended both on the concentration of cadmium, as well as on the type of plant organ and its developmental stage. Soybean tissues generally showed low levels of oxidative stress and reduced proline content likely due to activity or depletion by different mechanisms (respectively). The activity of catalases and guaiacol peroxidases was inhibited by cadmium concentrations only in younger leaves. The enzymatic activities of superoxide dismutases, chitinases and β-1,3-glucanases were highly variable depending on the cadmium concentration as well as the soybean organ analyzed. Our experiments revealed differences in defense strategies and regulatory mechanisms between plant organs as well as developmental stages of leaves in response to cadmium toxicity.

Role of TFE3 in Mitochondrial Adaptations to Skeletal Muscle Disuse

Prolonged muscle disuse is accompanied by a phenotypic shift characterized by declines in mitochondrial content and function within skeletal muscle. This loss in mitochondrial content can be partially attributed to elevations in various catabolic processes that occur with atrophy. One of these is termed mitophagy, a selective form of cellular recycling (autophagy) whereby dysfunctional mitochondria are degraded via lysosomes. TFEB and TFE3 are key transcription factors that regulate lysosomes by activating the expression of various lysosomal genes. Loss of TFE3 has been associated with depressed levels of autophagy and with mitochondrial dysfunction. It is speculated that these functional impairments are due to diminished clearance via the lysosomes, however to date this has not been examined. We hypothesized that the loss of TFE3 would amplify the mitochondrial dysfunction associated with muscle disuse, while paradoxically preserving muscle mass and mitochondrial content. Using a severe model of muscle disuse, sciatic denervation, we observed a 10% loss in hindlimb muscle mass within 7 days of denervation. In the absence of TFE3, a trend for muscle preservation was observed, as these animals lost 20% less muscle mass than WT counterparts. Reduced rates of respiration supported by complex I and II were observed irrespective of genotype, concurrent with elevated ROS emissions, suggesting an impaired oxidative capacity following 7 days of denervation. Surprisingly, TFE3 KO animals did exhibit lower levels of oxidative stress basally, but this too increased following 7 days of denervation, and taken relative to baseline the fold induction of ROS emission was 3 times greater than WT animals. Higher levels of mitophagy flux were observed in the absence of TFE3 basally, which supports the observed 35% decline in mitochondrial content as measured by COX activity, as well as the lower levels of ROS emissions. Following only 1 day of denervation, increases in mitophagy flux were observed in WT animals, while the response in KO animals was clearly attenuated. In the WT animals, denervation led to a 30% reduction in mitochondrial content, however no change was observed in the absence of TFE3. Finally, increases in a number of autophagy‐related markers such Beclin‐1 and ATG7 were observed following denervation irrespective of genotype. However, the mature form of Cathepsin B, a hydrolytic enzyme, was markedly reduced by 55% in the absence of TFE3 and did not increase to the same extent as WT following 7 days of denervation suggesting an impairment in lysosomal function. Together, our results suggest that TFE3 exerts multiple roles in skeletal muscle plasticity, as a partial mediator of muscle mass, and in the control of lysosomal function and mitophagy in response to the acute stress of muscle disuse.