Acute inhibitory effects of tire wear particles on the removal of biological phosphorus：The critical role of aging in improving environmentally persistent free radicals.

A comparative study explored how photoaging, ozonation aging, and Fenton aging affect tire wear particles (TWPs) and their phosphorus (P) removal in activated sludge. Aging altered TWPs' properties, increasing surface roughness, porosity, and generating more small particles, especially environmental persistent free radicals (EPFRs) in ozonation and Fenton aging. Post-aging TWPs (50 mg/L) inhibited sludge P removal significantly (p < 0.05), with rates of 44.3% and 59.6% for ozonation and Fenton aging, respectively. In addition, the metabolites involved in P cycling (poly-ß-hydroxyalkanoates: PHA and glycogen) and essential enzymes (Exopolyphosphatase: PPX and Polyphosphate kinase: PPK) were significantly inhibited (p < 0.05). Moreover, TWPs led to a decrease in microbial cells within the sludge and altered the community structure, a situation exacerbated by the aging of TWPs. P-removing bacteria decreased (e.g., Burkholderia, Candidatus), while extracellular polymeric substance-secreting bacteria increased (e.g., Pseudomonas, Novosphingobium). Pearson correlation analysis highlighted EPFRs' role in TWPs' acute toxicity to microbial cells, yet, emphasizing particle size's impact on the sludge system's purification and community structure.

Rod-Shaped Au@Ce Nano-Platforms for Enhancing Photodynamic Tumor Collaborative Therapy.

Tumor photodynamic therapy (PDT) relies on intratumoral free radicals, while the limited oxygen source and the depletion of tissue oxygen may exacerbate the hypoxia. As the treatment progresses, there will eventually be a problem of insufficient free radicals. Here, it is found that Au@CeO2 nano-rods (Au@Ce NRs), assembled by gold nano-rods (Au NRs) and ceria nanoparticles (CeO2 NPs), can efficaciously absorb near-infrared light (NIR) to promote the release of oxygen and free radicals. Au@Ce NRs exhibit a higher proportion of Ce3+ (Ce2O3) after oxygen release, while Ce3+ is subsequently oxidized to Ce4+ (CeO2) by trace H2O2. Interestingly, Au@Ce NRs re-oxidized by trace H2O2 can re-releasing oxygen and free radicals again upon NIR treatment, achieving oxygenation/oxygen evolution, similar to charging/discharging. This loop maximizes the conversion of limited oxygen source into highly cytotoxic free radicals. As a result, when B16-F10 cells are treated by NIR/Au@Ce NRs, more tumor cells undergo apoptosis, consistent with the higher level of free radicals. Importantly, NIR/Au@Ce NRs successfully suppresses tumor growth and promotes the generation of epidermal collagen fibers in the transplanted tumor model. Therefore, the rod-shaped Au@Ce NRs provide an ideal platform for maximizing the utilization of intratumoral oxygen sources and improving the treatment of melanoma.

Nicotine inhalation and metabolism triggers AOX-mediated superoxide generation with oxidative lung injury.

With the increasing use of vaping devices that deliver high levels of nicotine (NIC) to the lungs, sporadic lung injury has been observed. Commercial vaping solutions can contain high NIC concentrations of 150 mM or more. With high NIC levels, its metabolic products may induce toxicity. NIC is primarily metabolized to form NIC iminium (NICI) that is further metabolized by aldehyde oxidase (AOX) to cotinine. We determine that NICI in the presence of AOX is a potent trigger of superoxide generation. NICI stimulated superoxide generation from AOX with Km=2.7 µM and Vmax=794 nmol/min/mg measured by cytochrome-c reduction. EPR spin-trapping confirmed that NICI in the presence of AOX is a potent source of superoxide. AOX is expressed in the lungs and chronic e-cigarette exposure in mice greatly increased AOX expression. NICI or NIC stimulated superoxide production in lungs of control mice with even greater increase after chronic e-cigarette exposure. This superoxide production was quenched by AOX inhibition. Furthermore, e-cigarette-mediated NIC delivery triggered oxidative lung damage that was blocked by AOX inhibition. Thus, NIC metabolism triggers AOX-mediated superoxide generation that can cause lung injury. Therefore, high uncontrolled levels of NIC inhalation, as occur with e-cigarette use, can induce oxidative lung damage.

RESEARCH OF THE IMPACT OF ENVIRONMENTALLY PERSISTENT FREE RADICALS ON CHEMICAL ELEMENT BEHAVIOUR IN THE SOIL-PLANT SYSTEM.

Environmentally persistent free radicals (EPFRs) may pose a potential risk to the ecosystem and human health via oxidation stress and are considered emerging contaminants. Being stable with a lifetime of minutes or several months and abundant in transitional matrices (e.g. biochar), EPFRs continue to affect deposits (e.g. soil) and related media (plants) when the transitional matrices (e.g. biochar) are applied. The impact of EPFR on the plant uptake of chemical elements (CEs) was studied in the field conditions where, for two years, biochar and fertilisers were applied to the agricultural soil for winter triticale cultivation. EPFRs determination methods, along with the element uptake indices (bioaccumulation and biophilicity) and the method of the dynamic factors were applied. Results have shown that EPFRs have influenced the soil properties relevant to CE soil bioavailability and bioaccumulation in plants. The impact of EPFRs on CE transport in the soil-plant system was observed to influence the biogeochemical behaviour of CEs in the soil-plant system. This work provides the first findings on EPFRs-induces changes on CE bioavailability and bioaccumulation intensity, indicating the higher plant uptake risk of some potentially toxic elements (such as Cr).

Residential Wood Burning and Vehicle Emissions as Major Sources of Environmentally Persistent Free Radicals in Fairbanks, Alaska.

Environmentally persistent free radicals (EPFRs) play an important role in aerosol effects on air quality and public health, but their atmospheric abundance and sources are poorly understood. We measured EPFRs contained in PM2.5 collected in Fairbanks, Alaska, in winter 2022. We find that EPFR concentrations were enhanced during surface-based inversion and correlate strongly with incomplete combustion markers, including carbon monoxide and elemental carbon (R2 > 0.75). EPFRs exhibit moderately good correlations with PAHs, biomass burning organic aerosols, and potassium (R2 > 0.4). We also observe strong correlations of EPFRs with hydrocarbon-like organic aerosols, Fe and Ti (R2 > 0.6), and single-particle mass spectrometry measurements reveal internal mixing of PAHs, with potassium and iron. These results suggest that residential wood burning and vehicle tailpipes are major sources of EPFRs and nontailpipe emissions, such as brake wear and road dust, may contribute to the stabilization of EPFRs. Exposure to the observed EPFR concentrations (18 ± 12 pmol m-3) would be equivalent to smoking ∼0.4-1 cigarette daily. Very strong correlations (R2 > 0.8) of EPFR with hydroxyl radical formation in surrogate lung fluid indicate that exposure to EPFRs may induce oxidative stress in the human respiratory tract.

Theoretical study of the antioxidant mechanism and structure-activity relationships of 1,3,4-oxadiazol-2-ylthieno[2,3-d]pyrimidin-4-amine derivatives: a computational approach.

A theoretical thermodynamic study was conducted to investigate the antioxidant activity and mechanism of 1,3,4-oxadiazol-2-ylthieno[2,3-d]pyrimidin-4-amine derivatives (OTP) using a Density Functional Theory (DFT) approach. The study assessed how solvent environments influence the antioxidant properties of these derivatives. With the increasing prevalence of diseases linked to oxidative stress, such as cancer and cardiovascular diseases, antioxidants are crucial in mitigating the damage caused by free radicals. Previous research has demonstrated the remarkable scavenging abilities of 1,3,4-oxadiazole derivatives, prompting this investigation into their potential using computational methods. DFT calculations were employed to analyze key parameters, including bond dissociation enthalpy (BDE), ionization potential (IP), proton dissociation enthalpy (PDE), and electron transfer enthalpy (ETE), to delineate the antioxidant mechanisms of these compounds. Our findings indicate that specific electron-donating groups such as amine on the phenyl rings significantly enhance the antioxidant activities of these derivatives. The study also integrates global and local reactivity descriptors, such as Fukui functions and HOMO-LUMO energies, to predict the stability and reactivity of these molecules, providing insights into their potential as effective synthetic antioxidants in pharmaceutical applications.

Optimization and characterization of brown seaweed alginate for antioxidant, anticancer, antimicrobial, and antiviral properties.

Alginate is a natural polysaccharide obtained from brown seaweeds and having advantageous health usefulness, was employed extensively in nutraceutical sectors and the pharmaceutical industry. This research was devoted for optimization of alginate extraction from different brown seaweeds. A Box-Behnken Design (BBD) was used for the optimization of alginate extraction from Padina pavonica by analyzing the influence of temperature (30, 40, and 50 °C), time (60, 120, and 180 min), and alkaline concentration (1 %, 2 %, and 3 %) on extraction yield and uronic acid content. The optimal conditions recorded to maximize the alginate yield and its uronic content were an alkali concentration of 2.5 % and a temperature of 39.95 °C for 102.5 min. The optimized parameters achieved from BBD were used to compare alginate extraction from P. pavonica, Sargassum cinereum, Turbinaria turbinata, and Dictyota dichotoma. FTIR, 1H NMR, and HPLC were used to characterize the extracted alginate. The bioactivity of alginate against free radicals, breast cancer cells (MCF-7), some pathogenic microbes, and SARS-CoV-2 viruses was tested. Under the optimized conditions, alginate was extracted from P. pavonica at a rate of 21.13 ±â€¯2.47 % DW, S. cinereum at 24.08 ±â€¯0.33 % DW g/L, T. turbinata at 17.47 ±â€¯0.26 % DW, and D. dichotoma at a rate of 19.57 ±â€¯3.60 % DW. The alginate extracted from D. dichotoma showed the highest antioxidant, anticancer, and antiviral activity.

An evaluation of pyrite as a component of respirable coal dust.

Over the past two decades, the rise in coal worker's pneumoconiosis has prompted research into the effects of respirable coal dust components. This study explores how coal-pyrites produce hydroxyl radicals (•OH), a reactive oxygen species closely associated with particle toxicity, and assesses the ability of safe chemical additives to reduce •OH production at various pH levels. Promising candidates were evaluated in various solutions, including tap and process waters and simulated lung fluid. We employed electrokinetic measurements, infrared and X-ray photoelectron spectroscopies, and ab initio atomistic simulations to analyze particle surfaces. The study also looked at how surface aging affects •OH production. Our results show that •OH generation of the pyrite varies and is catalyzed by elements like silicon, aluminum, and iron in pyrite. Carboxymethyl cellulose was effective in reducing •OH production by targeting surface sulfide and silicon sites and affecting surface hydration and charge. Atmospheric aging was found to increase •OH production, especially in the pyrite with high iron and silicon and low calcium contents, relative to other samples. This highlights the role of the pyrite surface properties and chemical composition, and the solution pH and composition in •OH generation by coal-pyrites.

Fenton-conditioning of landfill leachate biological sludge enables biochar for efficient Cr(â ¥)removal: Occurrence of oxygen-centered free radicals.

Fenton-conditioning is commonly used to improve dewatering ability for municipal biological sludge, however, its application in industries is scarce. In this study, biochar (FT-BC) was successfully synthesized from a Fenton-conditioned landfill leachate biological sludge under oxygen-limited. As compared to the corresponding blank and poly ferric-pretreated biochars (BC and PF-BC), moderate Fenton conditioning of the sludge could enable good removal performance for Cr (Ⅵ) by FT-BC. It was found that the oxygen central free radicals (OCFRs) on the biochar surface was intensively promoted due to Fenton electrophilic addition of ·OH onto the oxygen-containing functional groups in biomass. The amounts of OCFRs correlated positively well with the removal efficiency, indicating these persistent free radicals (PFRs)would mainly responsible for the reductive immobilization of Cr(VI)on the FT-BC surface. This study is expected to provide a new method for reclamation of industrial biological sludges with poor agglomeration by introducing simple Fenton pre-conditioning.

Biomarker dosimetry of acute low level of thermal neutrons and radiation adaptive response effect on rats.

In this paper, we demonstrated the biological effects of acute low-dose neutrons on the whole body of rats and investigated the impact of that level of neutron dose to induce an in vivo radio-adaptive response. To understand the radio-adaptive response, the examined animals were exposed to acute neutron radiation doses of 5 and 10 mSv, followed by a 50 mSv challenge dose after 14 days. After irradiation, all groups receiving single and double doses were kept in cages for one day before sampling. The electron paramagnetic resonance (EPR) method was used to estimate the radiation-induced radicals in the blood, and some hematological parameters and lipid peroxidation (MDA) were determined. A comet assay was performed beside some of the antioxidant enzymes [catalase enzyme (CAT), superoxide dismutase (SOD), and glutathione (GSH)]. Seven groups of adult male rats were classified according to their dose of neutron exposure. Measurements of all studied markers are taken one week after harvesting, except for hematological markers, within 2 h. The results indicated lower production of antioxidant enzymes (CAT by 1.18-5.83%, SOD by 1.47-17.8%, and GSH by 11.3-82.1%). Additionally, there was an increase in red cell distribution width (RDW) (from 4.61 to 25.19%) and in comet assay parameters such as Tail Length, (from 6.16 to 10.81 µm), Tail Moment, (from 1.17 to 2.46 µm), and percentage of DNA in tail length (DNA%) (from 9.58 to 17.32%) in all groups exposed to acute doses of radiation ranging from 5 to 50 mSv, respectively. This emphasizes the ascending harmful effect with the increased acute thermal neutron doses. The values of the introduced factor of radio adaptive response for all markers under study reveal that the lower priming dose promotes a higher adaptation response and vice versa. Ultimately, the results indicate significant variations in DNA%, SOD enzyme levels, EPR intensity, total Hb concentration, and RDWs, suggesting their potential use as biomarkers for acute thermal neutron dosimetry. Further research is necessary to validate these measurements as biodosimetry for radiation exposure, including investigations involving the response impact of RAR with varied challenge doses and post-irradiation behavior.

Overlooked Roles and Transformation of Carbon-Centered Radicals Produced from Natural Organic Matter in a Thermally Activated Persulfate System.

The presence and induced secondary reactions of natural organic matter (NOM) significantly affect the remediation efficacy of in situ chemical oxidation (ISCO) systems. However, it remains unclear how this process relates to organic radicals generated from reactions between the NOM and oxidants. The study, for the first time, reported the vital roles and transformation pathways of carbon-centered radicals (CCR•) derived from NOM in activated persulfate (PS) systems. Results showed that both typical terrestrial/aquatic NOM isolates and collected NOM samples produced CCR• by scavenging activated PS and greatly enhanced the dehalogenation performance under anoxic conditions. Under oxic conditions, newly formed CCR• could be oxidized by O2 and generate organic peroxide intermediates (ROO•) to catalytically yield additional •OH without the involvement of PS. Nuclear magnetic resonance (NMR) and Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS) results indicated that CCR• predominantly formed from carboxyl and aliphatic structures instead of aromatics within NOM through hydrogen abstraction and decarboxylation reactions by SO4•- or •OH. Specific anoxic reactions (i.e., dehalogenation and intramolecular cross-coupling reactions) further promoted the transformation of CCR• to more unsaturated and polymerized/condensed compounds. In contrast, oxic propagation of ROO• enhanced bond breakage/ring cleavage and degradation of CCR• due to the presence of additional •OH and self-decomposition. This study provides novel insights into the role of NOM and O2 in ISCO and the development of engineered strategies for creating organic radicals capable of enhancing the remediation of specific contaminants and recovering organic carbon.

Dielectric barrier discharge low-temperature plasma modification of bamboo charcoal for supercapacitor applications.

Biochar is commonly utilized as an electrode material in supercapacitors. However, the conventional carbonization process often results in macromolecular compounds, which obstruct the porous structure of carbon materials, thereby reducing their capacitance. Dielectric barrier discharge low-temperature plasma (DLTP) is a technology that transforms gases into highly excited states, utilizing high-energy particles for enhanced energy applications. This study investigated the effects of DLTP on the electrochemical performance of bamboo charcoal (BC), utilizing bamboo shavings (BS) as the carbon source. The results indicated that the specific capacitance of BC varied under different atmospheric conditions, input voltages, and treatment durations, thereby achieving a maximum increase of 144 F/g. Furthermore, when combined with KOH activation, DLTP modification further enhanced the specific capacitance of BC to 237 F/g. The DLTP treatment enhanced the specific surface area and the types of functional groups in BC, thereby leading to a significant enhancement of its electrochemical properties.

Unlocking peak performance: The role of Nrf2 in enhancing exercise outcomes and training adaptation in humans.

Since the discovery of the nuclear factor erythroid-derived 2-like 2 (Nrf2) transcription factor thirty years ago, it has been shown that it regulates more than 250 genes involved in a multitude of biological processes, including redox balance, mitochondrial biogenesis, metabolism, detoxification, cytoprotection, inflammation, immunity, autophagy, cell differentiation, and xenobiotic metabolism. In skeletal muscle, Nrf2 signalling is primarily activated in response to perturbation of redox balance by reactive oxygen species or electrophiles. Initial investigations into human skeletal muscle Nrf2 responses to exercise, dating back roughly a decade, have consistently indicated that exercise-induced ROS production stimulates Nrf2 signalling. Notably, recent studies employing Nrf2 knockout mice have revealed impaired skeletal muscle contractile function characterised by reduced force output and increased fatigue susceptibility compared to wild-type counterparts. These deficiencies partially stem from diminished basal mitochondrial respiratory capacity and an impaired capacity to upregulate specific mitochondrial proteins in response to training, findings corroborated by inducible muscle-specific Nrf2 knockout models. In humans, baseline Nrf2 expression in skeletal muscle correlates with maximal oxygen uptake and high-intensity exercise performance. This manuscript delves into the mechanisms underpinning Nrf2 signalling in response to acute exercise in human skeletal muscle, highlighting the involvement of ROS, antioxidants and Keap1/Nrf2 signalling in exercise performance. Furthermore, it explores Nrf2's role in mediating adaptations to chronic exercise and its impact on overall exercise performance. Additionally, the influence of diet and certain supplements on basal Nrf2 expression and its role in modulating acute and chronic exercise responses are briefly addressed.

Tobacco cigarette smoking induces cerebrovascular dysfunction followed by oxidative neuronal injury with the onset of cognitive impairment.

While chronic smoking triggers cardiovascular disease, controversy remains regarding its effects on the brain and cognition. We investigated the effects of long-term cigarette smoke (CS) exposure (CSE) on cerebrovascular function, neuronal injury, and cognition in a novel mouse exposure model. Longitudinal studies were performed in CS or air-exposed mice, 2 hours/day, for up to 60 weeks. Hypertension and carotid vascular endothelial dysfunction (VED) occurred by 16 weeks of CSE, followed by reduced carotid artery blood flow, with oxidative stress detected in the carotid artery, and subsequently in the brain of CS-exposed mice with generation of reactive oxygen species (ROS) and secondary protein and DNA oxidation, microglial activation and astrocytosis. Brain small vessels exhibited decreased levels of endothelial NO synthase (eNOS), enlarged perivascular spaces with blood brain barrier (BBB) leak and decreased levels of tight-junction proteins. In the brain, amyloid-ß deposition and phosphorylated-tau were detected with increases out to 60 weeks, at which time mice exhibited impaired spatial learning and memory. Thus, long-term CSE initiates a cascade of ROS generation and oxidative damage, eNOS dysfunction with cerebral hypoperfusion, as well as cerebrovascular and BBB damage with intracerebral inflammation, and neuronal degeneration, followed by the onset of impaired cognition and memory.

Panax notoginseng: Pharmacological Aspects and Toxicological Issues.

Current evidence suggests a beneficial role of herbal products in free radical-induced diseases. Panax notoginseng (Burk.) F. H. Chen has long occupied a leading position in traditional Chinese medicine because of the ergogenic, nootropic, and antistress activities, although these properties are also acknowledged in the Western world. The goal of this paper is to review the pharmacological and toxicological properties of P. notoginseng and discuss its potential therapeutic effect. A literature search was carried out on Pubmed, Scopus, and the Cochrane Central Register of Controlled Trials databases. The following search terms were used: "notoginseng", "gut microbiota", "immune system", "inflammation", "cardiovascular system", "central nervous system", "metabolism", "cancer", and "toxicology". Only peer-reviewed articles written in English, with the full text available, have been included. Preclinical evidence has unraveled the P. notoginseng pharmacological effects in immune-inflammatory, cardiovascular, central nervous system, metabolic, and neoplastic diseases by acting on several molecular targets. However, few clinical studies have confirmed the therapeutic properties of P. notoginseng, mainly as an adjuvant in the conventional treatment of cardiovascular disorders. Further clinical studies, which both confirm the efficacy of P. notoginseng in free radical-related diseases and delve into its toxicological aspects, are mandatory to broaden its therapeutic potential.

Reactive Oxygen Species (ROS)-Mediated Antibacterial Oxidative Therapies: Available Methods to Generate ROS and a Novel Option Proposal.

The increasing emergence of multidrug-resistant (MDR) pathogens causes difficult-to-treat infections with long-term hospitalizations and a high incidence of death, thus representing a global public health problem. To manage MDR bacteria bugs, new antimicrobial strategies are necessary, and their introduction in practice is a daily challenge for scientists in the field. An extensively studied approach to treating MDR infections consists of inducing high levels of reactive oxygen species (ROS) by several methods. Although further clinical investigations are mandatory on the possible toxic effects of ROS on mammalian cells, clinical evaluations are extremely promising, and their topical use to treat infected wounds and ulcers, also in presence of biofilm, is already clinically approved. Biochar (BC) is a carbonaceous material obtained by pyrolysis of different vegetable and animal biomass feedstocks at 200-1000 °C in the limited presence of O2. Recently, it has been demonstrated that BC's capability of removing organic and inorganic xenobiotics is mainly due to the presence of persistent free radicals (PFRs), which can activate oxygen, H2O2, or persulfate in the presence or absence of transition metals by electron transfer, thus generating ROS, which in turn degrade pollutants by advanced oxidation processes (AOPs). In this context, the antibacterial effects of BC-containing PFRs have been demonstrated by some authors against Escherichia coli and Staphylococcus aureus, thus giving birth to our idea of the possible use of BC-derived PFRs as a novel method capable of inducing ROS generation for antimicrobial oxidative therapy. Here, the general aspects concerning ROS physiological and pathological production and regulation and the mechanism by which they could exert antimicrobial effects have been reviewed. The methods currently adopted to induce ROS production for antimicrobial oxidative therapy have been discussed. Finally, for the first time, BC-related PFRs have been proposed as a new source of ROS for antimicrobial therapy via AOPs.

Cannabinoid 2 receptor activation protects against diabetic cardiomyopathy through inhibition of AGE/RAGE-induced oxidative stress, fibrosis, and inflammasome activation.

Oxidative stress, fibrosis, and inflammasome activation from AGE-RAGE interaction contribute to diabetic cardiomyopathy (DCM) formation and progression. Our study revealed the impact of ß-caryophyllene (BCP) on activating CB2 receptors against diabetes complications and investigated the underlying cell signaling pathways in mice. The murine model of DCM was developed by feeding high-fat diet with streptozotocin injections. After the development of diabetes, the animals received a 12-week oral BCP treatment at a dosage of 50 mg/kg/body weight. BCP treatment showed significant improvement in glucose tolerance, insulin resistance, and enhanced serum insulin levels in diabetic animals. BCP treatment effectively reversed the heart remodeling and restored the phosphorylated troponin I and SERCA2a expression. Ultrastructural examination showed reduced myocardial cell injury in DCM mice treated with BCP. The preserved myocytes were found associated with reduced expression of AGE/RAGE in DCM mice hearts. BCP treatment mitigated oxidative stress by inhibiting expression of NOX4 and activating PI3K/AKT/Nrf2 signaling. BCP suppressed cardiac fibrosis and endothelial-to-mesenchymal transition (EndMT) in DCM mice by inhibiting TGF-ß/Smad signaling. Further, BCP treatment suppressed NLRP3 inflammasome activation in DCM mice and alleviated cellular injury to the pancreatic tissues evidenced by significant elevation of the number of insulin-positive cells. To demonstrate CB2 receptor dependent mechanism of BCP, another group of DCM mice were pretreated with AM630, a CB2 receptor antagonist AM630 and AM630 was observed to abrogate the beneficial effects of BCP in DCM mice. Taken together, BCP showed the potential to protect the myocardium and pancreas of DCM mice mediating CB2 receptor dependent mechanisms. Significance Statement 1. ß-caryophyllene (BCP), a cannabinoid type 2 receptor (CB2R) agonist. 2. BCP attenuates diabetic cardiomyopathy via activating CB2R in mice 3. CB2R activation by BCP shows strong protection against fibrosis and inflammasome activation 4. It regulates AGE/RAGE and PI3K/Nrf2/Akt signaling in mice.

Deciphering the Potential Therapeutic Effects of Hydnocarpus wightianus Seed Extracts using in vitro and in silico approaches.

Phytocompounds possess the potential to treat a broad spectrum of disorders due to their remarkable bioactivity. Naturally occurring compounds possess lower toxicity profiles, which making them attractive targets for drug development. Hydnocarpus wightianus seeds were extracted using ethanol, acetone, and hexane solvents. The extracts were evaluated for phytochemicals screening and other therapeutic characteristics, such as free radicals scavenging, anti α-amylase, anti α-glucosidase, and anti-bacterial activities. The ethanolic extract exhibited noteworthy antibacterial characteristics and demonstrated considerable antioxidant, and anti-diabetic effects. The IC50 value of the ethanolic extract for Dpph, α-amylase, and α-glucosidase were found to be 77.299 ± 3.381 µg/mL, 165.56 2.56 µg/mL, and 136.58 ± 5.82 µg/mL, respectively. The ethanolic extract was effective against Methicillin resistant Staphylococcus aureus (26 mm zone of inhibition at 100 µL concentration). Molecular docking investigations revealed the phytoconstituent's inhibitory mechanisms against diabetic, free radicals, and bacterial activity. Docking score for phytocompounds against targeted protein varies from -7.2 to -5.1 kcal/mol. The bioactive compounds present in the ethanolic extract were identified by Gas chromatography/Mass spectrometry analysis, followed by molecular docking and molecular dynamic simulation studies to further explore the phytoconstituent's inhibitory mechanism of α-glucosidase, ∝-amylase, radical scavenging, and bacterial activity. The electronic structure and possible pharmacological actions of the phytocompound were revealed through the use of Density Functional Theory (DFT) analysis. Computational and in vitro studies revealed that these identified compounds have anti-diabetic, anti-oxidant, and anti-bacterial activities against antibiotic-resistant strain of Staphylococcus aureus.

Coupled effects of Fenton-like systems with different concentrations of H2O2/Biochar on diethyl phthalate removal: Dominant role of environmental persistent free radicals (EPFRs).

To investigate the impact of different H2O2 concentrations on the Fenton-like systems of H2O2/biochar, this study examined the mechanism of the physical structure and environmental persistent free radicals (EPFRs) of biochar during diethyl phthalate (DEP) removal by the Fenton-like system. The peak-splitting method was utilized to differentiate EPFRs types in cotton stalk biochar produced at different temperatures. High-temperature environments promote π-electron delocalization, which facilitates phenyl π free radicals and σ-π oxygen-containing free radicals. By analyzing relationships between the removal rate K1 and removal constant Kobs of DEP with the structural properties of biochar, it was discovered that EPFRs concentrations in biochar had a significant positive correlation with K1 (r = 0.92) and Kobs (r = 0.97). Different H2O2 concentrations added to the biochar removal system resulted in varied DEP removal efficiency. Among them, CS500, CS550, and CS600 exhibited superior DEP removal efficiency when H2O2 concentration was 5 mM.

Study of Serum Gamma-Glutamyl Transferase Levels in Patients With Acute Ischemic Stroke.

Background Gamma-glutamyl transferase (GGT) mediates intracellular uptake of glutathione which is a known antioxidant. GGT levels are found to be elevated in conditions of oxidative stress. Ischemic stroke results in anoxic injury, which liberates free radicals, causing glutathione to rise, which may be accompanied by a rise in serum GGT levels. This study aimed to compare serum GGT levels in acute ischemic stroke patients with normal controls and to ascertain the relation of serum GGT levels with National Institute of Health Stroke Scale (NIHSS) scores. Materials and methods This cross-sectional study was carried out in a tertiary care hospital in South India from August 2023 to February 2024. The study included 57 patients who presented with acute ischemic stroke within 24 hours of onset and 57 age- and sex-matched controls. The serum GGT levels of the cases were compared with age- and sex-matched controls using an independent t-test. Mean serum GGT levels were compared among groups with varying NIHSS scores and different locations of infarction using the ANOVA test. Serum GGT levels were also compared based on age, gender, and various comorbidities. Results The mean serum GGT levels were significantly increased (p < 0.0001) in acute ischemic stroke patients, 43.96 ± 28.02 (mean ± SD), when compared to controls, 26.14 ± 5.93 (mean ± SD). The difference in serum GGT levels with NIHSS scores of 5-15 (moderate strokes) with 34.17 ± 18.39 (mean ± SD), 16-20 (moderate-severe strokes) with 46.64 ± 21.95 (mean ± SD), and >21 (severe stroke) with 84.62 ± 39.35 (mean ± SD) was significant (p < 0.00001). Serum GGT levels were not significant while comparing age, gender, location of infarction, type 2 diabetes mellitus, and hypertension. Conclusion Serum GGT levels were significantly elevated in acute ischemic stroke patients within 24 hours of presentation. Serum GGT levels were significantly elevated with increasing severity of stroke as calculated by NIHSS scores at the time of presentation. Serum GGT levels are a potential marker of ischemic stroke and its severity.