Oxygen Free Radicals Research Articles

Characteristics and mechanism of Glutathione in inhibiting coal spontaneous combustion

Inhibitors play an important role in preventing and controlling coal spontaneous combustion (CSC). In this study, the inhibitory effects of antioxidant-reduced glutathione (G-SH) on CSC were examined. Thermogravimetric-differential scanning calorimetry (TG-DSC), cross-point temperature (CPT), and oxidation product tests were used to examine the effect of G-SH on the tendency of CSC and compare the discrepancy in the inhibition effect of G-SH and the halogen inhibitor. The changes in the free radical type, concentration, and surface functional groups in coal before and after the addition of G-SH were analyzed using electron spin resonance spectroscopy (ESR) and Fourier transform infrared spectroscopy (FT-IR). Six common active radical models were constructed, and the thermodynamic parameters of the reaction were calculated using density functional theory (DFT). The results revealed that G-SH inhibits the spontaneous combustion of coal. The inhibitory effect of G-SH was significantly stronger than that of the halogen salt inhibitors CaCl2 and MgCl2, and the higher the concentration of G-SH, the stronger is the inhibitory effect. The characteristic temperature points in the thermogravimetric experiment of coal samples with G-SH shifted to a higher temperature zone, and the CO concentration and oxygen consumption were lower than those of raw coal. After G-SH treatment, the type and relative concentration of free radicals in coal were lower than those in raw coal, the content of aliphatic hydrocarbon functional groups and oxygen-containing functional groups decreased, and the content of sulfur-containing functional groups increased. According to the calculation of Gibbs free energy and reaction enthalpy, G-SH can effectively neutralize the active free radicals in the process of coal oxidation, and the reaction activity with the free radicals in the process of coal oxidation is ·OOH > ·OH > ·CH3 > RO· > R· > ROO·. According to the experimental results, it is inferred that G-SH continuously supplies a large number of hydrogen donors (·H) for the reaction during the oxidation process and simultaneously neutralizes carbon free radicals and carbon oxygen free radicals, thereby reducing the concentration and reactivity of free radicals in the whole chain reaction process and blocking the occurrence of coal-oxygen composite reaction.

Hollow-polydopamine-nanocarrier-based near-infrared-light/pH-responsive drug delivery system for diffuse alveolar hemorrhage treatment.

Introduction: Diffuse alveolar hemorrhage (DAH) is a serious complication caused by systemic lupus erythematosus (SLE). Tissue damage and changes in immune response are all associated with excessive free radical production. Therefore, removing excess reactive oxygen species are considered a feasible scheme for diffuse alveolar hemorrhage treatment. Cyclophosphamide is often used as the main therapeutic drug in clinics. However, CTX carries a high risk of dose-increasing toxicity, treatment intolerance, and high recurrence rate. The combination of therapeutic drugs and functional nanocarriers may provide an effective solution. PDA is rich in phenolic groups, which can remove the reactive oxygen species generated in inflammatory reactions, and can serve as excellent free radical scavengers. Methods: We developed a hollow polydopamine (HPDA) nanocarrier loaded with CTX by ionization to prepare the novel nanoplatform, CTX@HPDA, for DAH treatment. The monodisperse silica nanoparticles were acquired by reference to the typical Stober method. PDA was coated on the surface of SiO2 by oxidation self-polymerization method to obtain SiO2@PDA NPs. Then, HPDA NPs were obtained by HF etching. Then HPDA was loaded with CTX by ionization to prepare CTX@HPDA. Then we tested the photothermal effect, animal model therapeutics effect, and biosafety of CTX@HPDA. Results: Material tests showed that the CTX@ HPDA nanoplatform had a uniform diameter and could release CTX in acidic environments. The vitro experiments demonstrated that CTX@HPDA has good photothermal conversion ability and photothermal stability. Animal experiments demonstrated that the CTX@HPDA nanoplatform had good biocompatibility. The nanoplatform can dissociate in acidic SLE environment and trigger CTX release through photothermal conversion. Combining HPDA, which scavenges oxygen free radicals, and CTX, which has immunosuppressive effect, can treat pulmonary hemorrhage in SLE. Micro-CT can be used to continuously analyze DAH severity and lung changes in mice after treatment. The pulmonary exudation in the various treatment groups improved to varying degrees. Discussion: In this study, we report a photothermal/PH-triggered nanocarrier (CTX@HPDA) for the precise treatment of SLE-DAH. CTX@HPDA is a simple and efficient nanocarrier system for DAH therapy. This work provides valuable insights into SLE treatment.

Betalains in practical medicine

Betalains are plant pigments synthesized in the cells of Caryophyllales (red beets, opuntia, etc.). They are involved in the inactivation of reactive oxygen species and free radicals. The paper summarizes the data on the physical-chemical and pharmacological properties of betalains. Betalains eliminate the consequences of oxidative stress, effectively correct metabolic disorders in diabetes mellitus and abdominal obesity, and reduce the risk of cardiovascular diseases. A betalain-enriched diet has a wide range of anticancer effects. Betalains protect brain dopaminergic neurons from oxidative damage and reduce the severity of neurodegenerative disorders in Alzheimer’s and Parkinson’s disease. However, betalains are not stable enough to resist degradation during processing and storage of plant raw materials. Therefore, developing non-damaging technologies for betalain-containing treatment is highly relevant.

Involvement of oxidative stress in placental dysfunction, the pathophysiology of fetal death and pregnancy disorders.

Placental oxidative stress contributes to both normal and abnormal placentation during pregnancy. This review discusses the potential consequence of oxidative stress-induced placental dysfunction on pregnancies complicated by fetal death and pregnancies with a high risk of fetal death. The placenta is a source of reactive oxygen free radicals due to the oxidative metabolism required to meet the demands of the growing fetus. The placenta has an array of efficient antioxidant defense systems to deal with rising oxidative stress created by free radicals during pregnancy. Properly controlled physiological (low-level) free radical production is a necessary part of cellular signaling pathways and downstream activities during normal placental development; however, poorly controlled oxidative stress can cause aberrant placentation, immune disturbances and placental dysfunction. Abnormal placental function and immune disturbances are linked to many pregnancy-related disorders, including early and recurrent pregnancy loss, fetal death, spontaneous preterm birth, preeclampsia and fetal growth restriction. This review discusses the role of placental oxidative stress in both normal and pathological settings. Finally, based on previously published work, this review presents multiple lines of evidence for the strong association between oxidative stress and adverse pregnancy outcomes, including fetal death and pregnancies with a high risk of fetal death.

Mitigation of Hepatotoxicity via Boosting Antioxidants and Reducing Oxidative Stress and Inflammation in Carbendazim-Treated Rats Using Adiantum Capillus-Veneris L. Extract.

Exposure to food contaminants continues to be a substantial source of human health risks all over the world, particularly in developing countries. Carbendazim (CBZ) is a chemical fungicide used to control the spread of various fungi and other pathogens in the agriculture and veterinary sectors. The hazardous effects of CBZ on human health occur due to the accumulation of its residues in agricultural food products. In this study, the possible hepatoprotective effects of Adiantum capillus-veneris L. (ACVL) extract were evaluated in CBZ-treated rats. A GC-MS analysis revealed that ACVL extract contained several bioactive hydrocarbon components and fatty acids, and that the components exerted hepatic protection by mitigating oxidative stress via upregulating antioxidant agents and neutralizing nitrogen and oxygen free radicals. Moreover, ACVL extracts relieved hepatic inflammation via decreasing NO, NF-κB, and pro-inflammatory cytokines (TNF-a, IL-6) in the liver of CBZ-treated rats, both at protein and mRNA levels. In addition, the protective effect of ACVL has appeared in the histopathological figures and function markers in the livers of CBZ-treated rats. According to the present results, ACVL extract can protect the hepatic tissue and restore its functions to a control level in CBZ-treated rats; this effect may be attributed to its antioxidant and anti-inflammatory activities.

Synergistic toxicity of NiO nanoparticles and benzo[a]pyrene co-exposure in liver cells: Role of free oxygen radicals induced oxidative stress

Current attention has been given on health effects of combined exposure of nanoscale materials and organic pollutants. Nickel (II) oxide nanoparticles (NiO NPs) displays exceptional properties and is being used in various areas such as batteries, diesel–fuel additives, and biomedicals. Benzo[a]pyrene (BaP) is a ubiquitous pollutant. Cigarette smoke, diesel exhaust, and grilled foods are main sources of BaP exposure. Therefore, combined exposure of NiO NPs and BaP to humans is unavoidable. There is a dearth of knowledge on combined effects of NiO NPs and BaP in humans. This study was aimed to investigate co-exposure effects of NiO NPs and BaP in human liver cells (HepG2) and primary rat hepatocytes. We observed that individual and co-exposure of NiO NPs and BaP induced cytotoxicity, lactate dehydrogenase leakage, lipid peroxidation, depletion of mitochondrial membrane potential, and activation of caspases (-3 and -9) in both types of cells. Individual and co-exposure of NiO NPs and BaP further accelerated the generation of free oxygen radicals (reactive oxygen species and hydrogen peroxide) and depletion of antioxidants (glutathione and various antioxidant enzymes). Remarkably, NiO NPs and BaP exerted synergistic toxicity to both HepG2 cells and primary rat hepatocytes. Moreover, combined toxicity of NiO NPs and BaP in both cells was mediated through free oxygen radicals induced oxidative stress. This work warrants further research on risk assessment of co-exposure effects NiO NPs and BaP in an appropriate in vivo model.

Photoenhanced Radical Formation in Aqueous Mixtures of Levoglucosan and Benzoquinone: Implications to Photochemical Aging of Biomass-Burning Organic Aerosols.

The photochemical aging of biomass-burning organic aerosols (BBOAs) by exposure to sunlight changes the chemical composition over its atmospheric lifetime, affecting the toxicological and climate-relevant properties of BBOA particles. This study used electron paramagnetic resonance (EPR) spectroscopy with a spin-trapping agent, 5-tert-butoxycarbonyl-5-methyl-1-pyrroline-N-oxide (BMPO), high-resolution mass spectrometry, and kinetic modeling to study the photosensitized formation of reactive oxygen species (ROS) and free radicals in mixtures of benzoquinone and levoglucosan, known BBOA tracer molecules. EPR analysis of irradiated benzoquinone solutions showed dominant formation of hydroxyl radicals (•OH), which are known products of reaction of triplet-state benzoquinone with water, also yielding semiquinone radicals. In addition, hydrogen radicals (H•) were also observed, which were not detected in previous studies. They were most likely generated by photochemical decomposition of semiquinone radicals. The irradiation of mixtures of benzoquinone and levoglucosan led to substantial formation of carbon- and oxygen-centered organic radicals, which became prominent in mixtures with a higher fraction of levoglucosan. High-resolution mass spectrometry permitted direct observation of BMPO-radical adducts and demonstrated the formation of •OH, semiquinone radicals, and organic radicals derived from oxidation of benzoquinone and levoglucosan. Mass spectrometry also detected superoxide radical adducts (BMPO-OOH) that did not appear in the EPR spectra. Kinetic modeling of the processes in the irradiated mixtures successfully reproduced the time evolution of the observed formation of the BMPO adducts of •OH and H• observed with EPR. The model was then applied to describe photochemical processes that would occur in mixtures of benzoquinone and levoglucosan in the absence of BMPO, predicting the generation of HO2• due to the reaction of H• with dissolved oxygen. These results imply that photoirradiation of aerosols containing photosensitizers induces ROS formation and secondary radical chemistry to drive photochemical aging of BBOA in the atmosphere.

Shorter telomere length in children with autism spectrum disorder is associated with oxidative stress.

Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental disorder caused by a complex interaction between genetic and environmental risk factors. The balance between antioxidant capacity and oxidative stress (OS) induced free radicals may be crucial during the pathophysiological development of ASD. In this study, 96 children with ASD who met the diagnostic and statistical manual of mental disorders were collected, and the number of children in the typical development (TD) group was matched by 1:1. Digital PCR (dPCR) for telomere length (TL) expression in ASD in peripheral blood leukocytes. Urine levels of 8-hydroxy-2-deoxyguanosine (8-OHdG) content were measured by tandem triple quadrupole mass spectrometry and corrected by urinary creatinine levels. The levels of superoxide dismutase (SOD), catalase (CAT), and capacity (AOC) were detected by kits. The TL of the ASD group was shorter than the TD group (p < 0.01) and had some accurate predictive significance for the identification of ASD (AUC = 0.632, 95% CI: 0.533-0.710, p = 0.002). Both 8-OHdG content and SOD activity in the ASD group were significantly higher than those in the TD group (p < 0.05). Shortened TL (Monofactor: 2.20 (1.22, 3.96), p = 0.009; Multifactor: 2.22 (1.22, 4.00), p = 0.008) and reduced CAT activity (Monofactor: 2.31 (1.28, 4.17), p = 0.006; Multifactor: 2.31 (1.28, 4.18), p = 0.006) are risk factors for the development of ASD, while reduced 8-OHdG content (Monofactor: 0.29 (0.14, 0.60), p = 0.001; Multifactor: 0.27 (0.13, 0.57), p = 0.001) and reduced SOD activity (Monofactor: 0.55 (0.31, 0.98), p = 0.042; Multifactor: 0.54 (0.30, 0.98), p = 0.042) are protective factors for the development of ASD. In this study, TL and OS were significantly different between the ASD group and the TD group. As guanine-rich telomere sequences were likely damaged by oxygen free radicals, creating OS, which is a factor in the incidence and progression of ASDs. In conclusion, oxidative damage occurs in the bodies of children with ASD, which may lead to sustained disease progression and severe clinical manifestations. We assume that timely supplementation of antioxidants is very likely to be a potential treatment for early intervention in children with ASD. Identification and detection of OS-related biomarkers may contribute to early diagnosis and timely interventions in young patients with ASD.

Alpha-lipoic acid modulates the diabetes mellitus-mediated neuropathic pain via inhibition of the TRPV1 channel, apoptosis, and oxidative stress in rats.

Diabetes mellitus (DM) is a chronic syndrome involving neuropathic pain. Increased oxidative stress in DM is assumed to increase free reactive oxygen radicals (ROS) and causes diabetic damage. The sciatic nerve (ScN) and dorsal root ganglion (DRG) both contain high levels of the TRPV1 channel, which is triggered by capsaicin and ROSs and results in increased Ca2+ entry into the neurons. Alpha-lipoic acid (ALA) is considered an important part of the antioxidant system. To better characterize the protective effects of ALA on the DM-induced neuronal through TRPV1 modulation, we investigated the role of ALA on DM-induced neuropathic pain, oxidative ScN, and DRG damage in diabetic rats. Forty adult Wistar albino female rats were divided into four groups as control, ALA (50mg/kg for 14 days), streptozotocin (STZ and 45mg/kg and single dose), and STZ + ALA. Rats were used for the pain tests. After obtaining the DRGs and ScN, they were used for plate reader, patch-clamp, and laser confocal microscope analyses. We observed the modulator role of ALA on the thresholds of mechanical withdrawal pain (von Frey test) and hot sensitivity pain (hot plate test) in the STZ + ALA group. The treatment of ALA decreased STZ-induced increase of TRPV1 current densities, intracellular free Ca2+ concentrations (Fura-2 and Fluo - 3/AM), ROS, caspase 3, caspase 9, mitochondrial membrane potential, and apoptosis values in the ScN and DRG neurons, although its treatment induced the increase of cell viability and body weight gain. The treatment of ALA acted a neuroprotective role on the TRPV1 channel stimulation-mediated Ca2+ influx, neuropathic pain, and neuronal damage in diabetic rats. The neuroprotective role of ALA treatment can be explained by its modulating the TRPV1 channel activity, intracellular Ca2+ increase-induced oxidative stress, and apoptosis.

Erb‐(IL10)2 ameliorates radiation‐induced skin injury through eliminate oxygen free radicals

AbstractObjectiveRadiation‐induced skin injury (RISI) remains a serious concern during radiotherapy. IL‐10 is considered as an immune suppressive cytokine by inhibiting the secretion of the proinflammatory cytokines in cells. The aim of this study was to evaluate the protective role of Erb (IL10) 2 against ionizing radiation.MethodsWe fused Interleukin 10 (IL‐10) dimer onto an anti‐epidermal growth factor receptor antibody Cetuximab (Erbitux) to form a new bispecific protein Erb‐(IL10)2. The protective effect and biological activity of Erb‐(IL10)2 was measured in model of RISI.ResultsUnder the condition of 20 Gy irradiation, surviving cells in the IR group decreased significantly compared with the non‐IR group (p = 0.0021). The survival rates of HaCaT (p = 0.0038) and WS1 (p = 0.0003) cells were significantly increased after IL‐10 treatment. The apoptosis rates of HaCaT (p = 0.0048) and WS1 (p = 0.0074) cells in the IL‐10 group were significantly lower compared to the NC group. Under 20 Gy irradiation conditions, IL‐10 fusion protein reduced the level of reactive oxygen in HaCaT (p = 0.0046) and WS1 (p&lt;0.0001) cells compared to the control group. Relatively normal granular mitochondrial morphology was observed in the IL‐10 group after 20 Gy X‐ray irradiation compared with the NC group. Ater 35 Gy electron radiation, the levels of reactive oxygen species in the skin tissue of C57/B6 mice injected with IL‐10 fusion protein were significantly lower than those in the PBS group (p = 0.001). Compared with the PBS group and the other IL‐10 groups, the group treated with 0.2 mg/kg IL‐10 showed a significant decrease in MDA level (p = 0.0024). Compared with the PBS group, the thickness of the stratum corneum in groups treated with 0.05, 0.1 and 0.2 mg/kg IL‐10 decreased, and the skin appendages were well‐preserved. In the group treated with 0.2 mg/kg IL‐10, the skin tissue structure was still relatively intact, and the masson staining area was smaller than that of the PBS group.ConclusionIL‐10 plays a role in inhibiting radioactive fibrosis in radioactive skin injury. IL‐10 has a protective effect on skin cell damage after ionizing radiation irradiation both in vitro and in vivo. Moreover, IL‐10 plays a role in inhibiting radioactive fibrosis in radioactive skin injury.

Mechanisms Suggesting a Relationship between Vitamin D and Erectile Dysfunction: An Overview

Vitamin D deficiency (VDD) and erectile dysfunction (ED) heavily burden the male population. The higher prevalence of both conditions in the elderly suggests a possible relationship between the two conditions. In addition, in vitro, animal, and human studies have revealed several mechanisms that may relate VDD to ED. The main mechanism by which vitamin D might exert its action on sexual function appears to be through the regulation of endothelial function. Indeed, VDD correlates with several markers of endothelial function. The action of vitamin D on the endothelium would be exercised both indirectly through its intervention in inflammatory processes and through the production of oxygen free radicals, and directly through the regulation of vascular stiffness, the production of nitric oxide, and the regulation of vessel permeability. Furthermore, the ubiquitous distribution of the vitamin D receptor in the human body means that this hormone can also exert a beneficial effect on erectile function by interfering with those comorbidities significantly associated with ED, such as hypertension, diabetes mellitus, hypercholesterolemia, chronic kidney disease, and hypogonadism. In this review, we thoroughly and carefully presented the evidence and mechanisms that would appear to relate vitamin D levels to erectile function. Furthermore, we have summarized the meta-analytic evidence for and against this association to provide a true representation of this topic. Data published to date suggest that low levels of vitamin D could contribute to worsening erectile function through several mechanisms. Therefore, vitamin D levels should be measured in patients with ED and maintained at adequate levels by specific supplementation in case of deficiency. However, the low quality and heterogeneity of clinical trials evaluating the effects of vitamin D administration on erectile function and ED-associated comorbidities do not allow for a univocal conclusion, and indicate the need for further studies to analyze these aspects.

Whether Carotenoids and Quercetin Affect the Proliferation andExpression of PPARγ Protein in Leukemia K562 Cells

Carotenoids are some of the most abundant pigments in nature, ranging from yellow to red. Carotenoids can divide intotwo categories: carotenoids composed of hydrocarbon elements and lutein-containing oxygen elements. They are lipidsoluble pigments, and some contain carbonyl or enol groups, which are water-soluble. Carotenoids absorb visible lightfrom 400 nm to 600 nm, while special ones such as octa-hydro lycopene and hexahydrolycopene only absorb ultravioletlight. Quercetin is a flavonoid compound widely found in fruits and vegetables. Its chemical structure phenolic hydroxylgroup is the basis of antioxidant action, which can be used for hydrogen to quench oxygen free radicals. It is oxidizedto form a highly stable catechol structure. It has a variety of biological activities and pharmacological effects, such asexpanding coronary blood vessels and inhibiting tumor cell proliferation. This paper shows that the K562 cell growthrate in carotenoids and quercetin treatment groups was slower than the control group.

TO STUDY IN-HOSPITAL MORTALITY OF ALUMINIUM PHOSPHIDE POISONING IN RELATION TO TOTAL LEUCOCYTE COUNT

Background: Pesticide poisoning is a major problem worldwide. The incidence of aluminium phosphide poisoning has increased over decades. Phosphine, active form, binds cytochrome oxidase, induces oxidative stress with release of free oxygen radicals, lipid peroxidation, resulting acute inflammation leads to alteration of various haematological/biochemical parameters, including total leucocyte count (TLC). Objectives: 1.To study TLC in aluminium phosphide poisoning 2.To study severity of toxicity in relation to TLC 3.To study in-hospital mortality in relation to TLC Methods: A hospital based cross sectional study with sample size of 65. In-patients with aluminium phosphide poisoning attending Medicine Department in KR Hospital, Mysuru were studied. The parameters like complete hemogram including TLC, liver/renal function tests, electrolytes, electrocardiogram were assessed and correlated. With a confidence interval of 95%, level of significance was kept at 5% Results: Of the 65 subjects, mean age was 34.11 ±11.55 years and mean TLC was 10467.5 ±2991.2 . Subjects were categorised into non-severe(29%), severe(26%) and death(45%) groups. Mean TLC in non severe(8140.7±2445.9), severe(10980.3± 2471.1) and death(11691.4 ±2780.4). A high TLC was found in 15.8% non-severe, 41.2% severe and 69% death cases. A significant positive correlation of TLC with severity of toxicity and mortality of aluminium phosphide poisoning was obtained (p&lt;0.005). Conclusion: Total leucocyte count can be used as one of the easily available cost effective predictive variable to assess the outcome of aluminium phosphide poisoning.

Transcription Factor VvDREB2A from Vitis vinifera Improves Cold Tolerance.

Low temperatures restrict the growth of the grapevine industry. The DREB transcription factors are involved in the abiotic stress response. Here, we isolated the VvDREB2A gene from Vitis vinifera cultivar 'Zuoyouhong' tissue culture seedlings. The full-length VvDREB2A cDNA was 1068 bp, encoding 355 amino acids, which contained an AP2 conserved domain belonging to the AP2 family. Using transient expression in leaves of tobacco, VvDREB2A was localized to the nucleus, and it potentiated transcriptional activity in yeasts. Expression analysis revealed that VvDREB2A was expressed in various grapevine tissues, with the highest expression in leaves. VvDREB2A was induced by cold and the stress-signaling molecules H2S, nitric oxide, and abscisic acid. Furthermore, VvDREB2A-overexpressing Arabidopsis was generated to analyze its function. Under cold stress, the Arabidopsis overexpressing lines exhibited better growth and higher survival rates than the wild type. The content of oxygen free radicals, hydrogen peroxide, and malondialdehyde decreased, and antioxidant enzyme activities were enhanced. The content of raffinose family oligosaccharides (RFO) also increased in the VvDREB2A-overexpressing lines. Moreover, the expression of cold stress-related genes (COR15A, COR27, COR6.6, and RD29A) was also enhanced. Taken together, as a transcription factor, VvDREB2A improves plants resistance to cold stress by scavenging reactive oxygen species, increasing the RFO amount, and inducing cold stress-related gene expression levels.

Therapeutic potential of flavonoids in the management of obesity-induced Alzheimer's disease: an overview of preclinical and clinical studies.

Obesity is a global epidemic that affects people of all ages, genders, and backgrounds. It can lead to a plethora of disorders, including diabetes mellitus, renal dysfunction, musculoskeletal problems, metabolic syndrome, cardiovascular, and neurodegenerative abnormalities. Obesity has also been linked to neurological diseases such as cognitive decline, dementia, and Alzheimer's disease (AD), caused by oxidative stress, pro-inflammatory cytokines, and the production of reactive oxygen free radicals (ROS). Secretion of insulin hormone is impaired in obese people, leading to hyperglycaemia and increased accumulation of amyloid-β in the brain. Acetylcholine, a key neurotransmitter necessary for forming new neuronal connections in the brain, decreases in AD patients. To alleviate acetylcholine deficiency, researchers have proposed dietary interventions and adjuvant therapies that enhance the production of acetylcholine and assist in the management of AD patients. Such measures include dietary intervention with antioxidant and anti-inflammatory flavonoid-rich diets, which have been found to bind to tau receptors, reduce gliosis, and reduce neuroinflammatory markers in animal models. Furthermore, flavonoids like curcumin, resveratrol, epigallocatechin-3-gallate, morin, delphinidins, quercetin, luteolin, and oleocanthal have shown to cause significant reductions in interleukin-1β, increase BDNF levels, stimulate hippocampal neurogenesis and synapse formation, and ultimately prevent the loss of neurons in the brain. Thus, flavonoid-rich nutraceuticals can be a potential cost-effective therapeutic option for treating obesity-induced AD, but further well-designed, randomized, and placebo-controlled clinical studies are needed to assess their optimal dosages, efficacy, and long-term safety of flavonoids in humans. The main objectives of this review are to underscore the therapeutic potential of different nutraceuticals containing flavonoids that can be added in the daily diet of AD patients to enhance acetylcholine and reduce neuronal inflammation in the brain.

An insight into hypothesized biological mechanisms contributing to the Flash effect

In recent years, FLASH radiotherapy (FLASH RT) has gained attention in preclinical studies as a potential advancement in cancer treatment. The great advantage of FLASH RT is the ultra-fast, high doses delivery that have a similar or greater effect on cancer cells while sparing normal, healthy tissue surrounding the tumor site. This is known as the FLASH effect. However, currently, there are not enough in vitro and in vivo data to transpose FLASH RT to human trials. This mini review summarizes the available in vitro data on electron beam FLASH, focusing on possible mechanisms of the FLASH effect. Current studies have focused on various types of cancer, including lung cancer, glioblastoma, uterus adenocarcinoma, cervix carcinoma, prostate carcinoma, melanoma, breast cancer, head and neck squamous cell carcinoma, and colon adenocarcinoma. Several hypotheses have been proposed to explain the biological mechanisms contributing to the to the selective FLASH effect, including differences between healthy and cancer cells in production of reactive oxygen species and free radicals, limitation of Fenton reaction caused by high Fe2+/3+ levels in tumor cells, and impaired DNA damage repair mechanisms occurring in cancer.

Molecular mechanisms of effects of ionizing radiation action. Irradiation effect on protein (literary review)

Target effects (direct and indirect effects of ionizing radiation). When exposed to ionizing radiation, it damages vital intracellular biomolecules which leads to multiple damage to cells and tissues as well as pathophysiological diseases such as inflammation, immunosuppression, etc. Such damage can be caused by direct ionization of biomolecules, but in almost 70% of cases due to indirect radiolysis of intracellular water with the formation of reactive oxygen species and free radicals, which ultimately causes oxidative stress.Non-target effects (abscopal effect, adaptive response, bystander effect, genomic instability). Over the past 25 years, many studies have explored the molecular mechanisms underlying in nontargeted effects (also known as effects not aimed at DNA). It is shown that these effects are the result of a huge dynamic and complex process induced in irradiated cells, transmitted to neighboring cells and, to some extent, to the whole body through activation of the immune system.The irradiation effect on protein. Under the direct action of ionizing radiation on a protein, an electron is knocked out of it, resulting in a defective site devoid of an electron, which migrates along the polypeptide chain due to the transfer of electrons until it reaches a site with increased electron-donor properties. At this point, free radicals arise in the side chains of amino acids. Under the indirect effect of ionizing radiation, the formation of free radicals occurs when protein molecules interact with the products of water radiolysis.

Zn2 SiO4 Bioceramic Attenuates Cardiac Remodeling after Myocardial Infarction.

In the pursuit of therapeutic strategies for myocardial infarction (MI), a pivotal objective lies in the concurrent restoration of blood perfusion and reduction of cardiomyocyte apoptosis. However, achieving these dual goals simultaneously presents a considerable challenge. In this study, a Zn2 SiO4 bioceramic capable of concurrently sustaining the release of bioactive SiO3 2- and Zn2+ ions, which exhibit a synergistic impact on endothelial cell angiogenesis promotion, cardiomyocyte apoptosis inhibition, and myocardial mitochondrial protection against oxygen-free radical (reactive oxygen species) induced injury is developed. Furthermore, in vivo outcomes from a murine MI model demonstrate that either systemic administration via tail vein injection of Zn2 SiO4 extract or local application through intramyocardial injection of a Zn2 SiO4 composite hydrogel promotes cardiac function and reduces cardiac fibrosis, thus aiding myocardial repair. This research is the first to elucidate the advantageous effects of dual bioactive ions in myocardial protection and may offer a novel therapeutic avenue for ischemic heart disease based on meticulously engineered bioceramics.

Dexmedetomidine enables copper homeostasis in cerebral ischemia/reperfusion via ferredoxin 1

Excessive oxygen free radicals and toxic substances are generated in cerebral ischemia-reperfusion (I/R) process. Dexmedetomidine (DEX), a common anesthetic and sedative drug, can considerably boost glutathione (GSH), which has anti-copper influx effects. Focusing on cuproptosis, the mechanism of DEX in the I/R was revealed. Using the I/R rat model, the effects of DEX and the copper chelator D-penicillamine on cerebral infarct volume, copper levels, mitochondrial respiration and membrane potential, GSH content, and enrichment of cuproptosis functional proteins were examined. The involvement of ferredoxin 1 (FDX1) in the DEX regulatory pathway was verified by overexpressing FDX1 in vitro. DEX could significantly reduce cerebral infarction in rats, reduce copper levels, maintain mitochondrial functions, increase GSH, and reduce the content of key proteins related to cuproptosis. These aspects were replicated in vitro and revealed that FDX1 overexpression partially reversed the impacts of DEX. Together, cuproptosis occurs in the brain I/R process and DEX can enhance cell survival by blocking the primary pathway mediated by FDX1. KEY MESSAGES Dexmedetomidine reduces cerebral infarction in the I/R rat models. Dexmedetomidine reduces cuproptosis in the I/R rat models. FDX1, an upstream of protein fatty acylation, mediates regulation of Dexmedetomidine.

Imatinib-Functionalized Galactose Hydrogels Loaded with Nanohydroxyapatite as a Drug Delivery System for Osteosarcoma: In Vitro Studies.

This study reports an impact of structure (XRPD, FT-IR) and surface morphology (SEM-EDS) of imatinib-functionalized galactose hydrogels, loaded and unloaded with nHAp, on osteosarcoma cell (Saos-2 and U-2OS) viability, levels of free oxygen radicals, and nitric oxide, levels of BCL-2, p53, and caspase 3 and 9, as well as glycoprotein-P activity. It was investigated how the rough surface of the crystalline hydroxyapatite-modified hydrogel affected amorphous imatinib (IM) release. The imatinib drug effect on cell cultures has been demonstrated in different forms of administration-directly to the culture or the hydrogels. Administration of IM and hydrogel composites could be expected to reduce the risk of multidrug resistance development by inhibiting Pgp.