Free Radical Production Research Articles

Quantum Sensing for Detection of Zinc‐Triggered Free Radicals in Endothelial Cells

AbstractOxidative stress originating from the overproduction of free radicals poses a major threat to cell fate, therefore it is of great importance to address the formation of free radicals in cells subjected to various pathological stimuli. Here we investigate the free radical response of endothelial cells to biodegradable zinc. In addition to the standard free radical assays, relaxometry was used for determining the production of free radicals in cells exposed to non‐physiological concentrations of zinc ions. The cellular morphology, intracellular zinc accumulation, as well as the levels of reactive oxygen/nitrogen species, are determined using standard fluorescent methods. For endothelial cells subjected to 50% zinc extracts, deviations from the normal cell shape and cell agglomeration tendency are observed. The culture medium containing the highest amount of zinc ions caused nuclei fragmentation, blebbing, and cell shrinkage, indicating cell death. A potential explanation for the observed phenomena is an overproduction of free radicals. In the case of 1% and 10% zinc extracts, the formation of free radicals is clearly confirmed by relaxometry, while the results obtained by using fluorescent techniques are unambiguous. It is revealed that high concentrations of zinc ions released from biodegradable samples induce a deleterious effect on endothelial cells.

The Role of Captopril on Pentylenetetrazole-Induced Seizures in Rats

ABSTRACT: 
 Purpose: In recent years, experimental studies have shown that some angiotensin-converting enzyme (ACE) inhibitors with antihypertensive effects have anticonvulsant effects against seizures. After the seizure, the process of inflammation begins in the brain and body, with the production of free radicals. Renin has some effects on the central nervous system of the angiotensin system. The current study's objective was to examine how captopril, an ACE inhibitor, affects neuroinflammation in the hippocampus and cortical areas in acute epileptic seizures and post-seizures induced by pentylenetetrazole (PTZ).
 Material and Methods: Eighteen Wistar Albino rats were separated into three groups: control, PTZ (serum physiologic 1 ml/kg as solvent), and captopril (50 mg/kg/day for 7days). To produce epileptic seizures, PTZ (45 mg/kg) was delivered thirty minutes after the drug was administered. The animals were monitored during 30 minutes to record seizures scoring scale and the onset time of first myoclonic jerk (FMJ). In the brain tissue, the activity of TNF- α, IL-1 β, NF-kB, COX-1, and COX-2 were examined.
 Results: Captopril increased FMJ onset time and reduced seizure stage as compared to the PTZ group (p

Abstract 011: Cluster Of Differentiation 14 (CD14) Inhibits NADPH Oxidase 2 (NOX2)-Derived Oxidative Stress In Hematopoietic Cells And Modulates Dahl Salt-Sensitive Hypertension And Renal Damage

We recently discovered that genetic deletion of CD14 in Dahl SS rats (CD14-/-) amplifies the development of salt-sensitive hypertension and renal damage in females. Interestingly, the expression of CD14 in leukocytes and the level of plasma CD14 protein are increased in cardiovascular disease and hypertension in humans. An examination of macrophages from CD14-/- females revealed enhanced production of superoxide from NOX2 compared to Dahl SS. Furthermore, a double knockout Dahl SS strain lacking both CD14 and functional NOX2 (DKO) exhibits significantly reduced salt-induced hypertension and associated renal damage, indicating that free radical production from NOX2 is likely mediating the amplification of disease following CD14 deletion. The present study examined the specific effects of CD14 and NOX2 deletion in hematopoietic cells via a total body irradiation/bone marrow transfer (TBI/BMT) approach. Female Dahl SS recipients were irradiated (11Gy) then received either CD14 or DKO bone marrow transplantation via tail vein injection. Rats that received DKO hematopoietic cells had blunted mean arterial pressure (147±4 mmHg, n=3, p=0.052) versus those that received CD14-/- (179±19mmHg, n=3) in response to a 3-week high salt challenge (HS, 4.0% NaCl, AIN-76A). As an index of renal damage, albuminuria was significantly reduced in the DKO (110.3±7 mg/day, n=3, p<0.01) compared to the CD14-/- (280.9±42 mg/day, n=3) at HS day 21. Flow cytometric analysis of isolated renal immune cells indicated a reduction in renal inflammation in the DKO compared to the CD14-/-. There were fewer CD45+ total leukocytes (2.8x10 6 vs 3.8x10 6 cells/kidney, p<0.05) and CD11b/c+ monocytes/macrophages (2.4x10 6 vs 3.3x10 6 cells/kidney, n=3, p<0.05) in DKO versus CD14-/- kidneys. Finally, to document the TBI/BMT, macrophages from CD14-/- rats produced 7-fold greater superoxide from NOX2 when stimulated with 12-phorbol myristate 13-acetate compared to DKO macrophages. Together, these data suggest a regulatory role of CD14 in hematopoietic cells to reduce oxidative stress from NOX2 in the kidney of female Dahl SS rats during salt-sensitive hypertension and associated renal disease.

Abstract P318: INDOLE-3 ACETIC ACID: A NOVEL DUAL-ACTION INHIBITOR OF THE ENDOTHELIN SYSTEM FOR TREATING HYPERTENSION

Elevated levels of endothelin-1 (ET-1) stimulate potent vasoconstriction, free radical production, oxidative stress, and vascular inflammation, which are often present in salt-sensitive hypertension, pulmonary hypertension, drug-resistant hypertension, and hypertension among African Americans. There is currently no known drug that simultaneously targets both ET-1 receptors (ETRs) and the ET-1 synthesizing enzyme ECE-1, even though dual targeting of the ET system could lead to a new generation of drug molecules with improved therapeutic outcome. Using an integrated in vitro, in vivo and in silico approaches, here we report the discovery of indole-3 acetic acid (IAA) as an inhibitor of both ET-1 receptors and ECE-1. IAA is produced in the human body via tryptophan metabolism by gut microbiota. Our data demonstrates that IAA concentration-dependently inhibits ET-1-evoked vasoconstriction in rat resistance mesenteric arteries and ET-1-stimulated reactive oxygen species (ROS) production in smooth muscle cells (SMCs). Furthermore, IAA suppresses ET-1-induced endothelial cell (EC) activation, adhesion molecule overexpression, and leukocyte adhesion. IAA inhibits ET-1-stimulated, ET A R- and ET B R-mediated increases in [Ca 2+ ] i . Intriguingly, IAA produces a concentration-dependent inhibition of purified human ECE-1. Treatment of Dahl salt-sensitive (DSS) hypertensive rats, a model of augmented ET-1 signaling, with an oral extended-release formulation of IAA significantly inhibits blood pressure elevation in high-salt diet-fed (HSD) DSS rats. IAA-treated DSS arteries show intact acetylcholine- and sodium nitroprusside-induced vasodilation, suggesting that IAA preserves endothelial and smooth muscle function, respectively. IAA treatment also prevents arterial remodeling, oxidative stress, and kidney dysfunction in HSD DSS rats. Overall, our study identifies IAA as the first-in-class dual-action inhibitor of ETRs and ECE-1, which produces profound antihypertensive effect in vivo. IAA could also be therapeutically useful for other cardiovascular diseases in which ET-1 signaling is implicated.

Radiation-Chemical Transformations of Ethylene Glycol and Its Deuterated Derivative in Deaerated Aqueous Solutions

This study is devoted to the effect of complete deuteration of the ethylene glycol carbon skeleton on the formation of its radiation-induced free-radical transformations products in deaerated aqueous solutions at pH 7.00 ± 0.10 and a dose rate of 0.064 ± 0.002 Gy/s. It has been established that the chain process of fragmentation of carbon-centered ethylene glycol radicals (∙CH(OH)CH2OH) plays an important role in the formation of acetaldehyde. The replacement of protium atoms located at carbon atoms by deuterium decreased the radiation-chemical yield of acetaldehyde in aqueous 1 M solutions of diols by a factor of 8. The results of this study indicate that the use of deuterium exchange at the carbon skeleton of organic molecules is a promising way for increasing their resistance to radiation-induced free radical fragmentation processes.

Effects of structural characteristics of phenolic compounds on oxidation of glycerol trioleate: Action rule and mechanism

Effects of structural characteristics of phenolic compounds on the oxidation of glycerol trioleate were investigated, and the action rule and mechanism were further explored. By using thermal and multispectral analyses, all tested phenolic compounds significantly inhibited the oxidation of glycerol trioleate, and reduced the decomposition of CC and ester bonds of glycerol trioleate, which were attributed to their capability to inhibit the production of free radicals. Quercetin and gallic acid were the most effective among the condensed and hydrolyzable phenolic compounds in present study, respectively. For condensed phenolic compounds, the hydroxyl groups in B ring, substitution in C ring, and the structure of C ring played a crucial role in their inhibitory action. For hydrolyzable phenolic compounds, the amount of hydroxyl groups and their molecular weight had obvious effects on their inhibitory action. According to the measurement of molecular electrostatic potential and frontier molecular orbitals by density functional theory, the large maximum electrostatic potential and the small energy gap value were beneficial to enhance the inhibitory capability of phenolic compounds on the oxidation of glycerol trioleate. All present results suggested the potential action rule and molecular mechanism about the inhibitory effects of phenolic compounds on the oxidation of glycerol trioleate.

Improvement of spermatozoa concentration due to maximal exercise with Vitis gracilis Wall.

Context: Swimming is a common form of exercise; however, excessive exercise might reduce sperm count by lowering testosterone levels and increasing the production of free radicals, commonly known as reactive oxygen species (ROS). In Indonesia, Vitis gracilis Wall. is a traditional remedy for increasing stamina. Aims: To assess the concentration of spermatozoa after vigorous physical activity and V. gracilis administration, as well as the histological and apoptotic changes in testicular histology that occur via caspase-3 expression. Methods: This study was conducted on six groups of rats: the control group (G+), a group of rats subjected to vigorous swimming then administered 0.2 mg/kg BW vit C (GVitC), and three groups of rats subjected to vigorous swimming then administered 100, 125, or 150 mg/kg BW V. gracilis (G100, G125, and G150). Testicular tissue and blood serum samples were extracted from the rats subjected to vigorous swimming. Testicular tissue was immunohistochemically stained using caspase-3 antibody and TUNEL assays, while blood samples were analysed using ELISA. Results: V. gracilis administration significantly affected IL-6 and testosterone levels (p<0.00). Testosterone had a greater impact on spermatozoa concentration than IL-6. Caspase-3 expression and the proportion of apoptotic cells were both markedly reduced. Conclusions: Administering 125 mg/kg BW V. gracilis can help to increase sperm concentration by reducing apoptosis through altering caspase-3 and IL-6 levels, thereby preventing inflammation. This plant might be a viable molecular therapeutic target for staminal medicines.

Mechanism of Bimodal Effect of DL-Butyonine Sulfoximine of Constitutive Androstane and Pregnane X Receptors <i>in vitro</i>

The constitutive androstane receptor (CAR) and the pregnan X receptor (PXR) are nuclear receptors that are involved in the regulation of gene transcription of enzymes responsible for biotransformation and excretion of endo- and xenobiotics. The aim of the study was to study the effect of DL-butyonine sulfoximine (BSO, gamma-glutamylcysteine synthetase inhibitor) on the relative amount of CAR and PXR in Caco-2 cells and to evaluate its mechanisms. BSO was used in concentrations of 1‒500 μM and exposure duration of 24 and 72 h. The generation of reactive oxygen species (ROS) was determined using MitoTracker Red CM-H2 XRos fluorescent probes. Cytotoxicity was analyzed according to the results of the MTT test. The relative amount of CAR and PXR was estimated by the Western blot method. It was shown that BSO caused an increase in the formation of ROS at exposure duration of 24 h at concentrations of 10, 50 and 100 μM, at 72 h – at concentrations of 50, 100 μM. At the same time, at a concentration of 500 μM, BSO reduced the viability of cells during all periods of exposure. The relative amount of CAR increased at BSO concentrations of 50, 100 μM and exposure duration of 24 hours and 10, 50 μM at exposure of 72 h, and PXR – at concentrations of 100 and 500 μM and incubation of 24 h and 50, 100, 500 μM and incubation of 72 h. When used together with BSO, glutathione, the synthesis of which it blocks, it was found that at exposure time of 24 h and BSO concentrations of 50 μM and 72 h and concentrations of 10 and 50 μM, CAR induction was suppressed, and at 50 and 100 μM and exposure time of 72 h – PXR. The introduction of glutathione into the nutrient medium with BSO had no effect on PXR at xenobiotic concentrations of 100 and 500 μM (24 h) and 500 μM (72 h), on CAR – at concentrations of 100 μM (24 h) and 50 and 100 μM (72 h). Thus, BSO can induce CAR and PXR both by increasing the production of free radicals and the development of oxidative stress, and independently as a xenobiotic.

Antioxidant and antiaging activities of Cinnamomum burmannii, Michelia champaca and their combinations.

Aging is a natural skin process that occurs due to intrinsic and extrinsic factors, such as excessive exposure to ultraviolet light (photoaging). The mechanism of damage involves the production of excess free radicals that trigger oxidative stress in the skin. Determining the natural products that have high antioxidant activities as antiaging is important. Cinnamomum burmannii and Michelia champaca are typical Aceh plants that are believed to have high antioxidant effects. The aim of this study was to determining the contents of C. burmannii and M. champaca as well as to determine the antioxidant and antiaging activities of either individually or combinations. The qualitative phytochemical and semi-quantitative analysis of the extracts were measured using gas chromatography-mass spectroscopy (GC-MS). The antioxidant activity was examined by radical scavenging using the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical method while the antiaging activity was measured using the tyrosinase enzyme inhibition test. The phenolic and flavonoid contents of C. burmannii were higher than M. champaca (66.34 vs 24.71 mg gallic acid equivalent/gr and 80.52 vs 60.20 mg quercetin equivalent/gr, respectively. The inhibitory concentration (IC50) of M. champaca extract in inhibiting DPPH indicated that M. champaca had a better antioxidant activity than C. burmannii. The combination of C. burmannii and M. champaca extracts had a lower IC50 compared to M. champaca alone. C. burmannii and M. champaca extracts had a weak potential to inhibit tyrosinase activity (IC50 value ≥1000 μg/mL). In conclusion, this study indicates that M. champaca and C. burmannii have strong antioxidant activities and these might associate with polyphenol contents.

Is there a correlation between antibiotic use and the severity or post-infection conditions of COVID-19 and other viral infections?

Antibiotics are one of the most frequently prescribed medications in modern medicine; besides treating bacterial infections, they may often be utilized for prophylactic purposes, including during select viral infections. It has been shown that 74.9% of COVID-19 patients received antibiotics as a part of their treatment regimen during the pandemic. However, studies suggest that the actual incidence of bacterial coinfection was relatively uncommon with a mere 3.5% of overall cases reported. A recent study revealed that antibiotic administration would not improve disease progression or shorten the length of hospitalization in COVID-19 patients; additionally, some antibiotics, such as linezolid, promote the production of free radicals that might be responsible for exacerbated clinical symptoms during and post-infection. Notably, antibiotic use disturbs the normal gut microbiome, and this interference impedes antiviral immune response enhancing severity and susceptibility to a list of viral infections. Thus, resultant augmented severity of these infections may be a consequence of higher susceptibility to respiratory viral co-infection.

Activation of peroxymonosulphate using a highly efficient and stable ZnFe2O4 catalyst for tetracycline degradation

Tetracycline (TC) is a widely used antibiotic that adversely affects ecosystems and, therefore, must be removed from the environment. Owing to their strong ability to oxidise pollutants, including antibiotics, and selectivity for these pollutants, an improved oxidation method based on sulphate radicals (SO4·−) has gained considerable interest. In this study, a novel technique for removing TC was developed by activating peroxymonosulphate (PMS) using a ZnFe2O4 catalyst. Using the co-precipitation method, a ZnFe2O4 catalyst was prepared by doping zinc into iron-based materials, which increased the redox cycle, while PMS was active and facilitated the production of free radicals. According to electron paramagnetic resonance spectroscopy results, a ZnFe2O4 catalyst may activate PMS and generate SO4·−, HO·, O2·−, and 1O2 to eliminate TC. This research offers a new method for creating highly effective heterogeneous catalysts that can activate PMS and destroy antibiotics. The study proposes the following degradation pathways: hydroxylation and ring-opening of TC based on the products identified using ultra-performance liquid chromatography-mass spectrometry. These results illustrated that the prepared ZnFe2O4 catalyst effectively removed TC and exhibited excellent catalytic performance.

Identification and functional prediction of long non-coding RNAs related to oxidative stress in the jejunum of piglets.

Oxidative stress (OS) is a pathological process arising from the excessive production of free radicals in the body. It has the potential to alter animal gene expression and cause damage to the jejunum. However, there have been few reports of changes in the expression of long noncoding RNAs (lncRNAs) in the jejunum in piglets under OS. The purpose of this research was to examine how lncRNAs in piglet jejunum change under OS. The abdominal cavities of piglets were injected with diquat (DQ) to produce OS. Raw reads were downloaded from the SRA database. RNA-seq was utilized to study the expression of lncRNAs in piglets under OS. Additionally, six randomly selected lncRNAs were verified using quantitative real-time polymerase chain reaction (qRT‒PCR) to examine the mechanism of oxidative damage. A total of 79 lncRNAs were differentially expressed (DE) in the treatment group compared to the negative control group. The target genes of DE lncRNAs were enriched in gene ontology (GO) terms and Kyoto encyclopedia of genes and genomes (KEGG) signaling pathways. Chemical carcinogenesis-reactive oxygen species, the Foxo signaling pathway, colorectal cancer, and the AMPK signaling pathway were all linked to OS. Our results demonstrated that DQ-induced OS causes differential expression of lncRNAs, laying the groundwork for future research into the processes involved in the jejunum's response to OS.

The Impact of Heavy Elements on Public Health

Although many heavy metals have bio-toxic effects on human biochemistry, some of them have bio-importance as trace elements. The most frequent heavy metals to cause human poisonings are arsenic, mercury, lead, chromium, cadmium, and iron. Their wide distribution in the environment and detrimental effects on people are the results of their numerous industrial, domestic, agricultural, medical, and technological applications. These metals' carcinogenicity has been attributed to defects in DNA repair following the induction of oxidative stress and DNA damage by these metals. Metal toxicity is dependent on the dose ingested, the route of exposure, and the duration of the exposure, and it can cause a variety of disorders as well as excessive damage from oxidative stress brought on by the production of free radicals. In this review, their manufacturing and use, potential for human exposure, and molecular mechanisms of toxicity are all examined. The purpose of this article review is to discuss the effects that specific heavy metals may have on human health. Keywords: heavy metals, occurrence, uses, potential effect, toxicity mechanism

The pentose phosphate pathway in health and disease.

The pentose phosphate pathway (PPP) is a glucose-oxidizing pathway that runs in parallel to upper glycolysis to produce ribose 5-phosphate and nicotinamide adenine dinucleotide phosphate (NADPH). Ribose 5-phosphate is used for nucleotide synthesis, while NADPH is involved in redox homoeostasis as well as in promoting biosynthetic processes, such as the synthesis of tetrahydrofolate, deoxyribonucleotides, proline, fatty acids and cholesterol. Through NADPH, the PPP plays a critical role in suppressing oxidative stress, including in certain cancers, in which PPP inhibition may be therapeutically useful. Conversely, PPP-derived NADPH also supports purposeful cellular generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) for signalling and pathogen killing. Genetic deficiencies in the PPP occur relatively commonly in the committed pathway enzyme glucose-6-phosphate dehydrogenase (G6PD). G6PD deficiency typically manifests as haemolytic anaemia due to red cell oxidative damage but, in severe cases, also results in infections due to lack of leucocyte oxidative burst, highlighting the dual redox roles of the pathway in free radical production and detoxification. This Review discusses the PPP in mammals, covering its roles in biochemistry, physiology and disease.

Study of the Early Effects of Chitosan Nanoparticles with Glutathione in Rats with Osteoarthrosis.

Due to cartilage's limited capacity for regeneration, numerous studies have been conducted to find new drugs that modify osteoarthrosis's progression. Some evidence showed the capability of chitosan nanoparticles with glutathione (Np-GSH) to regulate the oxide-redox status in vitro in human chondrocytes. This work aimed to evaluate the capacity of Np-GSH in vivo, using Wistar rats with induced surgical osteoarthritis. Radiographic, biochemical (GSH and TBARS quantification), histopathological, and immunohistochemical (Col-2 and MMP-13) analyses were performed to evaluate the progress of the osteoarthritic lesions after the administration of a single dose of Np-GSH. According to the results obtained, the GSH contained in the NPs could be vectored to chondrocytes and used by the cell to modulate the oxidative state reduction, decreasing the production of ROS and free radicals induced by agents oxidizing xenobiotics, increasing GSH levels, as well as the activity of GPx, and decreasing lipid peroxidation. These results are significant since the synthesis of GSH develops exclusively in the cell cytoplasm, and its quantity under an oxidation-reduction imbalance may be defective. Therefore, the results allow us to consider these nanostructures as a helpful study tool to reduce the damage associated with oxidative stress in various diseases such as osteoarthritis.

Several dementia subtypes and mild cognitive impairment share brain reduction of neurotransmitter precursor amino acids, impaired energy metabolism, and lipid hyperoxidation.

Dementias and mild cognitive impairment (MCI) are associated with variously combined changes in the neurotransmitter system and signaling, from neurotransmitter synthesis to synaptic binding. The study tested the hypothesis that different dementia subtypes and MCI may share similar reductions of brain availability in amino acid precursors (AAPs) of neurotransmitter synthesis and concomitant similar impairment in energy production and increase of oxidative stress, i.e., two important metabolic alterations that impact neurotransmission. Sixty-five demented patients (Alzheimer's disease, AD, n = 44; frontotemporal disease, FTD, n = 13; vascular disease, VaD, n = 8), 10 subjects with MCI and 15 control subjects (CTRL) were recruited for this study. Cerebrospinal fluid (CSF) and plasma levels of AAPs, energy substrates (lactate, pyruvate), and an oxidative stress marker (malondialdehyde, MDA) were measured in all participants. Demented patients and subjects with MCI were similar for age, anthropometric parameters, biohumoral variables, insulin resistance (HOMA index model), and CSF neuropathology markers. Compared to age-matched CTRL, both demented patients and MCI subjects showed low CSF AAP tyrosine (precursor of dopamine and catecholamines), tryptophan (precursor of serotonin), methionine (precursor of acetylcholine) limited to AD and FTD, and phenylalanine (an essential amino acid largely used for protein synthesis) (p = 0.03 to <0.0001). No significant differences were found among dementia subtypes or between each dementia subtype and MCI subjects. In addition, demented patients and MCI subjects, compared to CTRL, had similar increases in CSF and plasma levels of pyruvate (CSF: p = 0.023 to <0.0001; plasma: p < 0.002 to <0.0001) and MDA (CSF: p < 0.035 to 0.002; plasma: p < 0.0001). Only in AD patients was the CSF level of lactate higher than in CTRL (p = 0.003). Lactate/pyruvate ratios were lower in all experimental groups than in CTRL. AD, FTD, and VaD dementia patients and MCI subjects may share similar deficits in AAPs, partly in energy substrates, and similar increases in oxidative stress. These metabolic alterations may be due to AAP overconsumption following high brain protein turnover (leading to phenylalanine reductions), altered mitochondrial structure and function, and an excess of free radical production. All these metabolic alterations may have a negative impact on synaptic plasticity and activity.

A Novel Therapeutic Formulation for the Improved Treatment of Indian Red Scorpion (Mesobuthus tamulus) Venom-Induced Toxicity-Tested in Caenorhabditis elegans and Rodent Models.

Indian Red Scorpion (Mesobuthus tamulus) stings are a neglected public health problem in tropical and sub-tropical countries, including India. The drawbacks of conventional therapies using commercial anti-scorpion antivenom (ASA) and α1-adrenoreceptor antagonists (AAA) have prompted us to search for an adequate formulation to improve treatment against M. tamulus stings. Novel therapeutic drug formulations (TDF) of low doses of commercial ASA, AAA, and ascorbic acid have remarkably improved in neutralising the in vivo toxic effects of M. tamulus venom (MTV) tested in Caenorhabditis elegans and Wistar strain albino rats in vivo models. The neutralisation of MTV-induced production of free radicals, alteration of the mitochondrial transmembrane potential, and upregulated expression of genes involved in apoptosis, detoxification, and stress response in C. elegans by TDF surpassed the same effect shown by individual components of the TDF. Further, TDF efficiently neutralized the MTV-induced increase in blood glucose level within 30 to 60 min post-treatment, organ tissue damage, necrosis, and pulmonary oedema in Wistar rats, indicating its clinical application for effecting treating M. tamulus envenomation. This study demonstrates for the first time that C. elegans can be a model organism for screening the neutralization potency of the drug molecules against a neurotoxic scorpion venom.

An economical pyrrhotite‐loaded sludge carbon composite effectively activated persulfate to sterilize Escherichia coli

AbstractBACKGROUNDPersulfate (PS) has the capability to yield free radicals via activators, thereby shaping an advanced oxidation process that can significantly contribute to effective sterilization. Central to this technology is the pursuit of appropriate activators.RESULTSIn our research, we successfully synthesized an economical and efficient PS activator, namely a pyrrhotite‐loaded sludge carbon (Pyr‐SC) composite. This was achieved via a straightforward procedure utilizing two environmentally friendly and cost‐efficient raw materials: pyrite and sludge. Pyr‐SC exhibited a specific surface area of 60.4 m2 g−1 and rich functional groups such as carbon–sulfur and sulfur–oxygen. The magnetic and graphitic carbon structures were formed at high temperatures during the preparation process, and the sludge carbon (SC) exhibited porous defects, which allowed the effective insertion of iron/sulfur into SC to form the stable Pyr‐SC structure. Pyr‐SC activated PS, which further sterilized Escherichia coli in the wastewater at a sterilization rate of 7.00 lg E. coli at 107 cfu mL−1 in 80 min. The sterilization rate was less affected by temperature and pH. We verified sulfate, hydroxyl and oxygen free radicals produced by the Pyr‐SC‐activated PS. The Pyr‐SC composite, thanks to its expedited electron transfer, could activate PS to engender free radicals. Furthermore, the oscillatory transformation of iron ions caused by the monosulfide ion on the Pyr‐SC surface augmented the production of free radicals. An assessment of Pyr‐SC's stability was conducted, adhering to the principles of magnetic separation. After five cycles in the Pyr‐SC/PS reaction system, the sterilization rate reached 3.29 lg, whereas the leaching rate of iron in Pyr‐SC decreased. The Pyr‐SC/PS reaction system also had a broad spectrum of wastewater.CONCLUSIONThe economically prepared Pyr‐SC composite provided an effective technology for activating PS and sterilizing microorganisms in wastewater. © 2023 Society of Chemical Industry.

Ozone Therapy in Medicine and Dentistry: A Review of the Literature.

Ozone has been successfully used in medicine for over 100 years due to its microbiological qualities. Its powerful oxidation impact, which results in the production of free radicals, and its ability to cause the direct death of nearly all microorganisms is the basis for its bactericide, virucide, and fungicide properties. Ozone also has a medicinal impact that speeds up blood flow and aids wound healing. Ozone may be applied as a gas or dissolved in water for medical purposes. Despite the benefits of using ozone therapeutically, concerns about its use in dentistry still exist. We aimed to provide a summary of the current uses of ozone in medicine and dentistry. An electronic search was performed for all English scientific papers published between 2012 and 2023 using PubMed, Cochrane, and Google Scholar search engines. Ozone, clinical applications, medicine, and dentistry were the search terms used. Seventy full-text articles describing the use of ozone therapy in medicine and dentistry were included in the present review. Ozone has shown several beneficial effects in the medical field. However, despite the encouraging in vitro evidence, the clinical use of ozone in dentistry has not yet been demonstrated as highly effective.

Phenylacetylglutamine and trimethylamine N-oxide: Two uremic players, different actions.

Chronic kidney disease (CKD) patients exhibit a heightened cardiovascular (CV) risk which may be partially explained by increased medial vascular calcification. Although gut-derived uremic toxin trimethylamine N-oxide (TMAO) is associated with calcium-phosphate deposition, studies investigating phenylacetylglutamine's (PAG) pro-calcifying potential are missing. The effect of TMAO and PAG in vascular calcification was investigated using 120 kidney failure patients undergoing living-donor kidney transplantation (LD-KTx), in an observational, cross-sectional manner. Uremic toxin concentrations were related to coronary artery calcification (CAC) score, epigastric artery calcification score, and markers of established non-traditional risk factors that constitute to the 'perfect storm' that drives early vascular aging in this patient population. Vascular smooth muscle cells were incubated with TMAO or PAG to determine their calcifying effects in vitro and analyse associated pathways by which these toxins may promote vascular calcification. TMAO, but not PAG, was independently associated with CAC score after adjustment for CKD-related risk factors in kidney failure patients. Neither toxin was associated with epigastric artery calcification score; however, PAG was independently, positively associated with 8-hydroxydeoxyguanosine. Similarly, TMAO, but not PAG, promoted calcium-phosphate deposition in vitro, while both uremic solutes induced oxidative stress. In conclusion, our translational data confirm TMAO's pro-calcifying effects, but both toxins induced free radical production detrimental to vascular maintenance. Our findings suggest these gut-derived uremic toxins have different actions on the vessel wall and therapeutically targeting TMAO may help reduce CV-related mortality in CKD.