Free Radical-induced Damage Research Articles

Synthesis and toxicity of monothiooxalamides against human red blood cells, brine shrimp (Artemia salina), and fruit fly (Drosophilamelanogaster)

A new family of monothiooxalamides derived from 2-aminobenzimidazole was synthesized, and their structures were confirmed by 1H and 13C one-dimensional and 2D NMR experiments (COSY, HSQC, and HMBC). The antioxidant capacity was evaluated by free radical scavenging assays: 1,1-diphenyl-2-picrylhydrazyl (DPPH•), 2,2′-azinobis(3-ethylbenzothiazoline-6-sulfonic acid) radical cation (ABTS•+), ferric reducing antioxidant power (FRAP), oxygen radical absorbance capacity (ORAC), and the Fe(II) chelating ability. Our work group has previously reported the synthesis and antioxidant activity of monothiooxalamides derived from 2-aminopyridine (I). In this study, the in vitro hemolytic activity of compounds from the 2-aminopyridine (I) and 2-aminobenzimidazole (II) families was evaluated against human red blood cells (RBCs). The concentration at which monothiooxalamides showed no hemolytic activity was chosen to assess their ability to inhibit free radical-induced membrane damage in human RBCs, acute toxicity in brine shrimp, and in vivo toxicity against Drosophila melanogaster. Compounds with morpholine fragments (1g, 1h, 2g, and 2h) showed time- and concentration-dependent protective effects against radical-induced oxidative hemolysis. Moreover, they had the lowest acute toxicity in the brine shrimp lethality assay and a significant increase in chelating activity compared with the other molecules. In particular, monothiooxalamide 2g showed lower toxicity and can be considered for further biological screening and application trials.

Studying the ability of olive leaves nanoparticles to reduce free radicals resulting from the effect of gamma rays on water

This study aims to explore the potential of olive leaves nanoparticles (OLNPs) in scavenging free radicals, particularly 2,2-diphenyl-1- picryl-hydrazyl-hydrate (DPPH), and their capability to mitigate the effects of ionizing radiation. The in vitro assessment of antioxidant activity revealed promising results for OLNPs, exhibiting effective DPPH scavenging within a concentration range of 0.00002 to 0.0001 g/l. Additionally, the natural nanoparticles demonstrated significant antioxidant capacity, suggesting their potential as radical scavengers against free radical-induced damages. Characterization of OLNPs was conducted using UV-Visible absorption spectroscopy, revealing surface Plasmon resonance absorption peaks around 287 nm. Furthermore, atomic force microscopy was employed to determine the morphology and size of the OLNPs, indicating an average diameter of 65 nm.

Hydrogen Sulfide can Scavenge Free Radicals to Improve Spinal Cord Injury by Inhibiting the p38MAPK/mTOR/NF-κB Signaling Pathway.

Spinal cord injury (SCI) causes irreversible cell loss and neurological dysfunctions. Presently, there is no an effective clinical treatment for SCI. It can be the only intervention measure by relieving the symptoms of patients such as pain and fever. Free radical-induced damage is one of the validated mechanisms in the complex secondary injury following primary SCI. Hydrogen sulfide (H2S) as an antioxidant can effectively scavenge free radicals, protect neurons, and improve SCI by inhibiting the p38MAPK/mTOR/NF-κB signaling pathway. In this report, we analyze the pathological mechanism of SCI, the role of free radical-mediated thep38MAPK/mTOR/NF-κB signaling pathway in SCI, and the role of H2S in scavenging free radicals and improving SCI.

Green Synthesis of Zinc Oxide Nanoparticles Using Currant Extracts and Study of Protective against Liver Necrosis of Rat

Abstract Aim: The goal of the current research was to synthesize zinc oxide nanoparticles (ZnONPs) via a simple, cheap, and eco-friendly method as an efficient antioxidant agent. Materials and Methods: ZnONPs are synthesized by reduction of zinc acetate dehydrate using extract of black currant (BC) as reductant. The characterization of stability, size, morphology, and the surface function groups present on synthesized ZnOBCNPs was achieved by Fourier transform infra red, scanning electron microscopy, and X-ray diffraction. In addition, the research included investigating the protective effect of prepared ZONPS on oxidative-stressed rats and evaluating its effectiveness in reducing free radical-induced damage by tracking the concentrations of liver enzymes and blood lipid profiles of rats. Results: The results showed that ZONPS has a positive, beneficial effect in the protection of the rat tissues and ameliorating side effects of oxidative stress. Conclusions: ZONPS can be produced in a simple way, quickly, and in an environmentally friendly manner without the use of hazardous reagents. In this method, zinc acetate dehydrate is reduced with an aqueous solution of BC. The ZONPS, thus produced, can be used as a tissue protectant against oxidative stress. The results showed that the concentrations of liver enzymes and blood lipid profile were stable within normal values in rats exposed to oxidative stress and treated with the prepared ZONPS solution. This indicates that the prepared nanoparticles reduced the harmful effect of oxidative stress through several proposed mechanisms mentioned previously.

Nutraceutical Potential of Underutilized Tropical Fruits and Their Byproducts: Phenolic Profile, Antioxidant Capacity, and Biological Activity of Jerivá (Syagrus romanzoffiana) and Butiá (Butia catarinensis).

Jerivá and butiá are under-valued tropical fruits lacking scientific evidence about their nutraceutical potential. Therefore, they were investigated for their phenolic compound composition and biological activities. Free, esterified, and insoluble-bound polyphenols were obtained from powdered jerivá and butiá pomace and seeds. The total phenolic estimation in seeds (jerivá, 36.45 mg GAE/g; butiá, 45.79 mg GAE/g) exceeded pomaces (jerivá, 23.77 mg GAE/g; butiá, 18.69 mg GAE/g). Phenolic extracts demonstrated antidiabetic and antiobesity potential, inhibiting α-glucosidase (30.51-98.43%) and pancreatic lipase (19.66-41.98%). They also suppressed free radical-induced damage to DNA (21.46-92.48%) and LDL-cholesterol (8.27-23.20%). Identified phenolics (51) included multiple phenolic acids, flavonoids, and tannins, predominantly gallic acid derivatives/conjugates. This is the first study to provide a detailed description of the phenolic profile of these fruits and their byproducts coupled with their bioactivities. Butiá and jerivá were demonstrated to be outstanding sources of polyphenols with high nutraceutical potential for bioeconomic exploration.

Oral Vitamin C Intake Ameliorates Crude Oil-Polluted Water-Induced Jejunal Contractile Dysfunctions in Wistar rats

Inhabitants of rural Niger-Delta oil communities in Nigeria often, unintentionally, consume crude oil polluted water (COCW) due to crude oil spills in the region. The impact of vitamin C supplementation during COCW ingestion on the contractile mechanism of the jejunum is not fully known. Hence, this study investigates the outcomes of COCW water and vitamin C intake on the smooth muscle activity of the jejunum in Wistar rats using standard techniques. Data obtained showed that jejunal tissue SOD concentration was significantly reduced, while jejunal tissue MDA concentration was significantly increased in the COCW-only treated group. Contraction mediated by acetylcholine was significantly increased in the COCW-only treated rats. Calcium and potassium ion influx significantly increased jejunal contraction in the COCW-only rats. Incubation of the jejunal tissue in nifedipine, indomethacin, and L-NAME significantly increased acetylcholine-mediated contractions in the jejunal tissue of the COCW-only treated rats when compared to other groups. COCW causes free radical-induced jejunal damage that results in impaired jejunal contractile activity mediated by the M2 muscarinic receptor, nitric oxide synthase activity, voltage-gated large-conductance calcium channels, potassium channels, and prostaglandins. However, the oral intake of Vitamin C supplementation significantly ameliorated impairments by enhancing jejunal antioxidant activity.

Isolation, characterization and modulatory potentials of β-stigmasterol, ergosterol and xylopic acid from Anchomanes difformis on mitochondrial permeability transition pore in vitro

ObjectiveSecondary metabolites and polyphenolic compounds from medicinal plants have been demonstrated to have multiple biological functions with promising research and development prospects. This study examined the effect of β-stigmasterol (with ergosterol) and xylopic acid isolated from Anchomanes difformis on liver mitochondrial permeability transition pore (mPTP). MethodsThe compounds were isolated by vacuum liquid chromatography. Mitochondrial swelling was assessed as changes in absorbance under succinate-energized conditions. Results1H and 13C NMR spectroscopic elucidation of the isolates affirmed the presence of β-stigmasterol with ergosterol (1:0.3) and xylopic acid. The isolates reversed the increase in lipid peroxidation and inhibited the opening of mitochondrial permeability transition pores caused by calcium and glucose. Pharmacological inhibition of mPTP offers a promising therapeutic target for the treatment of mitochondrial-associated disorders. ConclusionReduction in the activity of calcium ATPase and the expression of Caspase-3 and −9 were observed, suggesting that they could play a role in protecting physicochemical properties of membrane bilayers from free radical-induced severe cellular damage and be useful in the management of diseases where much apoptosis occurs.

Oxidative Stress Sensing System for 8-OHdG Detection Based on Plasma Coupled Electrochemistry by Transparent ITO/AuNTAs/PtNPs Electrode.

8-Hydroxydeoxyguanosine (8-OHdG) is the most widely used oxidative stress biomarker of the free radical-induced oxidative damage product of DNA, which may allow a premature assessment of various diseases. This paper designs a label-free, portable biosensor device to directly detect 8-OHdG by plasma-coupled electrochemistry on a transparent and conductive indium tin oxide (ITO) electrode. We reported a flexible printed ITO electrode made from particle-free silver and carbon inks. After inkjet printing, the working electrode was sequentially assembled by gold nanotriangles (AuNTAs) and platinum nanoparticles (PtNPs). This nanomaterial-modified portable biosensor showed excellent electrochemical performance for 8-OHdG detection from 10 μg/mL to 100 μg/mL by our self-developed constant voltage source integrated circuit system. This work demonstrated a portable biosensor for simultaneously integrating nanostructure, electroconductivity, and biocompatibility to construct advanced biosensors for oxidative damage biomarkers. The proposed nanomaterial-modified ITO-based electrochemical portable device was a potential biosensor to approach 8-OHdG point-of-care testing (POCT) in various biological fluid samples, such as saliva and urine samples.

Alpha-thiol deoxynucleotide triphosphates (S-dNTPs) as radioprotective agents: A novel approach

In this study, the ability of a mixture of four different alpha-thiol deoxynucleotide triphosphates (S-dNTPs) each at a concentration of 10μM when incorporated into the genomic DNA of proliferating human HL-60 and Mono-Mac-6 (MM-6) cells in vitro to provide protection from 2, 5, and 10 Gy of gamma radiation was investigated. Incorporation of the four different S-dNTPs into nuclear DNA at 10 μM concentration for five days was validated by agarose gel electrophoretic band shift analysis. S-dNTP-treated genomic DNA reacted with BODIPY-iodoacetamide demonstrated a band shift to higher molecular weight to confirm the presence of sulfur moieties in the resultant phosphorothioate DNA backbones. No overt signs of toxicity or obvious morphologic cellular differentiation were noted in the presence of 10 μM S-dNTPs even after 8 days in culture. Significantly reduced radiation-induced persistent DNA damage measured at 24 and 48 h post-exposure by γ-H2AX histone phosphorylation using FACS analysis in S-dNTP incorporated HL-60 and MM6 cells indicated protection against radiation-induced direct and indirect DNA damage. Statistically significant protection by S-dNTPs was noted at the cellular level by CellEvent™ Caspase-3/7 assay, which assess the extent of apoptotic events, and by trypan blue dye exclusion to assed cell viability. The results appear to support an innocuous antioxidant thiol radioprotective effect built into genomic DNA backbones as the last line of defense against ionizing radiation and free radical-induced DNA damage.

THE EFFECT OF KAFFIR LIME PEEL EXTRACT (Citrus hystrix) ON SPATIAL MEMORY OF MICE WITH DEMENTIA USING MORRIS WATER MAZE

Background: Antioxidants are a group of chemicals that protect biological systems against the potential harmful effects of oxidation processes or its reactions. Kaffir lime peel (Citrus hystrix) contains various potential antioxidants substances those are able to protect neurons from free radical-induced damage. Objective: To evaluate the effect of kaffir lime peel extract (Citrus hystrix) on the spatial memory of mice induced by Scopolamine (SCM). Methods: This research was a true experimental study with a post-test-only controlled group design. Thirty mice were randomly divided into 5 groups. SCM was injected intraperitoneally on day 1-7 and kaffir lime peel extract was given orally on day 2-7, the spatial memory testing of mice using Morris Water Maze on day 8. Data analysis used One-Way ANOVA test (α = 0.05) and continued with Post Hoc LSD test (α = 0.05). Results: The mean spatial memory of K+, K-, P1, P2,P3 were 16,33 ± 7,42; 70,00 ± 32,24; 25,66 ± 24,43; 23,00 ± 19,39; 25,00 ± 19,50 seconds respectively. There were significant differences in spatial memory in P1, P2, dan P3 to the negative control group, but there is no significant differences between treatment grups. Conclusion: Kaffir lime peel extract (Citrus hystrix) can improve the spatial memory of scopolamine-induced dementia (SCM) mice. There is no dose effect relationship between the treatment groups

The role of graphene quantum dots in mitigating lipid peroxidation.

Lipid peroxidation often underlies apoptosis and mitochondrial dysfunction, which are common pathological phenomena in neurodegenerative and lysosomal storage diseases. Graphene quantum dots (GQDs) have garnered considerable interest as a nanomedicine over the last several years due to their biocompatibility and ability to target cellular disorders associated with disease phenotypes. Recent work with cells containing α-synuclein aggregates (i.e., cells mimicking the onset of Parkinson's disease) has demonstrated that GQDs exhibit mitoprotective behavior. In these studies, GQDs were able to permeate the plasma membrane, inhibit mitochondrial deformation, and restore mitochondrial complex I activity. However, the mechanism by which GQDs interacted with mitochondria was neither examined nor understood. It is known that this type of mitochondrial dysfunction is associated with free radical-induced oxidative lipid damage. Therefore, we hypothesize that the observed mitoprotective properties of GQDs arise from the scavenging of reactive oxidative species that would otherwise interact with mitochondrial membranes. To test this hypothesis, we developed a system to examine lipid peroxidation in synthetic membranes while in the presence of GQDs. Here, we used the fluorescent sensor C11-BODIPY to monitor the kinetics of lipid peroxidation in the presence of hydroxyl free radicals. Comparison of peroxidation rates to first principles kinetic models confirmed that GQDs were indeed scavengers of free radicals. When membranes were incubated with GQDs, the lipid peroxidation rate decreased by 90%. Interestingly, when compared to other renowned antioxidants, such as ascorbic acid and Trolox, GQDs exhibited significantly higher antioxidant efficiency. Ascorbic acid and Trolox required substantially higher concentrations than GQDs to achieve comparable levels of reduction to lipid peroxidation rates. These results warrant further investigation of GQDs as a mitochondrial membrane protection agent.

Protective Effects of Auraptene against Free Radical-Induced Erythrocytes Damage.

Auraptene is the most abundant natural prenyloxycoumarin. Recent studies have shown that it has multiple biological and therapeutic properties, including antioxidant properties. Erythrocytes are constantly subjected to oxidative damage that can affect proteins and lipids within the erythrocyte membrane and lead to some hemoglobinopathies. Due to the lack of sufficient information about the antioxidant effects of auraptene on erythrocytes, this study intended to evaluate the potential of this compound in protecting radical-induced erythrocytes damages. The antioxidant activity of auraptene was measured based on DPPH and FRAP assays. Notably, oxidative hemolysis of human erythrocytes was used as a model to study the ability of auraptene to protect biological membranes from free radical-induced damage. Also, the effects of auraptene in different concentrations (25-400 µM) on AAPH-induced lipid/protein peroxidation, glutathione (GSH) content and morphological changes of erythrocytes were determined. Oxidative hemolysis and lipid/protein peroxidation of erythrocytes were significantly suppressed by auraptene in a time and concentration-dependent manner. Auraptene prevented the depletion of the cytosolic antioxidant GSH in erythrocytes. Furthermore, it inhibited lipid and protein peroxidation in a time and concentration-dependent manner. Likewise, FESEM results demonstrated that auraptene reduced AAPH-induced morphological changes in erythrocytes. Auraptene efficiently protects human erythrocytes against free radicals. Therefore, it can be a potent candidate for treating oxidative stress-related diseases.

Melatonin ameliorates myocardial infarction in obese diabetic individuals: The possible involvement of macrophage apoptotic factors.

In recent days, the hike in obesity-mediated epidemics across the globe and the prevalence of obesity-induced cardiovascular diseasehas become one of the chief grounds for morbidity and mortality. This epidemic-driven detrimental events in the cardiac tissues start with the altered distribution and metabolism pattern of high-density lipoproteinand low-density lipoprotein (LDL) leading to cholesterol (oxidized LDL) deposition on the arterial wall and atherosclerotic plaque generation, followed by vascular spasms and infarction. Subsequently, obesity-triggered metabolic malfunctions induce free radical generation which may further trigger pro-inflammatory signaling and nuclear factor kappa-light-chain-enhancer of activated B cellstranscriptional factor, thus inducing interferon-gamma, tumor necrosis factor-alpha, and inducible nitric oxide synthase. This terrifying cardiomyopathy can be further aggravated in type 2 diabetes mellitus, thereby makingobese diabetic patients prone towardthe development of myocardial infarction (MI) or stroke in comparison to their nondiabetic counterparts. The accelerated oxidative stress and pro-inflammatory response induced cardiomyocyte hypertrophy, followed by apoptosis in obese diabetic individuals, causing progression of athero-thrombotic vascular disease. Being an efficient antioxidative and anti-inflammatory indolamine, melatonin effectively inhibits lipid peroxidation, pro-inflammatory reactions, thereby resolving free radical-induced myocardial damages along with maintaining antioxidant reservoir to preserve cardiovascular integrity. Prolonged melatonin treatment maintains balanced body weight and serum total cholesterolconcentration by inhibiting cholesterol synthesis and promoting cholesterol catabolism. Additionally, melatonin promotes macrophage polarization toward the anti-inflammatory state, providing a proper shield during the recovery period. Therefore, the protective role of melatonin in maintaining the lipid metabolism homeostasis and blocking the atherosclerotic plaque rupture could be targeted as the possible therapeutic strategy for the management of obesity-induced acute MI. This review aimed at orchestrating the efficacy of melatonin in ameliorating irrevocable oxidative cardiovascular damage induced by the obesity-diabetes correlation.

Evaluating the Role of Salivary Oxidative Stress Marker Malondialdehyde in Dental Caries—A Comparative Study

Introduction: Free radical-induced damage on the lipids results in the creation of a novel oxidative stress marker—malondialdehyde (MDA). MDA-induced cell damage affects the immune mechanisms of saliva and may lead to the initiation and progression of bacterial diseases like periodontitis and even dental caries. Aim and Objectives: To determine the salivary levels of the oxidative stress marker—malondialdehyde (MDA) in subjects with dental caries before and after treatment to assess the role of MDA in the initiation and evolution of dental caries. Materials and Methods: The study included 40 patients in total. Based on the number of caries teeth present at the time of diagnosis, patients were divided into two groups: Group I: Subjects with dental caries in 1–2 teeth, N = 20; Group II: Subjects with dental caries in 3–4 teeth, N = 20. The patients were further divided into two groups after undergoing treatment: Group III: Group I subjects who undertook treatment for dental caries, N = 20; Group IV: Group II subjects who underwent treatment for dental caries, N = 20. The whole saliva was obtained from all subjects before treatment and one month after treatment. Estimation of MDA levels was done using ELISA. Statistical analysis was conducted using Student's t-test and Pearson's correlation coefficient. A P value ≤ 0.05 was considered significant. Results: Elevated levels of MDA were evident in subjects with greater carious lesions. The levels of MDA decreased significantly in post-treatment subjects. Pearson's correlation analysis also showed a strong positive correlation with the R-value of 0.832 between Group I and Group II. Conclusion: MDA levels increased with an increase in carious lesions and significantly reduced following treatment proving the role of salivary MDA in the evolution of dental caries.

Modulation of mitochondrial permeability transition pore opening by Myricetin and prediction of its-drug-like potential using in silico approach

Myricetin has been demonstrated to have multiple biological functions with promising research and development prospects. This study investigated the effect of myricetin on liver mitochondrial membrane permeability transition pores and its inhibitory potential on proteins that are important in the apoptotic process in silico. Mitochondrial swelling was assessed as changes in absorbance under succinate-energized conditions. Cytochrome c release, mitochondrial-lipid peroxidation, caspase 3 and 9 expressions, as well as calcium ATPase, were assessed. Pharmacokinetic properties of myricetin were predicted through the SwissADME server while the binding affinity of myricetin toward the proteins was computed using the AutodockVina Screening tool. The conformational stability of protein-ligand interactions was evaluated using molecular dynamics simulations analysis through the iMODS server. Myricetin inhibited the opening of the mitochondrial permeability transition pore and also reversed the increase in mitochondrial lipid peroxidation caused by calcium and other toxicants. Myricetin also caused a reduction in the expression of caspase 3 and 9 as well as calcium ATPase activity. The molecular docking results revealed that myricetin had a considerable binding affinity to the pocket site of caspase 3 and 9 as well as calcium ATPase. Myricetin showed a good drug-likeness based on the predicted pharmacokinetic properties as revealed by low CYP 450 inhibitory promiscuity and relatively low toxicity. It could therefore be suggested that myricetin could be useful in the management of diseases where too many apoptosis occur characterized by excessive tissue wastage such as neurodegenerative conditions and could as well play a role in protecting the physicochemical properties of membrane bilayers from free radical-induced severe cellular damage.

Comparative study between ethanolic and chloroform extracts of mucuna pruriens seeds extract in male wistar rats for the screening of anti-ulcer activity

Background: Well documented neuroprotective profile as well as antioxidant potential of mucuna pruriens seeds with lesser side effects, we are intended to compare study between ethanolic (MPEE) and chloroform extracts (MPCE) of mucuna pruriens seeds extract in albino Wistar rats for the screening of anti-ulcer activity. Materials and methods: The pylorus ligation induced ulcer was used to explore the activity of the ethanolic and chloroform extract. Male albino Wistar rats weighing 100-150g were selected and grouped them among normal control, standard (Omeprazole; 20mg/kg) and treatment groups (MPEE; 50 mg/kg and MPCE; 50 mg/kg) respectively. Results: In our study, the chloroform and ethanolic extract of the seeds of Mucuna pruriens showed antiulcer efficacy as evidenced by a considerable decrease in gastric volume, free and total acidities, ulcer index, and pH. Consequently it might be predicted that both the extracts prevent suppress gastric damage induced by aggressive factors. Preventive anti-oxidants like catalase (CAT) enzymes and reduced glutathione (GSH) constitute the first line of defense in order to combat reactive oxygen species. Conclusion: The ethanolic and chloroform extracts were significantly inhibited the growth of ulcers. Based on the findings, it was determined that the ethanolic extract had superior antiulcer activity over the chloroform extract. In comparison to ulcer control rats, the administration of herbal extract (50 mg/kg p.o.) raised CAT, SOD, and GSH levels, indicating its efficiency in reducing free radical-induced damage. The preliminary phytochemical investigation showed the presence of glycosides, flavonoids, carbohydrate, and tannins in the ethanolic extract, whereas glycosides, sterols, triterpines and tannins in the chloroform extract. The MPEE exhibited a better ulcer protective activity than the MPCE extract.

10-Hydroxydec-2-Enoic Acid Reduces Hydroxyl Free Radical-Induced Damage to Vascular Smooth Muscle Cells by Rescuing Protein and Energy Metabolism.

10-Hydroxydec-2-enoic acid (10-HDA), an unsaturated hydroxyl fatty acid from the natural food royal jelly, can protect against cell and tissue damage, yet the underlying mechanisms are still unexplored. We hypothesized that the neutralization of the hydroxyl free radical (•OH), the most reactive oxygen species, is an important factor underlying the cytoprotective effect of 10-HDA. In this study, we found that the •OH scavenging rate by 10-HDA (2%, g/ml) was more than 20%, which was achieved through multiple-step oxidization of the –OH group and C=C bond of 10-HDA. Moreover, 10-HDA significantly enhanced the viability of vascular smooth muscle cells (VSMCs) damaged by •OH (P < 0.01), significantly attenuated •OH-derived malondialdehyde production that represents cellular lipid peroxidation (P < 0.05), and significantly increased the glutathione levels in •OH-stressed VSMCs (P < 0.05), indicating the role of 10-HDA in reducing •OH-induced cytotoxicity. Further proteomic analyses of VSMCs identified 195 proteins with decreased expression by •OH challenge that were upregulated by 10-HDA rescue and were primarily involved in protein synthesis (such as translation, protein transport, ribosome, and RNA binding) and energy metabolism (such as fatty acid degradation and glycolysis/gluconeogenesis). Taken together, these findings indicate that 10-HDA can effectively promote cell survival by antagonizing •OH-induced injury in VSMCs. To the best of our knowledge, our results provide the first concrete evidence that 10-HDA-scavenged •OH could be a potential pharmacological application for maintaining vascular health.

Amomum subulatum mitigates total body irradiation-induced oxidative stress and its associated inflammatory response by enhancing the antioxidant status and regulating the pro-inflammatory cytokines

Free radical-induced oxidative damage and associated inflammatory responses play a crucial role in cancer radiotherapy (RT) mediated normal tissue toxicities. Supplementation of antioxidants or inflammation modulators may alleviate RT toxicity, thereby improving clinical outcomes. Amomum subulatum is a dietary spice rich in biologically active phytochemicals. The present study investigates radiation dose-modifying factor (DMF) and radioprotective efficacy of methanolic extract of Amomum subulatum dry fruits (MEAS) in mice exposed to different doses of total body irradiation (TBI). Administration of MEAS resulted in a DMF of 1.25 Gy, ascertaining its radioprotective efficacy. MEAS reversed X-ray-induced redox imbalance by enhancing antioxidant defense mechanisms. MEAS prevented TBI-induced hematopoietic damages by significantly (P<.01) enhancing bone marrow cellularity, total white blood cell count, and hemoglobin level. MEAS prevented p53-mediated apoptotic death of intestinal cells and increased the expression of cytoprotective genes Nrf2 (nuclear factor-erythroid factor 2-related factor 2) and HO-1 (heme oxygenase-1). Expression of apoptosis regulating genes revealed that MEAS reduced radiation-induced apoptotic death of intestinal cells. Treatment with MEAS also reduced inflammatory responses via reversing TBI-induced elevation in serum pro-inflammatory cytokine (TNF-α, IL-1β, IL-6) levels. Tissue histopathology further confirmed the protective effect of MEAS against TBI-induced inflammatory responses, suggesting the potential of MEAS in modulating inflammation. These effects might perhaps be attributed to the synergistic effect of biologically active polyphenols with antioxidant, anti-inflammatory, and Nrf2 activating potential in MEAS. Our findings demonstrated the radioprotective efficacy of MEAS, suggesting the possible nutraceutical application of Amomum subulatum in modulating oxidative stress and inflammation.

Protective Effect of Co Q10 and Candesartan on Bleomyycin Induced Lung Fibrosis in Rats

Fibrosis of the lungs is the final phase of many lung illnesses. Its characterized by excessive matrix production leading to the normal lung architecture destruction and eventually death. CoQ10 is an essential constituent of membrane oxidoreductase System. It is an intracellularly localized antioxidant&#x0D; &#x0D; enzyme that is endogenously synthesized in humans. CoQ10 protects cellular components from destruction by free radical-induced oxidative damage. candesartan is a selective antagonist of angiotensin II type 1 receptor (AT1) and is widely employed for treatment of hypertension. Most up to date research shows angiotensin II close involvement with damage and fibrosis process in tissues of organs of circulation.&#x0D; Objective: This animal study was designed to investigate the effect of Co Q10 and candesartan as antifibrotic agents against pulmonary fibrosis focusing on selected markers involved in pulmonary fibrosis.&#x0D; Materials and Method: 48 rats divided randomly into four groups, each consisting of 12 male rats. Group I: (Control group), the rats in this group received single injection of 0.2 ml normal saline via intratracheal route. Group II: (The BLM group), received BLM (8.3 U/kg) as a single dose via the intratracheal rout. Group III: (BLM+CoQ10 group) rats receive BLM (8.3 U/kg) as sulfate salt dissolved in 0.1 ml of normal saline via the intratracheal instillation concomitant with 100 mg/kg co Q 10 per day orally for 5 days before and 10 days after BLM injection. Group IV: (BLM+ candesartan group) rats receive BLM (8.3 U/kg) as sulfate salt dissolved in 0.1 ml of normal saline via the intratracheal instillation concomitant with (10 mg/kg) candesartan per day orally for 5 days before and 10 days after BLM injection. The studied serum biomarkers were glutathione, arachidonate 5 lipoxygenase in addition to histopathological examination using trichrome stain.&#x0D; Results: serum GSH concentration was lower in BLM group in comparison with the control group and the (BLM+ CoQ10) but this difference is not statistically significant. The serum GSH levels showed a significant(P&lt;0.05) elevation in (BLM+ Candesartan) group when compared with the levels in the BLM group. The serum ALOX5 concentration was significantly elevated in BLM group in comparison with the control group (P &lt; 0.05). The serum ALOX5 levels were highly significantly lower in (BLM +CoQ10) (P &lt; 0.01) and very highly significantly lower in the (BLM+ Candesartan) group (P &lt; 0.001) when comparing it with the levels in the BLM group. furthermore, histologically CoQ10 and candesartan showed reduction in the numbers of inflammation cells and a decrease in the damage to the lung architecture and fibrosis induced by bleomycin.&#x0D; Conclusion: CoQ10 and candesartan decrease pulmonary fibrosis induced by bleomycin in male rats.

Biomolecular Protective Effects of Bacopa Monnieri (L.) Pennell Leaf Extracts Against Oxidative Damage

In living systems, free radicals are constantly generated and they can cause extensive damage to tissues and biomolecules, leading to various disease conditions, especially degenerative diseases, and extensive lysis.The most effective way to eliminate free radicals which cause oxidative stress is with the help of antioxidants. Antioxidants prevent free radical-induced tissue damage by preventing the formation of radicals by scavenging them, or by promoting their decomposition. In the present study, the biomolecular protective effects of B. monnieri leaf extracts against oxidative stress induced damage to lipids and DNA in cell free systems and intact cells were analyzed. Results showed that the leaf extracts of B. monnieri rendered protection against oxidative stress induced damage in both cell-free systems and intact cells. Bangladesh J. Bot. 51(1): 123-129, 2022 (March)