Antioxidant Defense Research Articles

Dissecting the mechanism of synergistic interactions between Aspergillus fumigatus and the microalgae Synechocystis sp. PCC6803 under Cd(II) exposure: insights from untargeted metabolomics

Co-culturing fungi and microalgae may effectively remediate wastewater containing Cd and harvest microalgae. Nevertheless, a detailed study of the mechanisms underlying the synergistic interactions between fungi and microalgae under Cd(II) exposure is lacking. In this study, Cd(II) exposure resulted in a significant enhancement of antioxidants, such as glutathione (GSH), malondialdehyde (MDA), hydrogen peroxide (H2O2) and superoxide dismutase (SOD) compared to the control group, suggesting that the cellular antioxidant defense response was activated. Extracellular proteins and extracellular polysaccharides of the symbiotic system were increased by 60.61 % and ,24.29 %, respectively, after Cd(II) exposure for 72 h. The adsorption behavior of Cd(II) was investigated using three-dimensional fluorescence excitation-emission matrix (3D-EEM), fourier transform infrared spectroscopy (FTIR), and scanning electron microscope (SEM). Metabolomics results showed that the TCA cycle provided effective material and energy supply for the symbiotic system to resist the toxicity of Cd(II); Proline, histidine, and glutamine strengthened the synergistic adsorption capacity of the fungus and microalgae. Overall, the theoretical foundation for a deep comprehension of the beneficial interactions between fungi and microalgae under Cd(II) exposure and the role of the fungal-algal symbiotic system in the management of heavy metal pollution is provided by this combined physiological and metabolomic investigation.

Is Copper Still Safe for Us? What Do We Know and What Are the Latest Literature Statements?

Copper (Cu) is a precious metal and one of the three most abundant trace elements in the body (50-120 mg). It is involved in a large number of cellular mechanisms and pathways and is an essential cofactor in the function of cellular enzymes. Both its excess and deficiency may be harmful for many diseases. Even small changes in Cu concentration may be associated with significant toxicity. Consequently, it can be damaging to any organ or tissue in our body, beginning with harmful effects already at the molecular level and then affecting the degradation of individual tissues/organs and the slow development of many diseases, such as those of the immunological system, skeletal system, circulatory system, nervous system, digestive system, respiratory system, reproductive system, and skin. The main purpose of this article is to review the literature with regard to both the healthiness and toxicity of copper to the human body. A secondary objective is to show its widespread use and sources, including in food and common materials in contact with humans. Its biological half-life from diet is estimated to range from 13 to 33 days. The retention or bioavailability of copper from the diet is influenced by several factors, such as age, amount and form of copper in the diet, lifestyle, and genetic background. The upper limit of normal in serum in healthy adults is approximately 1.5 mg Cu/L, while the safe upper limit of average intake is set at 10-12 mg/day, the reference limit at 0.9 mg/day, and the minimum limit at 0.6-0.7 mg/day. Cu is essential, and in the optimal dose, it provides antioxidant defense, while its deficiency reduces the body's ability to cope with oxidative stress. The development of civilization and the constant, widespread use of Cu in all electrical devices will not be stopped, but the health of people directly related to its extraction, production, or distribution can be controlled, and the inhabitants of nearby towns can be protected. It is extremely difficult to assess the effects of copper on the human body because of its ubiquity and the increasing reports in the literature about its effects, including copper nanoparticles.

Effects of the dietary supplementation of manganese on growth, skeletal development, oxidative stress and bone metabolism related genes in gilthead seabream (Sparus aurata) larvae

Manganese (Mn) is an essential element necessary for normal growth, antioxidant defense and maintaining bone health. Knowledge about the effects of dietary Mn levels in gilthead seabream (Sparus aurata) larvae performance is still scarce. To determine the effects of dietary Mn levels on growth, survival, skeletal development and expression of antioxidant and bone metabolism related genes, gilthead seabream larvae were fed six experimental microdiets supplemented with manganese sulfate monohydrate (MnSO4.H2O) (contained 6.3, 39, 75, 79, 200 and 270 mg Mn/kg diet). After 26 days of feeding, dietary Mn levels had no effect on larval survival. However, larvae fed the non-supplemented diet (6.3 mg Mn/kg) showed signs of Mn deficiency, including growth reduction, low whole body Mn content, lower expression of mnsod, runx2, oc, and reduced bone mineralization. The poor vertebral body mineralization and low bone relative gene expression in seabream larvae was related to a marked increase in the number of fish with total skeletal anomalies and anomalies of the caudal vertebrae region. On the contrary, larvae fed with Mn supplemented diet up to 270 mg Mn/kg showed increased growth and whole body Mn content, up-regulated mnsod, runx2, alp, opn and oc expression, as well as increased bone mineralization, and reduced number of fish with skeletal anomalies. Therefore, the findings suggest that adequate dietary Mn supplementation positively influences the growth, skeletal development, and antioxidant defense of gilthead seabream larvae, preventing the manifestation of Mn deficiency-related issues.

A hollow mesoporous iron oxide nanoparticle to strengthen Fenton reaction and weaken antioxidant defense systems for high efficacy tumor ferroptosis therapy

Traditional drug delivery system (DDS) such as hollow mesoporous organosilica nanoparticle (HMON) can achieve efficient delivery of ferroptosis-inducing agents for tumor therapy due to its high drug loading content (DLC), but is limited by their slow degradation and the uselessness of their silicon-based compounds. In this study, a novel hollow mesoporous superparamagnetic iron oxide nanoparticle (HMSPION) was developed with 100 nm of hollow core and 40 nm of mesoporous shell with a high DLC (up to 22.9 %) of β-Lapachone (LAP), doxorubicin (DOX), sorafenib (SFN) and/or Zn2+. Furthermore, we propose a new strategy to strengthen Fenton reaction and weaken antioxidant defense systems in tumors by co-loading Zn2+ and LAP into HMSPION to generate LAP@HMSPION@Zn. Specifically, i) LAP@HMSPION@Zn is degraded into Fe2+/3+, Zn2+, and LAP in acidic tumor microenvironment. ii) LAP catalyzes O2 to be superoxide anion radical (O2•−) and Zn2+ raises the O2•− production in mitochondria. iii) The O2•− can be catalyzed into hydrogen peroxide (H2O2) via superoxide dismutase. iv) H2O2 and the released Fe2+ accelerate the Fenton reaction, generating highly toxic hydroxyl radical (•OH). v) The Fe3+ consumes GSH and LAP downregulates GSH level by NADPH consumption, thereby relieving the antioxidant defense systems in tumor cells.

Oxidative modulations in platelets stored in SSP+, PAS-G and Tyrode's buffer: a comparative analysis

BackgroundPlatelet additive solutions (PASs) improve the efficacy of stored platelets. Oxidative stress causes storage lesions and platelet functions deteriorate. Studies assessing the influence of oxidative stress on platelets stored in PASs are limited. This study compares variations in platelets in different storage solutions (SSP+, PAS-G and Tyrode's buffer). MethodsPlatelets isolated from the blood of Wistar rats were resuspended in SSP+, PAS-G and Tyrode's buffer and stored for seven days at 22°C. The markers of platelet metabolism, function, oxidative stress, antioxidant status and viability were analyzed on Days 1, 3, 5 and 7 of storage. Main resultsSSP+ is associated with platelet function, viability and antioxidant defenses (SOD, CAT and GSH); it decreased primary lipid peroxidation products and maintained the susceptible protein groups in reduced state. Platelet function, antioxidant defenses such as SOD and GSH improved, and lipids and thiols were protected from oxidation in PAS-G. SOD and GSH increased, and lipids and thiols were preserved in Tyrode's buffer. ConclusionSSP+ and PAS-G are more effective in maintaining platelet efficacy till Day 7 compared to Tyrode's buffer. Thus, PAS-G and ∼SSP+ are better than Tyrode's buffer in terms of platelet responses to oxidative stress during storage. This is the first comparative account on the influence of PASs (SSP+, PAS-G and Tyrode's buffer) on platelets in altering oxidative stress. It provides a comprehensive view of the differential responses of platelets in PASs.

Canola (Brassica napus) enhances sodium chloride and sodium ion tolerance by maintaining ion homeostasis, higher antioxidant enzyme activity and photosynthetic capacity fluorescence parameters.

Under salt stress, plants are forced to take up and accumulate large amounts of sodium (Na+ ) and chloride (Cl- ). Although most studies have focused on the toxic effects of Na+ on plants, Cl- stress is also very important. This study aimed to clarify physiological mechanisms underpinning growth contrasts in canola varieties with different salt tolerance. In hydroponic experiments, 150mM Na+ , Cl- and NaCl were applied to salt-tolerant and sensitive canola varieties. Both NaCl and Na+ treatments inhibited seedling growth. NaCl caused the strongest damage to both canola varieties, and stress damage was more severe at high concentrations of Na+ than Cl- . High Cl- promoted the uptake of ions (potassium K+ , calcium Ca2+ ) and induced antioxidant defence. Salt-tolerant varieties were able to mitigate ion toxicity by maintaining lower Na+ content in the root system for a short period of time, and elevating magnesium Mg2+ content, Mg2+ /Na+ ratio, and antioxidant enzyme activity to improve photosynthetic capacity. They subsequently re-established new K+ /Na+ and Ca2+ /Na+ balances to improve their salt tolerance. High concentrations of Cl salts caused less damage to seedlings than NaCl and Na salts, and Cl- also had a positive role in inducing oxidative stress and responsive antioxidant defence in the short term.

Gut microbiota-derived indole-3-propionic acid alleviates diabetic kidney disease through its mitochondrial protective effect via reducing ubiquitination mediated-degradation of SIRT1

IntroductionGut microbes and their metabolites play crucial roles in the pathogenesis of diabetic kidney disease (DKD). However, which one and how specific gut-derived metabolites affect the progression of DKD remain largely unknown. ObjectivesThis study aimed to investigate the potential roles of indole-3-propionic acid (IPA), a microbial metabolite of tryptophan, in DKD. MethodsMetagenomic sequencing was performed to analyze the microbiome structure in DKD. Metabolomics screening and validation were conducted to identify characteristic metabolites associated with DKD. The protective effect of IPA on DKD glomerular endothelial cells (GECs) was assessed through in vivo and in vitro experiments. Further validation via western blot, immunoprecipitation, gene knockout, and site-directed mutation elucidated the mechanism of IPA on mitochondrial injury. ResultsAlterations in gut microbial community structure and dysregulated tryptophan metabolism were evident in DKD mice. Serum IPA levels were significantly reduced in DKD patients and correlated with fasting blood glucose, HbA1c, urine albumin-to-creatinine ratio (UACR), and estimated glomerular filtration rate (eGFR). IPA supplementation ameliorated albuminuria, bolstered the integrity of the glomerular filtration barrier, and mitigated mitochondrial impairments in GECs. Mechanistically, IPA hindered SIRT1 phosphorylation-mediated ubiquitin–proteasome degradation, restoring SIRT1′s role in promoting PGC-1α deacetylation and nuclear translocation, thereby upregulating genes associated with mitochondrial biosynthesis and antioxidant defense. ConclusionOur findings underscore the potential of the microbial metabolite IPA to attenuate DKD progression, offering novel insights and potential therapeutic strategies for its management.

Virgin coconut oil mitigates ageing-associated oxidative stress and dyslipidaemia in male Wistar rats

Background and aimAgeing often leads to the deterioration of physiological functions, including a decline in antioxidant defences, which can result in various health complications. Exogenous antioxidants have been recognised for their potential to alleviate these age-related health complications. Virgin coconut oil (VCO), known for its antioxidant, anti-inflammatory and anti-lipidemic efficacies, has gained recognition as a functional food with promising benefits. However, the safety of VCO consumption among individuals of the aged and diseased population remains to be fully established. Methods and resultsFive experimental groups were established, consisting of one control group and four groups administered either “2 mL” or “4 mL” per kg body weight of “HP-VCO” or “F-VCO” daily for six weeks. Body weight, water, and feed intake were monitored. After six weeks, animals were euthanized, blood and organs were collected for analysis. Oxidative stress and dyslipidemia markers were analysed, and liver tissues underwent histological examination.HP-VCO-administered animals exhibited increased serum total cholesterol and triglycerides, whereas F-VCO-fed animals showed reduced triglyceride levels. LDL-cholesterol levels decreased in all VCO-fed groups, accompanied by increased HDL-cholesterol levels. Additionally, all treated groups showed a slight increase in the HMG Co. A/mevalonate ratio. Both VCO-fed animals displayed elevated reduced glutathione levels and reduced glutathione – S transferase activity. Consistent with these findings, decreased conjugated dienes and thiobarbituric acid reactive substances confirmed the improved redox status. ConclusionThe study indicated that F-VCO is advantageous over VCO prepared by hot pressing as it offers protection against oxidative stress and related degenerative diseases.

Selenium–nitrogen-co-doped carbon dots increase rice seedling growth and salt resistance

Soil salinity seriously affects the utilization of farmland and threatens the crop production. Here, a selenium-nitrogen-co-doped carbon dots was developed, which increased rice seedling growth and alleviated its inhibition by salt stress by foliar spraying. The treatment activated Ca2+ and jasmonic acid signaling pathways and increased iron homeostasis, antioxidant defense, and cell wall development of rice seedlings. It could be used to increase crop resistance to environmental stress.

Antioxidant Defense in the Toughest Animals on the Earth: Its Contribution to the Extreme Resistance of Tardigrades.

Tardigrades are unique among animals in their resistance to dehydration, mainly due to anhydrobiosis and tun formation. They are also very resistant to high-energy radiation, low and high temperatures, low and high pressure, and various chemical agents, Interestingly, they are resistant to ionizing radiation both in the hydrated and dehydrated states to a similar extent. They are able to survive in the cosmic space. Apparently, many mechanisms contribute to the resistance of tardigrades to harmful factors, including the presence of trehalose (though not common to all tardigrades), heat shock proteins, late embryogenesis-abundant proteins, tardigrade-unique proteins, DNA repair proteins, proteins directly protecting DNA (Dsup and TDR1), and efficient antioxidant system. Antioxidant enzymes and small-molecular-weight antioxidants are an important element in the tardigrade resistance. The levels and activities of many antioxidant proteins is elevated by anhydrobiosis and UV radiation; one explanation for their induction during dehydration is provided by the theory of "preparation for oxidative stress", which occurs during rehydration. Genes coding for some antioxidant proteins are expanded in tardigrades; some genes (especially those coding for catalases) were hypothesized to be of bacterial origin, acquired by horizontal gene transfer. An interesting antioxidant protein found in tardigrades is the new Mn-dependent peroxidase.

Insights Into the Role of Copper in Neurodegenerative Diseases and the Therapeutic Potential of Natural Compounds.

Neurodegenerative diseases encompass a collection of neurological disorders originating from the progressive degeneration of neurons, resulting in the dysfunction of neurons. Unfortunately, effective therapeutic interventions for these diseases are presently lacking. Copper (Cu), a crucial trace element within the human body, assumes a pivotal role in various biological metabolic processes, including energy metabolism, antioxidant defense, and neurotransmission. These processes are vital for the sustenance, growth, and development of organisms. Mounting evidence suggests that disrupted copper homeostasis contributes to numerous age-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), Wilson's disease (WD), Menkes disease (MD), prion diseases, and multiple sclerosis (MS). This comprehensive review investigates the connection between the imbalance of copper homeostasis and neurodegenerative diseases, summarizing pertinent drugs and therapies that ameliorate neuropathological changes, motor deficits, and cognitive impairments in these conditions through the modulation of copper metabolism. These interventions include Metal-Protein Attenuating Compounds (MPACs), copper chelators, copper supplements, and zinc salts. Moreover, this review highlights the potential of active compounds derived from natural plant medicines to enhance neurodegenerative disease outcomes by regulating copper homeostasis. Among these compounds, polyphenols are particularly abundant. Consequently, this review holds significant implications for the future development of innovative drugs targeting the treatment of neurodegenerative diseases.

Adenosine protects cardiomyocytes against acrolein-induced cardiotoxicity by enhancing mitochondrial homeostasis, antioxidant defense, and autophagic flux via ERK-activated FoxO1 upregulation

Acrolein is a ubiquitous gaseous air pollutant and endogenous toxicant, which poses strong risk for oxidative stress-related diseases such as cardiovascular disease. Adenosine has been identified as potential therapeutic agent for age-related cardiovascular disease, while the molecular mechanisms underlying its cardioprotection remain elusive. In the present study, we investigated the myocardial protective effects and the mechanism of adenosine on acrolein-induced toxicity in H9c2 cells and primary neonatal rat cardiomyocytes. We found that acrolein caused apoptosis of cardiomyocytes resulting from oxidative damage, autophagy defect, and mitochondrial dysfunction, as evidenced by loss of mitochondrial membrane potential, impairment of mitochondrial biogenesis, dynamics, and oxidative phosphorylation, decrease of mitochondrial deoxyribonucleic acid (mtDNA) copy number and adenosine 5’-triphosphate (ATP) production. Adenosine pretreatment protected against acrolein-induced cardiotoxicity by maintaining mitochondrial homeostasis, activating the phase II detoxifying enzyme system, promoting autophagic flux, and alleviating mitochondrial-dependent apoptosis. We further demonstrated that the up-regulation of forkhead box protein O1 (FoxO1) mediated by extracellular regulated protein kinases (ERK) activation contributes to the cardioprotection of adenosine. These results expand the application of adenosine in cardioprotection to preventing myocardial damages induced by environmental pollutant acrolein exposure, and uncover the adenosine-ERK-FoxO1 axis as the underlying mechanism mediating the protection of mitochondrial homeostasis, Nrf2-mediated antioxidant defense and autophagic flux, shedding light on the better understanding about the pathological mechanism of cardiovascular disease caused by environmental pollutants and applications of adenosine in cardioprotection.

From bacteria to fish: ecotoxicological insights into sulfamethoxazole and trimethoprim

Sulfamethoxazole (SMX) and trimethoprim (TRIM) are two of the most used antibiotics in the last 50 years, to prevent and treat bacterial infections; however, the available literature about toxicity to non-target organisms is quite discrepant and incomplete. This study aims to assess the SMX and TRIM ecotoxicological effects in standard species: Aliivibrio fischeri (bioluminescence inhibition), Escherichia coli ATCC 25922 (growth inhibition), Lemna minor (growth inhibition and biochemical biomarkers), Daphnia magna (immobilization/mortality, life history traits, and biochemical biomarkers), and Danio rerio (survival, hatching, abnormalities, and biochemical biomarkers). The species tested showed different acute sensitivities to SMX (A. fischeri < D. magna < E. coli < L. minor) and TRIM (L. minor < A. fischeri < D. magna < E. coli). Overall, TRIM reveals less toxicity than SMX, except for E. coli (Ecotoxicological approach based on Antimicrobial Susceptibility Testing – EcoAST procedure). Both antibiotics affect individually (e.g., growth and survival) and sub-individually (e.g., antioxidant defenses) L. minor, D. magna, and D. rerio. This study allowed us to generate relevant data and fill gaps in the literature regarding the effects of SMX and TRIM in aquatic organisms. The here-obtained results can be used to (i) complete and re-evaluate the Safety Data Sheet to improve the assessment of environmental safety and management of national and international entities; (ii) clarify the environmental risks of these antibiotics in aquatic ecosystems reinforcing the inclusion in the 4th Watch List of priority substances to be monitored in whole inland waters by the Water Framework Directive; and (iii) combat the development of antimicrobial resistance, as well as supporting the definition of environmental measurements in the context of European One Health Action Plan. However, it is essential to continue studying these antibiotics to better understand their toxicity at ecologically relevant concentrations and their long-term effects under different climatic change scenarios.

Toxicological response and bioaccumulation of strontium in Triticum durum (Nachit) and Triticum aestivum (Ibtissam)

The present study examines the toxicological effects and bioaccumulation of strontium (Sr2+) in two Moroccan wheat species, Triticum durum (Nachit) and Triticum aestivum (Ibtissam). Germination rates and seedling growth parameters were evaluated under Sr2+ concentrations of 0, 10, 100, and 1000 mM. Results revealed a significant decline in germination rates as Sr2+ concentrations increased, with T. aestivum showing higher sensitivity compared to T. durum. Low Sr2+ concentrations (10 mM) initially promoted stem growth in T. aestivum, but growth declined sharply at higher concentrations. Both species sustained growth at moderate Sr2+ concentrations (100 mM), but experienced a substantial reduction at 1000 mM, with T. durum demonstrating slightly better tolerance. Elevated Sr2+ concentrations notably affected root length and stem branching, indicating severe phytotoxic effects. Enzyme activity assays showed that at low Sr2+ concentration (10 mM), GST, CAT, POD, and SOD activities were similar to the control. At moderate concentrations (100 mM), GST and POD activities increased, suggesting enhanced detoxification. At high concentrations (1000 mM), all enzyme activities were significantly elevated, reflecting a robust antioxidative defense mechanism. This study provides valuable insights into the toxicological impacts and physiological responses of these wheat species to Sr2+ stress.

The state of the system of antioxidant protection of the body of dogs during toxocariasis invasion

Among the invasive diseases of dogs, the most common in our country and abroad is gastrointestinal helminthiasis, among which the leading place is occupied by toxocarosis. Adult toxocara cause an intestinal form of the disease, and the larvae – a visceral one. In the process of migration and vital activity, toxocar larvae cause severe damage to the body of dogs up to death. The work aimed to determine the effect of toxocariasis on the enzymatic and non-enzymatic links of the system of antioxidant protection of the dog's body. Twelve two- to four-month-old dogs were used for experimental research, and two groups of six animals each were formed: control and experimental. Puppies of the control group were clinically healthy. Puppies of the experimental group were experimentally infected with the causative agent of toxocarosis at a dose of 5,000 invasive T. canis eggs per kg of body weight. It was established that the antioxidant protection system of the dog's body is inhibited during toxocariasis infection, which is indicated by a decrease in the activity of the enzyme link and indicators of the glutathione system. Under the conditions of experimental toxocarosis invasion, a decrease in the activity of the enzyme link of the system of antioxidant protection of the dog's body was established, as indicated by a reduction in the activity of catalase by 51.9 %, superoxide dismutase by 33.4 %. The development of toxocariasis in dogs is also accompanied by depletion of the glutathione-dependent link of the antioxidant defense system. In infected dogs, a decrease in the content of reduced glutathione in their blood was established by 31.1 % (Р &lt; 0.01), glutathione peroxidase activity – by 26.6 % (Р &lt; 0.001), glutathione reductase activity – by 22.2 % (Р &lt; 0.001). The lowest activity of enzymes of the antioxidant system and the content of reduced glutathione in the blood of infected dogs of the experimental group was established on the 28th day of the experiment.

Exploring the Therapeutic Potential of Phytoconstituents for Addressing Neurodegenerative Disorders.

Neurodegenerative disorder is a serious condition that is caused by abnormal or no neurological function. Neurodegenerative disease is a major growing cause of mortality and morbidity worldwide, especially in the elderly. After World War Ⅱ, eugenics term was exterminated from medicines. Neurodegenerative disease is a genetically inherited disease. Lifestyle changes, environmental factors, and genetic modification, together or alone, are involved in the occurrence of this disorder. The major examples of neurodegenerative disorders are Alzheimer's and Parkinson's disease, in which apoptosis and necrosis are the two major death pathways for neurons. It has been determined from various studies that the etiology of the neurodegenerative disease involves the role of oxidative stress and anti-oxidant defence system, which are prime factors associated with the activation of signal transduction pathway that is responsible for the formation of synuclein in the brain and manifestation of toxic reactions in the form of functional abnormality, which ultimately leads to the dysfunction of neuronal pathway or cell. There has not been much success in the discovery of effective therapy to treat neurodegenerative diseases because the main cause of abnormal functioning or death of neurons is not well known. However, the use of natural products that are derived from plants has effective therapeutic potential against neurodegenerative disease. The natural compounds with medicinal properties to prevent neurological dysfunction are curcumin, wolfberry, ginseng, and Withania somnifera. The selection and use of natural compounds are based on their strong anti-inflammatory and anti-oxidant properties against neurodegenerative disease. Herbal products have active constituents that play an important role in the prevention of communication errors between neurons and neurotransmitters and their respective receptors in the brain, which influence their function. Considering this, natural products have great potential against neurodegenerative diseases. This article reviews the natural compounds used to treat neurodegenerative diseases and their mechanisms of action.

Role of Quercetin in DNA Repair: Possible Target to Combat Drug Resistance in Diabetes.

Diabetes Mellitus (DM) is referred to as hyperglycemia in either fasting or postprandial phases. Oxidative stress, which is defined by an excessive amount of reactive oxygen species (ROS) production, increased exposure to external stress, and an excessive amount of the cellular defense system against them, results in cellular damage. Increased DNA damage is one of the main causes of genomic instability, and genetic changes are an underlying factor in the emergence of cancer. Through covalent connections with DNA and proteins, quercetin has been demonstrated to offer protection against the creation of oxidative DNA damage. It has been found that quercetin shields DNA from possible oxidative stress-related harm by reducing the production of ROS. Therefore, Quercetin helps to lessen DNA damage and improve the ability of DNA repair mechanisms. This review mainly focuses on the role of quercetin in repairing DNA damage and compensating for drug resistance in diabetic patients. Data on the target topic was obtained from major scientific databases, including SpringerLink, Web of Science, Google Scholar, Medline Plus, PubMed, Science Direct, and Elsevier. In preclinical studies, quercetin guards against DNA deterioration by regulating the degree of lipid peroxidation and enhancing the antioxidant defense system. By reactivating antioxidant enzymes, decreasing ROS levels, and decreasing the levels of 8-hydroxydeoxyguanosine, Quercetin protects DNA from oxidative damage. In clinical studies, it was found that quercetin supplementation was related to increased antioxidant capacity and decreased risk of type 2 diabetes mellitus in the experimental group as compared to the placebo group. It is concluded that quercetin has a significant role in DNA repair in order to overcome drug resistance in diabetes.

Investigating intraspecific variability in the biological responses of sea urchins (Paracentrotus lividus) to seawater acidification

Alterations in seawater chemistry posed by acidification may lead to immunological and antioxidant defence impairment in sea urchins, with differences among local populations. Here, we analyzed the effects of reduced pH on Paracentrotus lividus, with a multibiomarker approach, and the possible intraspecific variations in sea urchin responses. Two groups of animals with different ecological histories (i.e., the pattern of environmental characteristics and pressures experienced throughout the organism’s lifetime) were maintained at ambient pH and pH reduced of 0.4 units for 8 months. Changes in gonadosomatic index (GSI), immunological, and oxidative stress biomarkers were assessed in coelomic fluid, gonads, and digestive tract. Animals maintained at reduced pH showed limited impact of seawater acidification compared to the ambient pH condition. However, sea urchins from the two sites were differently influenced by the seawater pH (as shown by multivariate analyses). GSI and immunological and antioxidant status were differentially modulated between the two sexes, with generally higher values in females, but differences between sexes in relation to the pH of exposure were limited. Overall, our findings highlight that the impact of environmental stressors may differ in sea urchins from different locations. This has implications for the maintenance of P. lividus wild populations under future global change scenarios.

Efficacy of propolis and royal jelly in attenuating cadmium-induced spermatogenesis and steroidogenesis dysregulation, causing infertility in rats.

Bee-derived pharmaceutical products, including propolis (PRO) and royal jelly (ROJ), possess outstanding pharmacological properties. However, their efficiency in counteracting the deleterious influences of cadmium (Cd) in testes and the relevant mechanisms entail further investigations. Therefore, this study sheds light on the therapeutic efficacy of PRO and ROJ against testicular dysfunction and infertility induced by Cd. Toward this end, 30 mature male Wistar albino rats were randomly divided into six groups (5 animals/group), including (I) control, (II) Cd, (III) PRO, (IV) ROJ, (V) PRO + Cd, and (VI) ROJ + Cd groups. Furthermore, antioxidant factors, semen quality, hormonal levels, steroidogenic enzymes, and genotoxicity were assessed. Moreover, histopathological and ultrastructural attributes and offspring rates were investigated. The Cd-treated group revealed marked reductions in reduced glutathione (GSH), total antioxidant capacity (TAC), and superoxide dismutase (SOD) with an amplification of lipid peroxidation in testes, indicating disruption of the antioxidant defense system. Furthermore, myeloperoxidase (MPO) activity and DNA damage were significantly heightened, implying inflammation and genotoxicity, respectively. Moreover, steroidogenic enzymes, including 17β-Hydroxy Steroid Dehydrogenase 3 (HSD17b3), 3β-Hydroxy Steroid Dehydrogenase 2 (HSD3b2), 17α-hydroxylase/17,20-lyase (CYP17A1), and steroid 5α-reductase 2 (SRD5A2) were markedly diminished accompanied with disorders in luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone. Besides, spermatozoa quality was reduced, associated with a diminution in the diameter of seminiferous tubules. By contrast, PRO or ROJ significantly protected and/or counteracted the Cd-induced pathophysiological consequences, ameliorating antioxidant and inflammatory biomarkers, steroidogenic enzymes, hormonal levels, and sperm properties, along with lessening DNA impairments. Critically, histological and ultrastructural analyses manifested several anomalies in the testicular tissues of the Cd-administered group, including the Leydig and Sertoli cells and spermatozoa. Conversely, PRO or ROJ sustained testicular tissues' structure, enhancing spermatozoa integrity and productivity. Interestingly, treatment with PRO or ROJ improved fertility indices through offspring rates compared to the Cd-animal group. Our data suggest that PRO is a more effective countermeasure than ROJ against Cd toxicity for securing the delicate testicular microenvironment for spermatogenesis and steroidogenesis.

Neuroprotective Effects of Isolated Mangiferin from Swertia chirayita Leaves Regulating Oxidative Pathway on Streptozotocin-Induced Diabetic Neuropathy in Experimental Rats.

Oxidative stress has an important role in the pathogenesis and development of diabetic peripheral neuropathy (DPN), the most common and debilitating complication of diabetes mellitus. Swertia chirayita is a rich source of phenolic constituents and has hypoglycemic, anti-inflammatory, and antioxidant properties. This study was performed to evaluate the neuroprotective effect in diabetes by enhancing antioxidant defense against oxidative stress, which exhibits a neuroprotective effect in streptozotocin- induced diabetic rats. The objective of this study was to elucidate the therapeutic potential of bioactive compounds of Swertia chirayita for diabetic complications. The present work focused on isolating the bioactive from the leaves of Swertia absinthe for acute toxicity studies, assessing its protective effects against diabetes and diabetic neuropathy as well as its mode of action in STZ-induced Wistar rats. The local area of Moradabad is the place from where the leaves of Swertia chirayita were gathered. Mangiferin was isolated and identified using spectroscopic techniques, such as UV, HPLC, 1H NMR, C13 NMR, MAS, and FTIR. Mangiferin was administered in doses of 15 and 30 mg/kg to test its effect on experimentally induced diabetes. The sciatic nerves of all groups were examined histopathologically. The protective effect of the drug against diabetes and diabetic neuropathy was demonstrated by measures, such as blood glucose level, body weight, food intake, thermal hyperalgesia, grip strength, spontaneous locomotor test, and lipid profile analysis. Sciatic nerve cells of the treated groups showed less inflammation, degeneration, and necrosis. The results of this study confirmed that mangiferin alleviated diabetic neuropathic pain, possibly by reducing inflammatory cytokines (TNF-α, TGF-β1, IL-1β, and IL-6), strong antioxidant activity, and NGF in sciatic nerves. It may be a therapeutic agent. Our results suggested that active phytochemicals of Swertia chirayita showed preventive and curative effects against STZ-induced diabetic neuropathy in rats, which might be due to its antioxidant, anti-inflammatory, and anti-apoptotic properties.