Oxidative Stress Defense System Research Articles

Impact of probiotics, prebiotics, and synbiotics on digestive enzymes, oxidative stress, and antioxidant defense in fish farming: current insights and future perspectives

There has been a surge of research in the aquaculture industry investigating probiotic, prebiotic, and synbiotic interventions on the physiological mechanisms of fish, specifically digestive enzymes, oxidative stress, and antioxidant defense. In fish, probiotics have been shown to improve nutrient utilization and growth performance by stimulating digestive enzymes. Meanwhile, probiotics, prebiotics and synbiotics have also been studied for their ability to modulate oxidative stress and antioxidant defense mechanisms in fish, highlighting their multifaceted health benefits. This review identified current trends, research gaps, and future considerations in this evolving field. Although promising findings have been made, a significant research gap exists in understanding the specific role of probiotics prebiotics, and synbiotics in modulating digestive enzymes, oxidative stress, and antioxidant defense systems in a variety of fish species. As this study investigate into the existing body of literature, it becomes evident that while certain aspects of these interactions have been elucidated, a nuanced and comprehensive understanding still needs to be discovered. The variations in experimental design, species-specific responses, and the lack of standardized methodologies contribute to the complexity of the field. Digestive physiology and antioxidant defense mechanisms vary among different fish species, so future research should focus on species-specific responses to probiotic, prebiotic, and synbiotic formulations. It will also be possible to establish robust correlations between dietary interventions and observed effects through a systematic experimental design and methodology approach. Accordingly, further research is needed to understand the interactions between probiotics, prebiotics, and synbiotics in fish and digestive enzymes, oxidative stress, and antioxidant defense. Identifying research gaps and adopting standardized methodologies can help develop tailored strategies to optimize aquaculture fish health and growth performance.

Effect of CB1 Receptor Deficiency on Mitochondrial Quality Control Pathways in Gastrocnemius Muscle.

This study aims to explore the complex role of cannabinoid type 1 receptor (CB1) signaling in the gastrocnemius muscle, assessing physiological processes in both CB1+/+ and CB1-/- mice. The primary focus is to enhance our understanding of how CB1 contributes to mitochondrial homeostasis. At the tissue level, CB1-/- mice exhibit a substantial miRNA-related alteration in muscle fiber composition, characterized by an enrichment of oxidative fibers. CB1 absence induces a significant increase in the oxidative capacity of muscle, supported by elevated in-gel activity of Complex I and Complex IV of the mitochondrial respiratory chain. The increased oxidative capacity is associated with elevated oxidative stress and impaired antioxidant defense systems. Analysis of mitochondrial biogenesis markers indicates an enhanced capacity for new mitochondria production in CB1-/- mice, possibly adapting to altered muscle fiber composition. Changes in mitochondrial dynamics, mitophagy response, and unfolded protein response (UPR) pathways reveal a dynamic interplay in response to CB1 absence. The interconnected mitochondrial network, influenced by increased fusion and mitochondrial UPR components, underlines the dual role of CB1 in regulating both protein quality control and the generation of new mitochondria. These findings deepen our comprehension of the CB1 impact on muscle physiology, oxidative stress, and MQC processes, highlighting cellular adaptability to CB1-/-. This study paves the way for further exploration of intricate signaling cascades and cross-talk between cellular compartments in the context of CB1 and mitochondrial homeostasis.

Significance of oxidative stress and antioxidant capacity tests as biomarkers of premature ovarian insufficiency: A case control study.

Premature ovarian insufficiency (POI) is a condition that causes secondary amenorrhea owing to ovarian hypofunction at an early stage. Early follicular depletion results in intractable infertility, thereby considerably reducing the quality of life of females. Given the continuum in weakened ovarian function, progressing from incipient ovarian failure (IOF) to transitional ovarian failure and further to POI, it is necessary to develop biomarkers for predicting POI. The oxidative stress states in IOF and POI were comprehensively evaluated via oxidative stress [diacron-reactive oxygen metabolites (d-ROMs)] test and antioxidant capacity [biological antioxidant potential (BAP)]. To explore the possibilities of oxidative stress and antioxidant capacity as biomarkers for the early detection of POI. Females presenting with secondary amenorrhea over 4 mo and a follicle stimulating hormone level of > 40 mIU/mL were categorized into the POI group. Females presenting with a normal menstrual cycle and a follicle stimulating hormone level of > 10.2 mIU/mL were categorized into the IOF group. Healthy females without ovarian hypofunction were categorized into the control group. Among females aged < 40 years who visited our hospital from January 2021 to June 2022, we recruited 11 patients into both POI and IOF groups. For the potential antioxidant capacity, the relative oxidative stress index (BAP/d-ROMs × 100) was calculated, and the oxidative stress defense system was comprehensively evaluated. d-ROMs were significantly higher in the POI and IOF groups than in the control group, (478.2 ± 58.7 U.CARR, 434.5 ± 60.6 U.CARR, and 341.1 ± 35.1 U.CARR, respectively) (U.CARR is equivalent to 0.08 mg/dL of hydrogen peroxide). However, no significant difference was found between the POI and IOF groups. Regarding BAP, no significant difference was found between the control, IOF, and POI groups (2078.5 ± 157.4 μmol/L, 2116.2 ± 240.2 μmol/L, and 2029.0 ± 186.4 μmol/L, respectively). The oxidative stress index was significantly higher in the POI and IOF groups than in the control group (23.7 ± 3.3, 20.7 ± 3.6, and 16.5 ± 2.1, respectively). However, no significant difference was found between the POI and IOF groups. High levels of oxidative stress suggest that evaluating the oxidative stress state may be a useful indicator for the early detection of POI.

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.

Chemo-photothermal nanoplatform with diselenide as the key for ferroptosis in colorectal cancer

Colorectal cancer (CRC) is a prevalent clinical malignancy of the gastrointestinal system, and its clinical drug resistance is the leading cause of poor prognosis. Mechanistically, CRC cells possess a specific oxidative stress defense mechanism composed of a significant number of endogenous antioxidants, such as glutathione, to combat the damage produced by drug-induced excessive reactive oxygen species (ROS). We report on a new anti-CRC nanoplatform, a multifunctional chemo-photothermal nanoplatform based on Camptothecin (CPT) and IR820, an indocyanine dye. The implementation of a GSH-triggered ferroptosis-integrated tumor chemo-photothermal nanoplatform successfully addressed the poor targeting ability of CPT and IR820 while exhibiting significant growth inhibitory effects on CRC cells. Mechanistically, to offset the oxidative stress created by the broken SeSe bonds, endogenous GSH was continuously depleted, which inactivated GPX4 to accumulate lipid peroxides and induce ferroptosis. Concurrently, exogenously administered linoleic acid was oxidized under photothermal conditions, resulting in an increase in LPO accumulation. With the breakdown of the oxidative stress defense system, chemotherapeutic efficacy could be effectively enhanced. In combination with photoacoustic imaging, the nanoplatform could eradicate solid tumors by means of ferroptosis-sensitized chemotherapy. This study indicates that chemotherapy involving a ferroptosis mechanism is a viable method for the treatment of CRC.

Modulation of mitochondrial activity by sugarcane (Saccharum officinarum L.) top extract and its bioactive polyphenols: a comprehensive transcriptomics analysis in C2C12 myotubes and HepG2 hepatocytes

Age-related mitochondrial dysfunction leads to defects in cellular energy metabolism and oxidative stress defense systems, which can contribute to tissue damage and disease development. Among the key regulators responsible for mitochondrial quality control, peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) is an important target for mitochondrial dysfunction. We have previously reported that bioactive polyphenols extracted from sugarcane top (ST) ethanol extract (STEE) could activate neuronal energy metabolism and increase astrocyte PGC-1α transcript levels. However, their potential impact on the mitochondria activity in muscle and liver cells has not yet been investigated. To address this gap, our current study examined the effects of STEE and its polyphenols on cultured myotubes and hepatocytes in vitro. Rhodamine 123 assay revealed that the treatment with STEE and its polyphenols resulted in an increase in mitochondrial membrane potential in C2C12 myotubes. Furthermore, a comprehensive examination of gene expression patterns through transcriptome-wide microarray analysis indicated that STEE altered gene expressions related to mitochondrial functions, fatty acid metabolism, inflammatory cytokines, mitogen-activated protein kinase (MAPK) signaling, and cAMP signaling in both C2C12 myotubes and HepG2 hepatocytes. Additionally, protein–protein interaction analysis identified the PGC-1α interactive-transcription factors-targeted regulatory network of the genes regulated by STEE, and the quantitative polymerase chain reaction results confirmed that STEE and its polyphenols upregulated the transcript levels of PGC-1α in both C2C12 and HepG2 cells. These findings collectively suggest the potential beneficial effects of STEE on muscle and liver tissues and offer novel insights into the potential nutraceutical applications of this material.Graphical

Advanced maternal age leads to changes within the insulin/IGF system and lipid metabolism in the reproductive tract and preimplantation embryo: insights from the rabbit model.

Reproductive potential in women declines with age. The impact of ageing on embryo-maternal interactions is still unclear. Rabbits were used as a reproductive model to investigate maternal age-related alterations in reproductive organs and embryos on Day 6 of pregnancy. Blood, ovaries, endometrium, and blastocysts from young (16-20 weeks) and advanced maternal age phase (>108 weeks, old) rabbits were analysed at the mRNA and protein levels to investigate the insulin-like growth factor (IGF) system, lipid metabolism, and stress defence system. Older rabbits had lower numbers of embryos at Day 6 of pregnancy. Plasma insulin and IGF levels were reduced, which was accompanied by paracrine regulation of IGFs and their receptors in ovaries and endometrium. Embryos adapted to hormonal changes as indicated by reduced embryonic IGF1 and 2 levels. Aged reproductive organs increased energy generation from the degradation of fatty acids, leading to higher oxidative stress. Stress markers, including catalase, superoxide dismutase 2, and receptor for advanced glycation end products were elevated in ovaries and endometrium from aged rabbits. Embryonic fatty acid uptake and β-oxidation were increased in both embryonic compartments (embryoblast and trophoblast) in old rabbits, associated with minor changes in the oxidative and glycative stress defence systems. In summary, the insulin/IGF system, lipid metabolism, and stress defence were dysregulated in reproductive tissues of older rabbits, which is consistent with changes in embryonic metabolism and stress defence. These data highlight the crucial influence of maternal age on uterine adaptability and embryo development.

Molecular Regulatory Mechanism of Exogenous Hydrogen Sulfide in Alleviating Low-Temperature Stress in Pepper Seedlings.

Pepper (Capsicum annuum L.) is sensitive to low temperatures, with low-temperature stress affecting its plant growth, yield, and quality. In this study, we analyzed the effects of exogenous hydrogen sulfide (H2S) on pepper seedlings subjected to low-temperature stress. Exogenous H2S increased the content of endogenous H2S and its synthetase activity, enhanced the antioxidant capacity of membrane lipids, and protected the integrity of the membrane system. Exogenous H2S also promoted the Calvin cycle to protect the integrity of photosynthetic organs; enhanced the photosynthetic rate (Pn), stomatal conductance (Gs), transpiration rate (Tr), and photosynthesis; and reduced the intercellular CO2 concentration (Ci). Moreover, the activities of superoxide dismutase, peroxidase, catalase, and anti-cyclic glutathione (ASA-GSH) oxidase were improved to decompose excess reactive oxygen species (ROS), enhance the oxidative stress and detoxification ability of pepper seedlings, and improve the resistance to low-temperature chilling injury in 'Long Yun2' pepper seedlings. In addition, the H2S scavenger hypotaurine (HT) aggravated the ROS imbalance by reducing the endogenous H2S content, partially eliminating the beneficial effects of H2S on the oxidative stress and antioxidant defense system, indicating that H2S can effectively alleviate the damage of low temperature on pepper seedlings. The results of transcriptome analysis showed that H2S could induce the MAPK-signaling pathway and plant hormone signal transduction; upregulate the expression of transcription factors WRKY22 and PTI6; induce defense genes; and activate the ethylene and gibberellin synthesis receptors ERF1, GDI2, and DELLA, enhancing the resistance to low-temperature chilling injury of pepper seedlings. The plant-pathogen interaction was also significantly enriched, suggesting that exogenous H2S also promotes the expression of genes related to plant-pathogen interaction. The results of this study provide novel insights into the molecular mechanisms and genetic modifications of H2S that mitigate the hypothermic response.

DNA repair and oxidative stress defense systems in radiation-resistant Deinococcus murrayi.

Deinococcus murrayi is a bacterium isolated from hot springs in Portugal, and named after Dr. Robert G.E. Murray in recognition of his research on the genus Deinococcus. Like other Deinococcus species, D. murrayi is extremely resistant to ionizing radiation. Repair of massive DNA damage and limitation of oxidative protein damage are two important factors contributing to the robustness of Deinococcus bacteria. Here, we identify, among others, the DNA repair and oxidative stress defense proteins in D. murrayi, and highlight special features of D. murrayi. For DNA repair, D. murrayi does not contain a standalone uracil-DNA glycosylase (Ung), but it encodes a protein in which Ung is fused to a DNA photolyase domain (PhrB). UvrB and UvrD contain large insertions corresponding to inteins. One of its endonuclease III enzymes lacks a [4Fe-4S] cluster. Deinococcus murrayi possesses a homolog of the error-prone DNA polymerase IV. Concerning oxidative stress defense, D. murrayi encodes a manganese catalase in addition to a heme catalase. Its organic hydroperoxide resistance protein Ohr is atypical because the redox active cysteines are present in a CXXC motif. These and other characteristics of D. murrayi show further diversity among Deinococcus bacteria with respect to resistance-associated mechanisms.

Remediation of soil polluted with Pb and Cd and alleviation of oxidative stress in Brassica rapa plant using nanoscale zerovalent iron supported with coconut-husk biochar

Accumulation of toxic elements by plants from polluted soil can induce the excessive formation of reactive oxygen species (ROS), thereby causing retarded plants' physiological attributes. Several researchers have remediated soil using various forms of zerovalent iron; however, their residual impacts on oxidative stress indicators and health risks in leafy vegetables have not yet been investigated. In this research, nanoscale zerovalent iron supported with coconut-husk biochar (nZVI-CHB) was synthesized through carbothermal reduction process using Fe2O3 and coconut-husk. The stabilization effects of varying concentrations of nZVI-CHB and CHB (250 and 500 mg/kg) on cadmium (Cd) and lead (Pb) in soil were analyzed, and their effects on toxic metals induced oxidative stress, physiological properties, and antioxidant defence systems of the Brassica rapa plant were also checked. The results revealed that the immobilization of Pb and Cd in soil treated with CHB was low, leading to a higher accumulation of metals in plants grown. However, nZVI-CHB could significantly immobilize Pb (57.5–62.12%) and Cd (64.1–75.9%) in the soil, leading to their lower accumulation in plants below recommended safe limits and eventually reduced carcinogenic risk (CR) and hazard quotient (HQ) for both Pb and Cd in children and adults below the recommended tolerable range of <1 for HQ and 10−6 – 10−4 for CR. Also, a low dose of nZVI-CHB significantly mitigated toxic metal-induced oxidative stress in the vegetable plant by inhibiting the toxic metals uptake and increasing antioxidant enzyme activities. Thus, this study provided another insightful way of converting environmental wastes to sustainable adsorbents for soil remediation and proved that a low-dose of nZVI-CHB can effectively improve soil quality, plant physiological attributes and reduce the toxic metals exposure health risk below the tolerable range.

Investigation of Oxidative/Antioxidant Effects of Turmeric (Curcuma longa L.) Supplementation on Heart Tissue in Adult Rats

n present study, the effects of curcumin supplementation on oxidative stress and antioxidant defense system in heart tissue in adult rats were investigated. Sixteen rats (8-weeks-old) were selected and divided into two groups. The first group is the experimental group and these rats (n=8) were gavaged with curcumin, dissolved in corn oil, at a dose of 300 mg/kg per day for 28 days. The second group is the control group, rats in this group were given curcumin and equal amount of corn oil to eliminate the porter effect. Euthanasia was performed and total antioxidant capacity (TAS), total oxidant capacity (TOS), malondialdehyde (MDA) and glutathione (GSH) levels were analyzed from heart tissues. Curcumin supplementation resulted in significantly increased GSH levels(P0.05). The total antioxidant capacity (TAS) and total oxidant capacity (TOS) ratios were found to be statistically significant. In the other group supplemented with curcumin, MDA levels tended to decrease compared to the control group, and there was no statistically significant difference between the two groups. Curcumin supplementation protects the heart tissue against oxidative damage and strengthens the antioxidant defense system in adult rats.

Protective effect of resveratrol on mitochondrial biogenesis during hyperoxia-induced brain injury in neonatal pups

BackgroundNeonatal hyperoxic brain injury is caused by exposure to hyperphysiological oxygen content during the period of incomplete development of the oxidative stress defence system, resulting in a large number of reactive oxygen species (ROS) and causing damage to brain tissue. Mitochondrial biogenesis refers to the synthesis of new mitochondria from existing mitochondria, mostly through the PGC-1α/Nrfs/TFAM signalling pathway. Resveratrol (Res), a silencing information regulator 2-related enzyme 1 (Sirt1) agonist, has been shown to upregulate the level of Sirt1 and the expression of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α). We speculate that Res has a protective effect on hyperoxia-induced brain injury through mitochondrial biogenesis.MethodsSprague-Dawley (SD) pups were randomly divided into the nonhyperoxia (NN) group, the nonhyperoxia with dimethyl sulfoxide (ND) group, the nonhyperoxia with Res (NR) group, the hyperoxia (HN) group, the hyperoxia with dimethyl sulfoxide (HD) group, and the hyperoxia with Res (HR) group within 12 h after birth. The HN, HD, and HR groups were placed in a high-oxygen environment (80‒85%), and the other three groups were placed in the standard atmosphere. The NR and HR groups were given 60 mg/kg Res every day, the ND and HD groups were given the same dose of dimethyl sulfoxide (DMSO) every day, and the NN and HN groups were given the same dose of normal saline every day. On postnatal day (PN) 1, PN7, and PN14, brain samples were acquired for HE staining to assess pathology, TUNEL to detect apoptosis, and real-time quantitative polymerase chain reaction and immunoblotting to detect the expression levels of Sirt1, PGC-1α, nuclear respiratory factor 1 (Nrf1), nuclear respiratory factor 2 (Nrf2) and mitochondrial transcription factor A (TFAM) in brain tissue.ResultsHyperoxia induced brain tissue injury; increased brain tissue apoptosis; inhibited Sirt1, PGC-1α, Nrf1, Nrf2, TFAM mRNA expression in mitochondria; diminished the ND1 copy number and ND4/ND1 ratio; and decreased Sirt1, PGC-1α, Nrf1, Nrf2, and TFAM protein levels in the brain. In contrast, Res reduced brain injury and attenuated brain tissue apoptosis in neonatal pups and increased the levels of the corresponding indices.ConclusionRes has a protective effect on hyperoxia-induced brain injury in neonatal SD pups by upregulating Sirt1 and stimulating the PGC-1α/Nrfs/TFAM signalling pathway for mitochondrial biogenesis.

The effect of Inflamma-X supplementation on oxidative stress and antioxidant defense system markers following of SWPT-SWFT combination Test in young wrestlers

زمینه و هدف: کشتی ورزشی برخوردی با انقباض‌های برون‌گرای مکرر و با شدت بالاست. چنین فعالیت‌هایی که با انقباض‌های برون‌گرای شدید انجام می‌گیرد، با اختلالات مکانیکی و متابولیکی همراه است. چنین شدت بالایی از فعالیت در کشتی به‌طور چشمگیری به تولید ناگهانی گونه‌های اکسیژن واکنش‌پذیر بنیان‌های آزاد در حین رقابت و بازیافت پس از هر مسابقه منجر می‌شود، به‌طوری‌که حتی ممکن است طی انجام این دسته از فعالیت‌ها، ذخیرة ضداکسایشی به‌شدت کاسته و تخلیه شود و به‌دنبال ناکارامدی دستگاه اکسایشی، فشار اکسایشی رخ دهد که کاهش عملکرد ورزشی را در پی دارد و با تسریع بروز خستگی همراه می‌شود. ازاین‌رو پژوهش حاضر با هدف تعیین تأثیر مکمل‌دهی کوتاه‌مدت اینفلاما ایکس بر شاخص‌های فشار اکسایشی و دستگاه دفاع ضداکسایشی پس از اجرای دو دوره پشت سر هم آزمون ترکیبی SWPT-SWFTدر کشتی‌گیران جوان انجام گرفت.مواد و روش‌ها: از بین داوطلبان واجد شرایط، ۲۴ کشتی‌گیر جوان به‌صورت تصادفی به دو گروه مکمل-تمرین (۱۲ نفر) و دارونما-تمرین (۱۲ نفر) تقسیم شدند. از کشتی‌گیران در گروه مکمل–تمرین درخواست شد به مدت ده روز تا پیش از اجرای آزمون ترکیبی، روزانه دو عدد مکمل اینفلاما ایکس 15 میلی‌گرمی را به‌صورت ناشتا به‌همراه 200 میلی‌لیتر آب مصرف کنند. گروه دارونما نیز قرص‌های نشاسته با همان مقدار و تعداد گروه مکمل- تمرین دریافت کردند. آزمون ترکیبی SWFT-SWPT شامل دو آزمون عملکردی ویژة کشتی (SWPT) و آزمون آمادگی بدنی ویژة کشتی (SWFT) است. آزمون ترکیبی سه دقیقه و 40 ثانیه بود که یک نوبت به‌شمار می‌رفت و هر مرحله نیز شامل دو نوبت بود. به‌منظور بررسی تغییرات شاخص‌های فشار اکسایشی و دستگاه دفاع ضداکسایشی کشتی‌گیران، خون‌گیری اولیه پیش از شروع آزمون ترکیبی SWPT-SWFT انجام گرفت. چهار خون‌گیری بعدی شامل بلافاصله پس از مراحل اول، دوم و چهارم آزمون مذکور و آخرین خون‌گیری نیز 48 ساعت پس از آزمون ترکیبی SWPT-SWFT اجرا شد. نمونه‌های جمع‌آوری‌شده به‌منظور بررسی سطوح مالون دی‌آلدهید، ظرفیت تام ضداکسایشی و سوپراکسید دیسموتاز با روش الایزا ارزیابی شدند. به‌منظور تجزیه‌وتحلیل داده‌ها از روش تحلیل واریانس با اندازه‌گیری مکرر ترکیبی (Mixed Anova) استفاده شد. نتایج: یافته‌ها نشان داد که مقادیر ظرفیت تام ضداکسایشی گروه مکمل در همة مراحل بیشتر از گروه دارونما بود؛ با این حال تفاوت دو گروه فقط در زمان‌های خون‌گیری سوم، چهارم و پنجم معنادار بود (05/‌0>P)، ولی در مراحل خون‌گیری اول و دوم بین دو گروه تفاوت معناداری مشاهده نشد (05/‌0<P). همین‌طور در هیچ‌یک از مراحل خون‌گیری در مقادیر سرمی سوپراکسید دیسموتاز تفاوت معناداری بین دو گروه وجود نداشت (05/‌0<P). همچنین در مراحل خون‌گیری دوم، سوم، چهارم و پنجم بین دو گروه در مقادیر سرمی مالون دی‌آلدهید تفاوت معناداری وجود داشت (05/‌0>P).نتیجه‌گیری: به‌نظر می‌رسد مصرف مکملInflamma-X می‌تواند برای جلوگیری از آسیب اکسایشی و حتی تسهیل دورة بازیافت بین هر رقابت کشتی سودمند باشد.

Deciphering the contribution of PerR to oxidative stress defense system in Clostridium tyrobutyricum

AbstractAs a next‐generation probiotic, Clostridium tyrobutyricum, which is considered obligate anaerobe, has been extensively considered a promising candidate for future use to promote health benefits. The industrial applications were limited by its weak tolerance to oxygen stress during fermentation. Here, we enhanced the oxidative stress tolerance of C. tyrobutyricum L319 by deleting the peroxide response regulator gene perR using an endogenous CRISPR‐Cas system. The mutant strain exhibited greatly improved growth when exposed to oxygen, which also showed a shortened lag phase compared with the control strain. Consistently, a concomitant increase in butyric acid productivity from 0.08 to 0.13 g/L/h in the presence of oxygen was observed. Decreased intracellular ROS level sand NAD+/NADH ratios were also observed in the mutant strain. Furthermore, transcriptome and binding target analysis revealed that genes encoding transcriptional regulators and proteins related to redox balance were upregulated. Changes in carbohydrate, amino acid and purine metabolisms upon oxygen exposure were also observed. Importantly, phylogenomic analysis indicated that PerR may be a universal engineering target in diverse Clostridium species. These findings will contribute to the development of robust C. tyrobutyricum strains for efficient butyric acid production in the food industry.

Recent advances in nanomaterial-mediated bacterial molecular action and their applications in wound therapy.

Because of the multi-pathway antibacterial mechanisms of nanomaterials, they have received widespread attention in wound therapy. However, owing to the complexities of bacterial responses toward nanomaterials, antibacterial molecular mechanisms remain unclear, making it difficult to rationally design highly efficient antibacterial nanomaterials. Fortunately, molecular dynamics simulations and omics techniques have been used as effective methods to further investigate the action targets of nanomaterials. Therefore, the review comprehensively analyzes the antibacterial mechanisms of nanomaterials from the morphology-dependent antibacterial activity and physicochemical/optical properties-dependent antibacterial activity, which provided guidance for constructing excellently efficient and broad-spectrum antibacterial nanomaterials for wound therapy. More importantly, the main molecular action targets of nanomaterials from the membranes, DNA, energy metabolism pathways, oxidative stress defense systems, ribosomes, and biofilms are elaborated in detail. Furthermore, nanomaterials used in wound therapy are reviewed and discussed. Finally, future directions of nanomaterials from mechanisms to nanomedicine are further proposed.

Implication of Oxidative Stress and Antioxidant Defence Systems in Symptomatic and Asymptomatic &amp;lt;i&amp;gt;Plasmodium falciparum&amp;lt;/i&amp;gt; Malaria Infection among Children Aged 1 to 15 Years in the Mount Cameroon Area

It is known that the pathogenicity of Plasmodium induces the breakdown of haemoglobin, which leads to the induction of oxidative stress. This study aimed to identify the possible effects of oxidative stress and antioxidant defence systems in symptomatic and asymptomatic Plasmodium falciparum malaria infection in children (1 - 15 years old) in the Mount Cameroon vicinity. This cross-sectional study involved blood samples collected from 473 children and examined for malaria parasitaemia. Full blood counts were performed using an automated haemoanalyser. Serum oxidative stress status (malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and vitamin C (Vit C)) were each determined by colorimetric enzymatic assays. The prevalence of malaria parasite infection was 32.1% among the participants. Out of that, 62.5% of patients with parasitaemia were symptomatic. Anaemia prevalence increased significantly with parasite density. MDA levels were significantly higher in patients with malaria symptoms than in those without symptoms. A significant and positive correlation was detected between MDA (r = 0.831, P < 0.05), NO (r = 0.779, P < 0.05), and malaria parasite density while, a significant and negative relationship occurred between parasite density and GSH (r = ?0.763, P < 0.05) and Vit C (r = ?0.826, P < 0.05) levels, SOD (r = ?0.621, P < 0.05) and CAT (r = ?0.817, P < 0.05) activities. The SOD activity and GSH level significantly decreased (P < 0.05) with an increase in the MDA levels. These findings showed that MDA and nitric oxide levels increased both in malaria participants with or without symptoms. A similar decrease in the antioxidant defence system was observed in both symptomatic and asymptomatic patients. Therefore, there is a need to develop public health policies that encourage routine diagnosis and treatment of malaria in seemingly healthy people (asymptomatic cases), and this will play an essential role in controlling malaria in tropical countries.

Improving the productivity of malic acid by alleviating oxidative stress during Aspergillus niger fermentation

BackgroundAs an attractive platform chemical, malic acid has been commonly used in the food, feed and pharmaceutical field. Microbial fermentation of biobased sources to produce malic acid has attracted great attention because it is sustainable and environment-friendly. However, most studies mainly focus on improving yield and ignore shortening fermentation time. A long fermentation period means high cost, and hinders the industrial applications of microbial fermentation. Stresses, especially oxidative stress generated during fermentation, inhibit microbial growth and production, and prolong fermentation period. Previous studies have shown that polypeptides could effectively relieve stresses, but the underlying mechanisms were poorly understood.ResultsIn this study, polypeptides (especially elastin peptide) addition improves the productivity of malic acid in A. niger, resulting in shortening of fermentation time from 120 to 108 h. Transcriptome and biochemical analyses demonstrated that both antioxidant enzyme-mediated oxidative stress defense system, such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and nonenzymatic antioxidant system, such as glutathione, were enhanced in the presence of elastin peptide, suggesting elastin peptide relieving oxidative stresses is involved in many pathways. In order to further investigate the relationship between oxidative stress defense and malic acid productivity, we overexpressed three enzymes (Sod1, CAT, Tps1) related to oxidation resistance in A. niger, respectively, and these resulting strains display varying degree of improvement in malic acid productivity. Especially, the strain overexpressing the Sod1 gene achieved a malate titer of 91.85 ± 2.58 g/L in 96 h, corresponding to a productivity of 0.96 g/L/h, which performs better than elastin peptide addition.ConclusionsOur investigation provides an excellent reference for alleviating the stress of the fungal fermentation process and improving fermentation efficiency.

The Antitumor and Toxicity Effects of Ruthenium(II) Complexes on Heterotopic Murine Colon Carcinoma Model

Abstract The aim of the present study was to examine the antitumor and toxicity effects of ruthenium(II) complexes, [Ru(Cltpy)(en)Cl][Cl] (Ru-1) and [Ru(Cl-tpy)(dach)Cl][Cl] (Ru-2) on heterotopic murine colon carcinoma model. For tumor induction, 1×106 CT26 cells suspended in 100 μl of DMEM were injected subcutaneously into flank of male BALB/c mice. Treatment groups were as follows: Ru-1, Ru-2, oxaliplatin and control (saline). The intraperitoneal administration of the tested complexes began on 6th day after CT26 cells inoculation. Each complex was administered at dose of 5 mg/kg, twice weekly, four doses in total. To assess toxicity, serum values of urea, creatinine, AST and ALT were determined and histopathological analysis of organs and tumor were performed. In order to assess the effects of Ru(II) complexes on markers of oxidative stress and antioxidant defense system, we determined the TBARS, GSH, SOD and CAT in the homogenate of tumor, heart, liver, lungs and kidney tissues. The findings indicate that Ru-1 and Ru-2 exerts equal or better antitumor activity in comparison with oxaliplatin, but with pronounced toxic effects such as reduced survival rate, cardiotoxicity, nephrotoxicity and hepatotoxicity. The increased index of lipid peroxidation in the tissues of the kidneys and heart, but decreased in tumor tissue, after Ru(II) complexes administration, indicates the importance of the induction of oxidative stress as a possible mechanism of nephrotoxicity and cardiotoxicity, but not the mechanism by which they realize antitumor activity. Additional studies are needed to elucidate the mechanism of antitumor activity and toxicity of the Ru(II) complexes.

Photothermal Conjugated Polymer Nanoparticles for Suppressing Breast Tumor Growth by Regulating TRPA1 Ion Channels.

Cancer cells survive by relying on oxidative stress defense against the accumulation of reactive oxygen species (ROS) during tumor formation. ROS-sensitive TRPA1 ion channels are overexpressed in breast cancer cells and induce a large influx of Ca2+ which upregulates the anti-apoptotic pathway to lead breast cancer cells to produce oxidative stress defense and enhance the resistance to ROS related chemotherapy. Targeting and inhibiting the TRPA1 ion channels are critical for breaking down the oxidative stress defense system and overcoming cellular resistance. Here, near-infrared (NIR) light-responsive conjugated polymer nanoparticles are designed and prepared to promote apoptosis of breast cancer cells, reduce cell drug resistance and suppress tumor growth through the remote and precise regulation of TRPA1 ion channels. Upon 808nm laser irradiation, the nanoparticles block the formation of Ca2+ /CaM complex and regulate the content of MCL-1 protein. Especially, the nanoparticles overcome drug resistance of cancer cells, therefore accelerating apoptosis of cancer cells and suppressing tumor growth in mice. Compared with carboplatin, the volume of tumor induced by NPs-H decreases by 54.1%. This work provides a strategy to disrupt the oxidative stress defense system and downregulate the antiapoptotic signaling pathway in cancer cells.

Simultaneous Elevation Of Antioxidant And Endocannabinoid Defense System May Prevent Dementia And Improve Cognitive Function In Humans

The incidence of dementia with or without Alzheimer’s disease (AD) is increasing despite extensive mechanistic studies and holistic approaches. There are no effective strategies for prevention or treatment with drugs. Analysis of cellular and molecular investigations suggest that increased oxidative stress is the earliest damage that initiates subsequent cellular defects such as chronic inflammation, mitochondrial dysfunction, increased production of Ab1-42 by cleavage of amyloid precursor protein (APP), hyperphosphorylation of tau protein, proteasome inhibition, and shortening of telomere, which are involved in increasing the risk of dementia. Humans have developed an antioxidant defense system (ADS) and endocannabinoid defense system (ECDS) to protect against external and internal stressors. Increased oxidative stress and chronic inflammation damage both defense systems. Therefore, the simultaneous elevation of these two defense systems may reduce the risk of dementia, improve cognitive function, and the effectiveness of drug therapy. Treatment with individual antioxidant compounds or elevation of endocannabinoids alone has failed to achieve the above goals. This review has proposed that a comprehensive mixture of micronutrients together with a stimulator of ECDS may simultaneously enhance the levels of ADS and ECDS, which can lead to a decrease in the risk of dementia, enhanced cognitive function, and improved efficacy of drug therapy in humans. Such an approach would simultaneously reduce the levels of oxidative damage and markers of chronic inflammation. Pre-clinical and clinical studies should be initiated to test the effectiveness of the proposed hypothesis.