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  1. Nelson VK, Pullaiah CP, Saleem Ts M, Roychoudhury S, Chinnappan S, Vishnusai B, et al.
    Adv Exp Med Biol, 2022;1391:161-179.
    PMID: 36472822 DOI: 10.1007/978-3-031-12966-7_10
    Prostate cancer is the most commonly diagnosed and frequently occurred cancer in the males globally. The current treatment strategies available to treat prostate cancer are not much effective and express various adverse effects. Hence, there is an urgent need to identify novel treatment that can improve patient outcome. From times immemorial, natural products are highly recognized for novel drug development for various diseases including cancer. Cancer cells generally maintain higher basal levels of reactive oxygen species (ROS) when compared to normal cells due to its high metabolic rate. However, initiation of excess intracellular ROS production can not be tolerated by the cancer cells and induce several cell death signals which are in contrast to normal cells. Therefore, small molecules of natural origin that induce ROS can potentially kill cancer cells in specific and provide a better opportunity to develop a novel drug therapy. In this review, we elaborated various classes of medicinal compounds and their mechanism of killing prostate cancer cells through direct or indirect ROS generation. This can generate a novel thought to develop promising drug candidate to treat prostate cancer patients.
    Matched MeSH terms: Oxidative Stress
  2. Tan BL, Norhaizan ME, Liew WP
    Oxid Med Cell Longev, 2018;2018:9719584.
    PMID: 29643982 DOI: 10.1155/2018/9719584
    There are different types of nutritionally mediated oxidative stress sources that trigger inflammation. Much information indicates that high intakes of macronutrients can promote oxidative stress and subsequently contribute to inflammation via nuclear factor-kappa B- (NF-κB-) mediated cell signaling pathways. Dietary carbohydrates, animal-based proteins, and fats are important to highlight here because they may contribute to the long-term consequences of nutritionally mediated inflammation. Oxidative stress is a central player of metabolic ailments associated with high-carbohydrate and animal-based protein diets and excessive fat consumption. Obesity has become an epidemic and represents the major risk factor for several chronic diseases, including diabetes, cardiovascular disease (CVD), and cancer. However, the molecular mechanisms of nutritionally mediated oxidative stress are complex and poorly understood. Therefore, this review aimed to explore how dietary choices exacerbate or dampen the oxidative stress and inflammation. We also discussed the implications of oxidative stress in the adipocyte and glucose metabolism and obesity-associated noncommunicable diseases (NCDs). Taken together, a better understanding of the role of oxidative stress in obesity and the development of obesity-related NCDs would provide a useful approach. This is because oxidative stress can be mediated by both extrinsic and intrinsic factors, hence providing a plausible means for the prevention of metabolic disorders.
    Matched MeSH terms: Oxidative Stress/physiology*
  3. Matough FA, Budin SB, Hamid ZA, Alwahaibi N, Mohamed J
    Sultan Qaboos Univ Med J, 2012 Feb;12(1):5-18.
    PMID: 22375253
    Diabetes is considered to be one of the most common chronic diseases worldwide. There is a growing scientific and public interest in connecting oxidative stress with a variety of pathological conditions including diabetes mellitus (DM) as well as other human diseases. Previous experimental and clinical studies report that oxidative stress plays a major role in the pathogenesis and development of complications of both types of DM. However, the exact mechanism by which oxidative stress could contribute to and accelerate the development of complications in diabetic mellitus is only partly known and remains to be clarified. On the one hand, hyperglycemia induces free radicals; on the other hand, it impairs the endogenous antioxidant defense system in patients with diabetes. Endogenous antioxidant defense mechanisms include both enzymatic and non-enzymatic pathways. Their functions in human cells are to counterbalance toxic reactive oxygen species (ROS). Common antioxidants include the vitamins A, C, and E, glutathione (GSH), and the enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GRx). This review describes the importance of endogenous antioxidant defense systems, their relationship to several pathophysiological processes and their possible therapeutic implications in vivo.
    Matched MeSH terms: Oxidative Stress*
  4. Alqahtani T, Deore SL, Kide AA, Shende BA, Sharma R, Dadarao Chakole R, et al.
    Mitochondrion, 2023 Jul;71:83-92.
    PMID: 37269968 DOI: 10.1016/j.mito.2023.05.007
    Misfolded proteins in the central nervous system can induce oxidative damage, which can contribute to neurodegenerative diseases in the mitochondria. Neurodegenerative patients face early mitochondrial dysfunction, impacting energy utilization. Amyloid-ß and tau problems both have an effect on mitochondria, which leads to mitochondrial malfunction and, ultimately, the onset of Alzheimer's disease. Cellular oxygen interaction yields reactive oxygen species within mitochondria, initiating oxidative damage to mitochondrial constituents. Parkinson's disease, linked to oxidative stress, α-synuclein aggregation, and inflammation, results from reduced brain mitochondria activity. Mitochondrial dynamics profoundly influence cellular apoptosis via distinct causative mechanisms. The condition known as Huntington's disease is characterized by an expansion of polyglutamine, primarily impactingthe cerebral cortex and striatum. Research has identified mitochondrial failure as an early pathogenic mechanism contributing to HD's selective neurodegeneration. The mitochondria are organelles that exhibit dynamism by undergoing fragmentation and fusion processes to attain optimal bioenergetic efficiency. They can also be transported along microtubules and regulateintracellular calcium homeostasis through their interaction with the endoplasmic reticulum. Additionally, the mitochondria produce free radicals. The functions of eukaryotic cells, particularly in neurons, have significantly deviated from the traditionally assigned role of cellular energy production. Most of them areimpaired in HD, which may lead to neuronal dysfunction before symptoms manifest. This article summarizes the most important changes in mitochondrial dynamics that come from neurodegenerative diseases including Alzheimer's, Parkinson's, Huntington's and Amyotrophic Lateral Sclerosis. Finally, we discussed about novel techniques that can potentially treat mitochondrial malfunction and oxidative stress in four most dominating neuro disorders.
    Matched MeSH terms: Oxidative Stress/physiology
  5. Low LE, Wang Q, Chen Y, Lin P, Yang S, Gong L, et al.
    Nanoscale, 2021 Jun 17;13(23):10197-10238.
    PMID: 34027535 DOI: 10.1039/d1nr02127c
    Neurodegenerative disorder is an illness involving neural dysfunction/death attributed to complex pathological processes, which eventually lead to the mortality of the host. It is generally recognized through features such as mitochondrial dysfunction, protein aggregation, oxidative stress, metal ions dyshomeostasis, membrane potential change, neuroinflammation and neurotransmitter impairment. The aforementioned neuronal dysregulations result in the formation of a complex neurodegenerative microenvironment (NME), and may interact with each other, hindering the performance of therapeutics for neurodegenerative disease (ND). Recently, smart nanoassemblies prepared from functional nanoparticles, which possess the ability to interfere with different NME factors, have shown great promise to enhance the diagnostic and therapeutic efficacy of NDs. Herein, this review highlights the recent advances of stimuli-responsive nanoassemblies that can effectively combat the NME for the management of ND. The first section outlined the NME properties and their interrelations that are exploitable for nanoscale targeting. The discussion is then extended to the controlled assembly of functional nanoparticles for the construction of stimuli-responsive nanoassemblies. Further, the applications of stimuli-responsive nanoassemblies for the enhanced diagnosis and therapy of ND are introduced. Finally, perspectives on the future development of NME-tailored nanomedicines are given.
    Matched MeSH terms: Oxidative Stress
  6. Ang TN, Young BR, Burrell R, Taylor M, Aroua MK, Baroutian S
    Chemosphere, 2021 Feb;264(Pt 2):128535.
    PMID: 33045509 DOI: 10.1016/j.chemosphere.2020.128535
    The emission of waste anaesthetic gas is a growing contributor to global warming and remains a factor in atmospheric ozone depletion. Volatile anaesthetics in medical waste gases could be removed via adsorption using suitable activated carbon materials possessing an enhanced affinity to anaesthetic molecules. In this work, the effects of surface physical and chemical properties on sevoflurane adsorption were investigated by oxidative hydrothermal surface modification of a commercial activated carbon using only distilled water. The hydrothermal surface modification was carried out at different treatment temperatures (150-300 °C) for varying durations (10-30 min), and adsorption was conducted under fixed conditions (bed depth = 10 cm, inlet concentration = 528 mg/L, and flow rate = 3 L/min). The hydrothermal treatment generally increased the BET surface area of the activated carbons. At oxidation temperatures above 200 °C, the micropore volume of the samples diminished. The relative amount of surface oxygen was enriched as the treatment temperature increased. Treatment duration did not significantly affect the introduction of relative amount of surface oxygen, except at higher temperatures. There were no new types of functional groups introduced. However, disappearance and re-formation of oxygen functional groups containing C-O structures (as in hydroxyl and ether groups) occurred when treatment temperature was increased from 150 to 200 °C, and when treatments were conducted above 200 °C, respectively. The ester/acetal groups were enriched under the temperature range studied. The findings suggested that the re-formation of surface oxygen functionalities might lead to the development of functional groups that improve sevoflurane adsorption.
    Matched MeSH terms: Oxidative Stress*
  7. Guan R, Van Le Q, Yang H, Zhang D, Gu H, Yang Y, et al.
    Chemosphere, 2021 May;271:129499.
    PMID: 33445014 DOI: 10.1016/j.chemosphere.2020.129499
    Phytochemicals refer to active substances in plant-based diets. Phytochemicals found in for example fruits, vegetables, grains and seed oils are considered relatively safe for consumption due to mammal-plant co-evolution and adaptation. A number of human diseases are related to oxidative stress caused by for example chemical environmental contaminants in air, water and food; while also lifestyle including smoking and lack of exercise and dietary preferences are important factors for disease development in humans. Here we explore the dietary sources of antioxidant phytochemicals that have beneficial effects on oxidative stress, cardiovascular and neurological diseases as well as cancer. Plant-based diets usually contain phenolic acids, flavonoids and carotenoids, which have strong antioxidant properties, and therefore remove the excess of active oxygen in the body, and protect cells from damage, reducing the risk of cardiovascular and Alzheimer's disease. In most cases, obesity is related to diet and inactivity and plant-based diets change lipid composition and metabolism, which reduce obesity related hazards. Cruciferous and Allium vegetables are rich in organic sulphides that can act on the metabolism of carcinogens and therefore used as anti-cancer and suppressing agents while dietary fibres and plant sterols may improve intestinal health and prevent intestinal diseases. Thus, we recommend a diet rich in fruits, vegetables, and grains as its content of phytochemicals may have the potential to prevent or improve a broad sweep of various diseases.
    Matched MeSH terms: Oxidative Stress*
  8. Shazia Q, Mohammad ZH, Rahman T, Shekhar HU
    Anemia, 2012;2012:270923.
    PMID: 22645668 DOI: 10.1155/2012/270923
    Beta thalassemia major is an inherited disease resulting from reduction or total lack of beta globin chains. Patients with this disease need repeated blood transfusion for survival. This may cause oxidative stress and tissue injury due to iron overload, altered antioxidant enzymes, and other essential trace element levels. The aim of this review is to scrutinize the relationship between oxidative stress and serum trace elements, degree of damage caused by oxidative stress, and the role of antioxidant enzymes in beta thalassemia major patients. The findings indicate that oxidative stress in patients with beta thalassemia major is mainly caused by tissue injury due to over production of free radical by secondary iron overload, alteration in serum trace elements and antioxidant enzymes level. The role of trace elements like selenium, copper, iron, and zinc in beta thalassemia major patients reveals a significant change of these trace elements. Studies published on the status of antioxidant enzymes like catalase, superoxide dismutase, glutathione, and glutathione S-transferase in beta thalassemia patients also showed variable results. The administration of selective antioxidants along with essential trace elements and minerals to reduce the extent of oxidative damage and related complications in beta thalassemia major still need further evaluation.
    Matched MeSH terms: Oxidative Stress*
  9. Nazmi NASM, Razak FIA, Mokhtar WNAW, Ibrahim MNM, Adam F, Yahaya N, et al.
    Environ Sci Pollut Res Int, 2022 Jan;29(1):1009-1020.
    PMID: 34341936 DOI: 10.1007/s11356-021-15733-1
    The world faces the challenge to produce ultra-low sulfur diesel with low-cost technology. Therefore, this research emphasised on production of low sulfur fuel utilising nanoparticle catalyst under mild condition. A small amount of cobalt oxide (10-30 wt%) was introduced into the Fe/Al2O3 catalyst through the wet impregnation method. Cobalt modification induces a positive effect on the performance of the iron catalyst. Hence, the insertion of cobalt species into Fe/Al2O3 led to the formation of lattice fringes in all directions which resulted in the formation of Co3O4 and Fe3O4 species. The optimised catalyst, Co/Fe-Al2O3, calcined at 400 °C with a dopant ratio of 10:90 indicating the highest desulfurisation activity by removing 96% of thiophene, 100% of dibenzothiophene (DBT) and 92% of 4,6-dimethyl dibenzothiophene (4,6-DMDBT). Based on the density functional theory (DFT) on Co/Fe-Al2O3, two pathways with the overall energy of -40.78 eV were suggested for the complete oxidation of DBT.
    Matched MeSH terms: Oxidative Stress*
  10. Mathialagan RD, Abd Hamid Z, Ng QM, Rajab NF, Shuib S, Binti Abdul Razak SR
    PMID: 32823552 DOI: 10.3390/ijerph17165865
    Hematopoietic stem/progenitor cells (HSPCs) are susceptible to benzene-induced genotoxicity. However, little is known about the mechanism of DNA damage response affecting lineage-committed progenitors for myeloid, erythroid, and lymphoid. Here, we investigated the genotoxicity of a benzene metabolite, 1,4-benzoquinone (1,4-BQ), in HSPCs using oxidative stress and lineage-directed approaches. Mouse bone marrow cells (BMCs) were exposed to 1,4-BQ (1.25-12 μM) for 24 h, followed by oxidative stress and genotoxicity assessments. Then, the genotoxicity of 1,4-BQ in lineage-committed progenitors was evaluated using colony forming cell assay following 7-14 days of culture. 1,4-BQ exposure causes significant decreases (p < 0.05) in glutathione level and superoxide dismutase activity, along with significant increases (p < 0.05) in levels of malondialdehyde and protein carbonyls. 1,4-BQ exposure induces DNA damage in BMCs by significantly (p < 0.05) increased percentages of DNA in tail at 7 and 12 μM and tail moment at 12 μM. We found crucial differences in genotoxic susceptibility based on percentages of DNA in tail between lineage-committed progenitors. Myeloid and pre-B lymphoid progenitors appeared to acquire significant DNA damage as compared with the control starting from a low concentration of 1,4-BQ exposure (2.5 µM). In contrast, the erythroid progenitor showed significant damage as compared with the control starting at 5 µM 1,4-BQ. Meanwhile, a significant (p < 0.05) increase in tail moment was only notable at 7 µM and 12 µM 1,4-BQ exposure for all progenitors. Benzene could mediate hematological disorders by promoting bone marrow oxidative stress and lineage-specific genotoxicity targeting HSPCs.
    Matched MeSH terms: Oxidative Stress*
  11. Khor YP, Wan SY, Tan CP, Zhao G, Li C, Wang Y, et al.
    Food Res Int, 2021 03;141:109897.
    PMID: 33641946 DOI: 10.1016/j.foodres.2020.109897
    Basa catfish is a good source for fish oil extraction, which was believed to have good thermo-oxidative stability because of its similar fatty acid composition to that of palm olein (PO). The thermo-oxidative stability of PO, basa catfish oil (FO), and palm olein-basa fish oil blend (PO-FO; ratio 1:1) was evaluated after 75 frying cycles. No significant difference was observed in p-anisidine value, TOTOX value, conjugated trienes, monomeric oxidized triacylglycerols, and free fatty acids concentration after frying. Moreover, compared to PO, FO exhibited lighter color, lower acid value, conjugated dienes, polymerized triacylglycerol, and total polar content. The PO-FO blend also demonstrated a more favorable frying stability compared to the other two frying systems. These findings indicated that FO could be proposed as a promising alternative to common PO, and its blending with other vegetable oils at an appropriate ratio might improve the overall oil frying quality for future industrial applications.
    Matched MeSH terms: Oxidative Stress
  12. Azman KF, Safdar A, Zakaria R
    Exp Gerontol, 2021 07 15;150:111372.
    PMID: 33905879 DOI: 10.1016/j.exger.2021.111372
    Aging is associated with a variety of morphological and functional changes in the liver. Oxidative stress and inflammation are now widely accepted as the main mechanisms involved in the aging process that may subsequently cause severe injury to mitochondrial DNA which leads to apoptosis. As aging may increase the risks for various liver diseases and plays as an adverse prognostic factor increasing the mortality rate, knowledge regarding the mechanisms of age-related liver susceptibility and the possible therapeutic interventions is imperative. Due to cost and time constraints, a mimetic aging model is generally preferred to naturally aged animals to study the underlying mechanisms of aging liver. The use of D-galactose in aging research is dated back to 1962 and has since been used widely. This review aims to comprehensively summarize the effects of D-galactose-induced aging on the liver and the underlying mechanisms involved. Its potential therapeutic interventions are also discussed. It is hoped that this invaluable information may facilitate researchers in choosing the appropriate aging model and provide a valuable platform for testing potential therapeutic strategies for the prevention and treatment of age-related liver diseases.
    Matched MeSH terms: Oxidative Stress
  13. Zhang C, Ho SH, Chen WH, Wang R, Show PL, Ong HC
    J Biotechnol, 2021 Sep 10;338:81-90.
    PMID: 34298023 DOI: 10.1016/j.jbiotec.2021.07.009
    Microalgae are a promising feedstock for carbon-neutral biofuel production due to their superior cellular composition. Alternatively, oxidative torrefaction has been recognized as a potential thermochemical technique for microalgal solid biofuel upgrading. Herein, by using microalga N. oceanica as a feedstock, several characterizations are adopted for evaluating the potential of oxidative torrefaction towards microalgal solid biofuel production. The oxidatively torrefied microalgae can be upgraded as lignite. After in-depth analysis, significant change in the surface microstructure of oxidatively torrefied microalgae is largely changed (via wrinkle and fragmentation) The hydrophobicity, thermal decomposition, thermal stability, and aromatization of oxidatively torrefied microalgae can be largely enhanced as the oxidative torrefaction severity increase. With the increasing torrefaction temperature, the hydrophobicity of oxidative torrefied microalgae gradually improved. The decomposition of C-2/3/5, and -OCH3, the CO bonds of CH3CO-, and the aromatization occurs via oxidative torrefaction according to the NMR analysis. For XPS analysis, torrefaction operation significantly decreases the carbide carbon and enhances the graphitization. As a result, the thermal stability of oxidatively torrefied microalgae is improved. Conclusively, the information obtained in this study can provide insights into the evaluation of oxidative torrefaction performance and fuel properties of microalgal solid biofuel, which may help accelerate the advancement of oxidative torrefaction industrialization.
    Matched MeSH terms: Oxidative Stress
  14. Wisam, Nabil lbrahim, Norsidah KZ, Samsul D, Zamzila A, Rafidah HM
    MyJurnal
    Essential hypertension is a multifactorial disease. Many experimental studies have elucidated
    the role of oxidative stress and atherosclerosis in the pathogenesis of essential hypertension. Apolipoprotein
    E is a plasma protein that is found to have antioxidant properties, and it also protects against atherosclerosis.
    Interestingly, the biological function of apolipoprotein E is strongly affected by polymorphisms in its gene.
    Based on this evidence, our aim was to investigate the association of apolipoprotein E gene polymorphisms with
    essential hypertension.
    Matched MeSH terms: Oxidative Stress
  15. Choo BKM, Shaikh MF
    Curr Neuropharmacol, 2021;19(9):1496-1518.
    PMID: 33998991 DOI: 10.2174/1570159X19666210517120413
    Curcuma longa (Turmeric) is a tropical herbaceous perennial plant of the family Zingiberaceae and contains curcuminoids, sesquiterpenoids and monoterpenoids as its major components. Given the broad range of activities that Curcuma longa possesses and also its use as a traditional epilepsy remedy, this review attempts to systematically review the experimentally proven activities of Curcuma longa and its bioactive components, which are related to the management of epileptic seizures. Using the PRISMA model, five databases (Google Scholar, PubMed, ScienceDirect, SCOPUS and SpringerLink) were searched using the keywords ["Curcuma longa" AND "Epilepsy"] and ["Curcuma longa" AND "Seizures"], leaving 34 articles that met the inclusion criteria. The present systematic review elaborated on the experimentally proven potential of Curcuma longa components, such as an aqueous extract of Curcuma longa itself, Curcuma longa oil and active constituents like curcuminoids and bisabolene sesquiterpenoids found in Curcuma longa with anti-seizure potential. Using human equivalent dose calculations, human treatment parameters were suggested for each component by analysing the various studies in this review. This review also determined that the principal components possibly exert their anti-seizure effect via the reduction of corticosterone, modulation of neurotransmitters signalling, modulation of sodium ion channels, reduction of oxidative DNA damage, reduction of lipid peroxidation, upgregulation of brain-derived neurotrophic factor (BDNF) and γ-aminobutyric acid (GABA) mediated inhibition. It is anticipated that this review will help pave the way for future research into the development of Curcuma longa and its neuroactive constituents as potential drug candidates for the management of epilepsy.
    Matched MeSH terms: Oxidative Stress
  16. Abdulhameed EA, Al-Rawi NH, Omar M, Khalifa N, Samsudin ABR
    PeerJ, 2022;10:e12951.
    PMID: 35261818 DOI: 10.7717/peerj.12951
    BACKGROUND: Titanium dioxide dental implants have a controversial effect on reactive oxygen species (ROS) production. ROS is necessary for cellular signal transmission and proper metabolism, but also has the ability to cause cell death as well as DNA, RNA, and proteins damage by excessive oxidative stress. This study aimed to systematically review the effect of titanium dioxide dental implant-induced oxidative stress and its role on the osteogenesis-angiogenesis coupling in bone remodeling.

    METHODS: This systematic review was performed conforming to preferred reporting items for systematic review and meta-analysis (PRISMA) model. Four different databases (PubMed, Science Direct, Scopus and Medline databases) as well as manual searching were adopted. Relevant studies from January 2000 till September 2021 were retrieved. Critical Appraisal Skills Programme (CASP) was used to assess the quality of the selected studies.

    RESULTS: Out of 755 articles, only 14 which met the eligibility criteria were included. Six studies found that titanium dioxide nanotube (TNT) reduced oxidative stress and promoted osteoblastic activity through its effect on Wnt, mitogen-activated protein kinase (MAPK) and forkhead box protein O1 (FoxO1) signaling pathways. On the other hand, three studies confirmed that titanium dioxide nanoparticles (TiO2NPs) induce oxidative stress, reduce ostegenesis and impair antioxidant defense system as a significant negative correlation was found between decreased SIR3 protein level and increased superoxide (O2 •-). Moreover, five studies proved that titanium implant alloy enhances the generation of ROS and induces cytotoxicity of osteoblast cells via its effect on NOX pathway.

    CONCLUSION: TiO2NPs stimulate a wide array of oxidative stress related pathways. Scientific evidence are in favor to support the use of TiO2 nanotube-coated titanium implants to reduce oxidative stress and promote osteogenesis in bone remodeling. To validate the cellular and molecular cross talk in bone remodeling of the present review, well-controlled clinical trials with a large sample size are required.

    Matched MeSH terms: Oxidative Stress
  17. Apparoo Y, Phan CW, Kuppusamy UR, Sabaratnam V
    Exp Gerontol, 2022 Dec;170:111982.
    PMID: 36244584 DOI: 10.1016/j.exger.2022.111982
    Healthy ageing is a crucial process that needs to be highlighted as it affects the quality of lifespan. An increase in oxidative stress along with ageing is the major factor related to the age-associated diseases, especially neurodegenerative disorders. An antioxidant-rich diet has been proven to play a significant role in the ageing process. Targeting ageing mechanisms could be a worthwhile approach to improving health standards. Ergothioneine (EGT), a hydrophilic compound with specific transporter known as OCTN1, has been shown to exert anti-ageing properties. In addition to its antioxidant effect, EGT has been reported to have anti-senescence, anti-inflammatory and anti-neurodegenerative properties. This review aims to define the pivotal role of EGT in major signalling pathways in ageing such as insulin/insulin-like growth factor (IGF) signalling (IIS), sirtuin 6 (SIRT6) and mammalian target of rapamycin complex (mTOR) pathways. The review further discusses evidence of EGT on neurodegeneration in its therapeutic context in various model organisms, providing new insights into improving health. In conclusion, an ergothioneine-rich diet may be beneficial in preventing age-related diseases, resulting in a healthy ageing population.
    Matched MeSH terms: Oxidative Stress
  18. Foo SC, Chapman IJ, Hartnell DM, Turner AD, Franklin DJ
    Environ Sci Pollut Res Int, 2020 Nov;27(31):38916-38927.
    PMID: 32638304 DOI: 10.1007/s11356-020-09729-6
    The application of hydrogen peroxide (H2O2) as a management tool to control Microcystis blooms has become increasingly popular due to its short lifetime and targeted action. H2O2 increases intracellular reactive oxygen species resulting in oxidative stress and subsequently cell death. H2O2 is naturally produced in freshwater bodies as a result of photocatalytic reactions between dissolved organic carbon and sunlight. Previously, some studies have suggested that this environmental source of H2O2 selectively targets for toxigenic cyanobacteria strains in the genus Microcystis. Also, past studies only focused on the morphological and biochemical changes of H2O2-induced cell death in Microcystis with little information available on the effects of different H2O2 concentrations on growth, esterase activity and membrane integrity. Therefore, this study investigated the effects of non-lethal (40-4000 nM) concentrations on percentage cell death; with a focus on sub-lethal (50 μM) and lethal (275 μM; 500 μM) doses of H2O2 on growth, cells showing esterase activity and membrane integrity. The non-lethal dose experiment was part of a preliminary study. Results showed a dose- and time-dependent relationship in all three Microcystis strains post H2O2 treatment. H2O2 resulted in a significant increase in intracellular reactive oxygen species, decreased chlorophyll a content, decreased growth rate and esterase activity. Interestingly, at sub-lethal (50 μM H2O2 treatment), percentage of dead cells in microcystin-producing strains was significantly higher (p 
    Matched MeSH terms: Oxidative Stress
  19. Amir Yusri MA, Sekar M, Wong LS, Gan SH, Ravi S, Subramaniyan V, et al.
    Drug Des Devel Ther, 2023;17:1079-1096.
    PMID: 37064431 DOI: 10.2147/DDDT.S389977
    Celastrol is a naturally occurring chemical isolated from Tripterygium wilfordii Hook. f., root extracts widely known for their neuroprotective properties. In this review, we focus on the efficacy of celastrol in mitigating memory impairment (MI) in both in vivo and in vitro models. Scopus, PubMed and Web of Science databases were utilised to locate pertinent literatures that explore the effects of celastrol in the brain, including its pharmacokinetics, bioavailability, behavioral effects and some of the putative mechanisms of action on memory in many MI models. To date, preclinical studies strongly suggest that celastrol is highly effective in enhancing the cognitive performance of MI animal models, particularly in the memory domain, including spatial, recognition, retention and reference memories, via reduction in oxidative stress and attenuation of neuro-inflammation, among others. This review also emphasised the challenges and potential associated enhancement of medication delivery for MI treatment. Additionally, the potential structural alterations and derivatives of celastrol in enhancing its physicochemical and drug-likeness qualities are examined. The current review demonstrated that celastrol can improve cognitive performance and mitigate MI in several preclinical investigations, highlighting its potential as a natural lead molecule for the design and development of a novel neuroprotective medication.
    Matched MeSH terms: Oxidative Stress
  20. Allam VSRR, Paudel KR, Gupta G, Singh SK, Vishwas S, Gulati M, et al.
    Environ Sci Pollut Res Int, 2022 Sep;29(42):62733-62754.
    PMID: 35796922 DOI: 10.1007/s11356-022-21454-w
    Asthma is a chronic inflammatory disease primarily characterized by inflammation and reversible bronchoconstriction. It is currently one of the leading causes of morbidity and mortality in the world. Oxidative stress further complicates the pathology of the disease. The current treatment strategies for asthma mainly involve the use of anti-inflammatory agents and bronchodilators. However, long-term usage of such medications is associated with severe adverse effects and complications. Hence, there is an urgent need to develop newer, novel, and safe treatment modalities for the management of asthma. This has therefore prompted further investigations and detailed research to identify and develop novel therapeutic interventions from potent untapped resources. This review focuses on the significance of oxidative stressors that are primarily derived from both mitochondrial and non-mitochondrial sources in initiating the clinical features of asthma. The review also discusses the biological scavenging system of the body and factors that may lead to its malfunction which could result in altered states. Furthermore, the review provides a detailed insight into the therapeutic role of nutraceuticals as an effective strategy to attenuate the deleterious effects of oxidative stress and may be used in the mitigation of the cardinal features of bronchial asthma.
    Matched MeSH terms: Oxidative Stress
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