Reactive oxygen species, toxicity, oxidative stress, and antioxidants: chronic diseases and aging

Archives of Toxicology, Journal Year: 2023, Volume and Issue: 97(10), P. 2499 - 2574

Published: Aug. 19, 2023

Abstract A physiological level of oxygen/nitrogen free radicals and non-radical reactive species (collectively known as ROS/RNS) is termed oxidative eustress or “good stress” characterized by low to mild levels oxidants involved in the regulation various biochemical transformations such carboxylation, hydroxylation, peroxidation, modulation signal transduction pathways Nuclear factor-κB (NF-κB), Mitogen-activated protein kinase (MAPK) cascade, phosphoinositide-3-kinase, nuclear factor erythroid 2–related 2 (Nrf2) other processes. Increased ROS/RNS, generated from both endogenous (mitochondria, NADPH oxidases) and/or exogenous sources (radiation, certain drugs, foods, cigarette smoking, pollution) result a harmful condition stress (“bad stress”). Although it widely accepted, that many chronic diseases are multifactorial origin, they share common denominator. Here we review importance mechanisms through which contributes pathological states an organism. Attention focused on chemistry ROS RNS (e.g. superoxide radical, hydrogen peroxide, hydroxyl radicals, peroxyl nitric oxide, peroxynitrite), their role damage DNA, proteins, membrane lipids. Quantitative qualitative assessment biomarkers also discussed. Oxidative pathology cancer, cardiovascular diseases, diabetes, neurological disorders (Alzheimer’s Parkinson’s Down syndrome), psychiatric (depression, schizophrenia, bipolar disorder), renal disease, lung disease (chronic pulmonary obstruction, cancer), aging. The concerted action antioxidants ameliorate effect achieved antioxidant enzymes (Superoxide dismutases-SODs, catalase, glutathione peroxidase-GPx), small molecular weight (vitamins C E, flavonoids, carotenoids, melatonin, ergothioneine, others). Perhaps one most effective vitamin first line defense against peroxidation promising approach appears be use flavonoids), showing weak prooxidant properties may boost cellular systems thus act preventive anticancer agents. Redox metal-based enzyme mimetic compounds potential pharmaceutical interventions sirtuins therapeutic targets for age-related anti-aging strategies

Language: Английский

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Role of Oxidative Stress in Blood–Brain Barrier Disruption and Neurodegenerative Diseases

Antioxidants, Journal Year: 2024, Volume and Issue: 13(12), P. 1462 - 1462

Published: Nov. 28, 2024

Upregulation of reactive oxygen species (ROS) levels is a principal feature observed in the brains neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s (AD). In these diseases, oxidative stress can disrupt blood–brain barrier (BBB). This disruption allows neurotoxic plasma components, blood cells, pathogens to enter brain, leading increased ROS production, mitochondrial dysfunction, inflammation. Collectively, factors result protein modification, lipid peroxidation, DNA damage, and, ultimately, neural cell damage. this review article, we present mechanisms by which damage leads BBB breakdown brain diseases. Additionally, summarize potential therapeutic approaches aimed at reducing that contributes

Language: Английский

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Astaxanthin Inhibits H2O2-Induced Excessive Mitophagy and Apoptosis in SH-SY5Y Cells by Regulation of Akt/mTOR Activation

Marine Drugs, Journal Year: 2024, Volume and Issue: 22(2), P. 57 - 57

Published: Jan. 24, 2024

Oxidative stress, which damages cellular components and causes mitochondrial dysfunction, occurs in a variety of human diseases, including neurological disorders. The clearance damaged mitochondria via mitophagy maintains the normal function facilitates cell survival. Astaxanthin is an antioxidant known to have neuroprotective effects, but underlying mechanisms remain unclear. This study demonstrated that astaxanthin inhibited H

Language: Английский

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Protective effect of flavonoids on oxidative stress injury in Alzheimer’s disease

Natural Product Research, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 28

Published: June 23, 2024

Alzheimer's disease (AD) is the most common neurodegenerative disease, which mainly caused by damage of structure and function central nervous system. At present, there are many adverse reactions in market-available drugs, can't significantly inhibit occurrence AD. Therefore, current focus research to find safe effective therapeutic drugs improve clinical treatment Oxidative stress bridges different mechanism hypotheses AD plays a key role Numerous studies have shown that natural flavonoids good antioxidant effects. They can directly or indirectly resist ­oxidative stress, Aβ aggregation Tau protein hyperphosphorylation activating Nrf2 other oxidation-antioxidation-related signals, regulating synaptic function-related pathways, promoting mitochondrial autophagy, etc., play neuroprotective In this review, we summarised inhibiting oxidative injury recent years. Moreover, because shortcomings poor biofilm permeability low bioavailability flavonoids, advantages progress nano-drug delivery systems such as liposomes solid lipid nanoparticles were highlighted. We hope review provides useful way explore treatments.

Language: Английский

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Microglial polarization in Alzheimer's disease: Mechanisms, implications, and therapeutic opportunities

Journal of Alzheimer s Disease, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 2, 2025

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-β plaques, neurofibrillary tangles, and chronic neuroinflammation. Microglial cells, resident immune cells in central nervous system, play crucial role pathogenesis AD. Microglia can undergo polarization, shifting between pro-inflammatory (M1) anti-inflammatory (M2) phenotypes response to different stimuli. Dysregulation microglial polarization towards phenotype leads release inflammatory cytokines, oxidative stress, synaptic dysfunction. These processes contribute neuronal damage cognitive decline However, several challenges remain this field. The complex molecular mechanisms governing AD need be further elucidated. In review, we discuss underlying its implications progression.

Language: Английский

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Chemical composition, antioxidant activities, and enzyme inhibitory effects of Lespedeza bicolour Turcz. essential oil

Journal of Enzyme Inhibition and Medicinal Chemistry, Journal Year: 2025, Volume and Issue: 40(1)

Published: Feb. 6, 2025

Lespedeza bicolour Turcz. is a traditional medicinal plant with wide range of ethnomedicinal values. The main components L. essential oil (EO) were β-pinene (15.41%), β-phellandrene (12.43%), and caryophyllene (7.79%). EO showed antioxidant activity against ABTS radical DPPH an IC50 value 0.69 ± 0.03 mg/mL 10.44 2.09 mg/mL, respectively. FRAP was 81.96 6.17 μmol/g. had activities acetylcholinesterase, α-glucosidase, β-lactamase values 309.30 11.16 μg/mL, 360.47 35.67 27.54 1.21 Molecular docking methyl dehydroabietate docked well all tested enzymes. Sclareol (+)-borneol acetate the strongest binding affinity to α-glucosidase β-lactamase, present study provides direction for searching enzyme inhibitors three enzymes shows possesses potential treat series diseases.

Language: Английский

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Integrated spatial metabolomics and network pharmacology to explore the pharmacodynamic substances and mechanism of Radix ginseng-Schisandra chinensis Herb Couple on Alzheimer’s disease

Analytical and Bioanalytical Chemistry, Journal Year: 2024, Volume and Issue: 416(19), P. 4275 - 4288

Published: June 10, 2024

Language: Английский

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Alkaloid-rich fraction from Luffa cylindrica Linn fruit enhances memory and mitigates oxidative stress in hippocampus of ozone-exposed sprague Dawley rat via LCMS and network pharmacology approach

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: 289, P. 117686 - 117686

Published: Jan. 1, 2025

Luffa cylindrica (L.), is a medicinal plant aimed to investigate the efficacy of alkaloid-rich fraction (ARF) extracted from L. cylindrica. The study employed behavioural analysis rat using Morris water maze (MWM), biochemical apoptotic proteins, Immunohistochemistry caspase 3 protein and network pharmacology approach. ozone-induced group exhibited complex behavioral changes. Western blot revealed altered expression SOD2, Caspase 3, Cytochrome C which play integral roles in oxidative stress, apoptosis, mitochondrial function. Histopathological hippocampus further supported neuroprotective potential cylindrica, demonstrating reduction neuropathological lesions improved memory processes. Network Pharmacology showed implication GSK3β neuronal damage. ARF promise preventing In summary, this comprehensive sheds light on its applications by vivo molecular analyses. It provides holistic understanding properties ARF, encouraging exploration for therapeutic interventions neurological diseases.

Language: Английский

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Gp93 safeguards tissue homeostasis by preventing ROS-JNK-mediated apoptosis

Redox Biology, Journal Year: 2025, Volume and Issue: 81, P. 103537 - 103537

Published: Feb. 8, 2025

Reactive oxygen species (ROS) play a pivotal role in maintaining tissue homeostasis, yet their overabundance can impair normal cellular functions, induce cell death, and potentially lead to neurodegenerative disorders. This study identifies Drosophila Glycoprotein 93 (Gp93) as crucial factor that safeguards homeostasis preserves neuronal functions by preventing ROS-induced, JNK-dependent apoptotic death. Firstly, loss of Gp93 induces apoptosis primarily through the induction ROS. Secondary, neuro-specific depletion results ROS-JNK-mediated neurodegeneration. Thirdly, overexpression effectively curtails oxidative stress neurodegeneration caused paraquat exposure or aging process. Furthermore, these be substituted its human ortholog, HSP90B1. Lastly, HSP90B1 cultured cells triggers ROS production, JNK activation, apoptosis. Thus, this not only unveils novel physiological function Gp93, but also provides valuable insights for understanding pathological

Language: Английский

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Cremastra appendiculata Polysaccharides Alleviate Neurodegenerative Diseases in Caenorhabditis elegans: Targeting Amyloid-β Toxicity, Tau Toxicity and Oxidative Stress

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(8), P. 3900 - 3900

Published: April 20, 2025

Alzheimer’s disease (AD) is characterized by oxidative stress, amyloid-beta (Aβ) deposition, and tau hyperphosphorylation. While polysaccharides have demonstrated anti-AD effects, the properties of Cremastra appendiculata (CAPs) remain underexplored. This study evaluates physicochemical properties, antioxidant activity, underlying mechanisms CAP in vitro Caenorhabditis elegans (C. elegans) AD models. CAP, containing 22.37% uronic acid, stable below 270 °C adopts a triple helix structure. Scanning electron microscopy (SEM) reveals an irregular layered architecture. In vitro, exhibits significant protecting PC12 cells from Aβ-induced cytotoxicity. C. elegans, extends lifespan concentration-dependent manner without affecting growth, alleviating tau-induced locomotor defects, reducing paralysis serotonin hypersensitivity, decreasing Aβ deposition 79.96% at 2.0 mg/mL. enhances capacity heat resistance reactive oxygen species (ROS) levels increasing glutathione S-transferase 4 (GST-4) peroxidase (GSH-Px) activities. Additionally, upregulates key genes insulin/insulin-like growth factor signaling pathway, including daf-16 skn-1, along with their downstream targets (sod-3, ctl-1, gst-4, hsp-70). These findings suggest that has potent Aβ- toxicity, may serve as promising therapeutic agent for disease.

Language: Английский

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