Free Radical Research最新文献

Cutting-edge insights into Helicobacter research. 对螺旋杆菌研究的前沿见解。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-11-06 DOI: 10.1080/10715762.2024.2421174

Hideki Mori, Hidekazu Suzuki

{"title":"Cutting-edge insights into Helicobacter research.","authors":"Hideki Mori, Hidekazu Suzuki","doi":"10.1080/10715762.2024.2421174","DOIUrl":"https://doi.org/10.1080/10715762.2024.2421174","url":null,"abstract":"Non-Helicobacter pylori Helicobacter (NHPH) species are emerging as significant gastric pathogens. Despite their clinical importance, NHPH infections are less studied compared to Helicobacter pylori (H. pylori) due to their lower prevalence and diagnostic challenges. Zoonotic transmission, particularly from pigs, dogs, and cats, underscores the need for improved diagnostic methods and heightened clinical awareness. Gastric cancer (GC) remains a major global health issue, with H. pylori being a primary risk factor. The eradication of H. pylori reduces GC risk, but post-eradication surveillance is essential. Endoscopic findings, especially those from the Kyoto classification, and noninvasive biomarkers play crucial roles in early GC detection and risk assessment. The increasing antibiotic resistance in H. pylori necessitates new treatment strategies. Novel therapies, such as vonoprazan-based regimens, and alternatives like sitafloxacin and rifabutin, are being developed to improve eradication success rates. Understanding the fundamental mechanisms of gastric carcinogenesis, including the roles of oxidative stress and cancer stem cells, is key to advancing treatment. Targeting specific molecular pathways offers potential for more effective therapies.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Protective effect of alpha-tocopherol on lipogenesis and oxysterol production in hypercholesterolemia-induced nonalcoholic steatohepatitis. α-生育酚对高胆固醇血症诱发的非酒精性脂肪性肝炎的脂肪生成和氧杂环醇产生的保护作用

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-10-30 DOI: 10.1080/10715762.2024.2421173

Ali Sahin, Tugce Demirel-Yalciner, Erdi Sozen, Nesrin Kartal Ozer

{"title":"Protective effect of alpha-tocopherol on lipogenesis and oxysterol production in hypercholesterolemia-induced nonalcoholic steatohepatitis.","authors":"Ali Sahin, Tugce Demirel-Yalciner, Erdi Sozen, Nesrin Kartal Ozer","doi":"10.1080/10715762.2024.2421173","DOIUrl":"10.1080/10715762.2024.2421173","url":null,"abstract":"Despite limited number of studies, oxysterols are known to contribute to the progression of nonalcoholic steatohepatitis (NASH) by affecting lipid/cholesterol metabolism and elevating proinflammatory and profibrotic processes. Accordingly, we used a high cholesterol-mediated in vivo NASH model and aimed to determine alterations in fatty acid content and oxysterol levels together with their effects on cholesterol/lipid metabolism during the progression of the disease. We further investigated the beneficial role of α-tocopherol. To this end, in our hypercholesterolemic rabbit model, we determined fatty acid profile by GC-MS while 25-, 27-, 4β-, 7α, and 24(S)-Hydroxycholesterol levels by means of LC-MS/MS. Additionally, lipid (SREBP-1c, PPARα, PPARγ) and cholesterol metabolism-related proteins (LXRα, SREBP2 and ABCA1) were determined by immunoblotting. In conclusion, the present findings provide a complete analysis of the hepatic alterations in lipid and oxysterol profiles mediated by a high-cholesterol diet. In addition, this study explains the protective effect of α-tocopherol on lipogenesis and oxysterol production in hypercholesterolemia-induced NASH. We believe that present study will guide to novel theories in the progression and therapeutic targeting of fatty liver diseases.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Redox factors in the antioxidant activity of nitroxides toward DNA guanyl and 2-deoxyribose-peroxyl radicals. 硝基化合物对 DNA 鸟苷酸和 2-脱氧核糖过氧自由基的抗氧化活性中的氧化还原因素。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-10-24 DOI: 10.1080/10715762.2024.2417278

Wen Qi, Smitha U Nair, David I Pattison, Robert F Anderson

{"title":"Redox factors in the antioxidant activity of nitroxides toward DNA guanyl and 2-deoxyribose-peroxyl radicals.","authors":"Wen Qi, Smitha U Nair, David I Pattison, Robert F Anderson","doi":"10.1080/10715762.2024.2417278","DOIUrl":"https://doi.org/10.1080/10715762.2024.2417278","url":null,"abstract":"A series of eight nitroxide compounds (four substituted piperidines, three pyrrolidines and one oxo-piperidine) are found to undergo electron transfer to 2'-deoxyribose-peroxyl and the guanyl radical. One-electron oxidation potentials of the nitroxides to oxoammonium cations (oxoammonium reduction potential), E0', have been measured against a common redox indicator, chlorpromazine, and found to span the range 751 ± 15 mV to 973 ± 15 mV. Fast chemical reduction of the 2'-deoxyribose-peroxyl radical to the hydroperoxide, generated by •OH radical attack on 2-deoxyribose, dR, in oxygenated aqueous solution, is a redox-dependent reaction, with rate constants of 0.8-3.5 x 107 M-1 s-1.The guanyl radicals, produced upon one-electron oxidation of 2'-deoxyguanosine monophosphate, dG, by the selenite radical, SeO3•-, react with the nitroxides in a redox-independent reaction with diffusion rate constants of 1-2 x 108 M-1 s-1. These findings represent a possible antioxidant role for nitroxides in the fast chemical repair of DNA radicals, which is supported by an in vitro strand break study using a plasmid.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142497944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The impact of hyperbaric oxygen therapy on the redox balance of patients with diabetic foot syndrome. 高压氧疗法对糖尿病足综合征患者氧化还原平衡的影响。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-10-19 DOI: 10.1080/10715762.2024.2417286

Paweł Sutkowy, Jarosław Paprocki, Jacek Piechocki, Alina Woźniak

{"title":"The impact of hyperbaric oxygen therapy on the redox balance of patients with diabetic foot syndrome.","authors":"Paweł Sutkowy, Jarosław Paprocki, Jacek Piechocki, Alina Woźniak","doi":"10.1080/10715762.2024.2417286","DOIUrl":"https://doi.org/10.1080/10715762.2024.2417286","url":null,"abstract":"Diabetic foot wounds associated with oxidative stress are treated with hyperbaric oxygen (HBO), but that may also induce the stress itself; therefore, we studied the effect of HBO treatments on the oxidant-antioxidant balance in the venous blood of patients with diabetic foot syndrome. In addition, blood counts were also examined. 14 male patients (24-74 years), at risk of lower limb amputation were treated with 30 HBO procedures (60 min of the inhalation of pure oxygen at a pressure of 2.5 atm per day, 5 days a week). The control group consisted of 29 healthy male volunteers aged 25-69 years. No members of the group had been subjected to HBO therapy previously (ClinicalTrials.gov, no. NCT06401941). The analyzed redox parameters did not change during the experiment in the patients (p > 0.05). The concentration of thiobarbituric acid reactive substances (TBARS) in the plasma was higher in the patients before the first and after the thirtieth HBO treatments when compared to the control group. In contrast, the TBARS concentration in erythrocytes was lower in the patients after the first treatment vs. the controls. Moreover, the higher activity of catalase in the patients' erythrocytes was noted before the therapy and after the first and last treatments compared to the controls. HBO therapy increased the percentage of monocytes and platelet volume, but it decreased the volume of platelets in the patients' blood. HBO therapy does not affect the oxidant-antioxidant balance disturbed in diabetic foot patients.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metformin suppresses metabolic dysfunction-associated fatty liver disease by ferroptosis and apoptosis via activation of oxidative stress. 二甲双胍通过激活氧化应激，抑制铁凋亡和细胞凋亡，从而抑制代谢功能障碍相关性脂肪肝。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-10-18 DOI: 10.1080/10715762.2024.2417279

Zhiyu Li, Chao Cui, Liang Xu, Mingfeng Ding, Yinghui Wang

{"title":"Metformin suppresses metabolic dysfunction-associated fatty liver disease by ferroptosis and apoptosis via activation of oxidative stress.","authors":"Zhiyu Li, Chao Cui, Liang Xu, Mingfeng Ding, Yinghui Wang","doi":"10.1080/10715762.2024.2417279","DOIUrl":"https://doi.org/10.1080/10715762.2024.2417279","url":null,"abstract":"Metformin is known for its antioxidant properties and ability to ameliorate metabolic dysfunction-associated fatty liver disease (MAFLD) and is the focus of this study. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is linked to MAFLD risk. This study investigated the effects of metformin on ferroptosis in free fatty acid (FFA)-treated Huh7 hepatoma cells and its association with MAFLD risk. Using Western blot, immunofluorescence, and ELISA, this study revealed that FFA treatment led to increased intracellular fat and iron accumulation, heightened Lp-PLA2 expression, reduced levels of the cysteine transporter SLC7A11 and glutathione peroxidase 4 (GPX4), altered glutathione (GSH)/oxidized glutathione (GSSG) ratios, generation of reactive oxygen species (ROS), and initiation of lipid peroxidation, which ultimately resulted in cell ferroptosis. Importantly, metformin reversed FFA-induced iron accumulation, and this effect was attenuated by ferrostatin-1 but enhanced by erastin, RSL3, and si-GPX4. Additionally, metformin activated antioxidant and antiapoptotic mechanisms, which reduced lipid peroxidation and suppressed Lp-PLA2 expression in FFA-treated Huh7 cells. In conclusion, our findings indicate that metformin may protect against MAFLD by inhibiting iron accumulation and Lp-PLA2 expression through the ROS, ferroptosis, and apoptosis signaling pathways. This study highlights potential therapeutic strategies for managing MAFLD-related risks and emphasizes the diverse roles of metformin in maintaining hepatocyte balance.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Redox remodeling of central metabolism as a driving force for cellular protection, proliferation, differentiation, and dysfunction. 中枢代谢的氧化还原重塑是细胞保护、增殖、分化和功能障碍的驱动力。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-09-24 DOI: 10.1080/10715762.2024.2407147

Junichi Fujii

{"title":"Redox remodeling of central metabolism as a driving force for cellular protection, proliferation, differentiation, and dysfunction.","authors":"Junichi Fujii","doi":"10.1080/10715762.2024.2407147","DOIUrl":"https://doi.org/10.1080/10715762.2024.2407147","url":null,"abstract":"The production of reactive oxygen species (ROS) is elevated via metabolic hyperactivation in response to a variety of stimuli such as growth factors and inflammation. Tolerable amounts of ROS moderately inactivate enzymes via oxidative modification, which can be reversed back to the native form in a redox-dependent manner. The excessive production of ROS, however, causes cell dysfunction and death. Redox-reactive enzymes are present in primary metabolic pathways such as glycolysis and the tricarboxylic acid cycle, and these act as floodgates for carbon flux. Oxidation of a specific form of cysteine inhibits glyceraldehyde-3-phosphate dehydrogenase, which is reversible, and causes an accumulation of upstream intermediary compounds that increases the flux of glucose-6-phosphate to the pentose phosphate pathway. These reactions increase the NADPH and ribose-5-phosphate that are available for reductive reactions and nucleotide synthesis, respectively. On the other hand, oxidative inactivation of mitochondrial aconitase increases citrate, which is then recruited to synthesize fatty acids in the cytoplasm. Decreases in the use of carbohydrate for ATP production can be compensated via amino acid catabolism, and this metabolic change makes nitrogen available for nucleic acid synthesis. Coupling of the urea cycle also converts nitrogen to urea and polyamine, the latter of which supports cell growth. This metabolic remodeling stimulates the proliferation of tumor cells and fibrosis in oxidatively damaged tissues. Oxidative modification of these enzymes is generally reversible in the early stages of oxidizing reactions, which suggests that early treatment with appropriate antioxidants promotes the maintenance of natural metabolism.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142344616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The inhibitory potential of 4,7-dihydroxycoumarin derivatives on ROS-producing enzymes and direct HOO•/o2• - radical scavenging activity - a comprehensive kinetic DFT study. 4,7-二羟基香豆素衍生物对产生 ROS 的酶的抑制潜力和直接清除 HOO-/o2- 自由基的活性--一项全面的动力学 DFT 研究。

IF 3.3 3区生物学

Free Radical Research Pub Date : 2024-09-12 DOI: 10.1080/10715762.2024.2400674

Žiko Milanović,Svetlana Jeremić,Marko Antonijević,Dušan Dimić,Đura Nakarada,Edina Avdović,Zoran Marković

{"title":"The inhibitory potential of 4,7-dihydroxycoumarin derivatives on ROS-producing enzymes and direct HOO•/o2• - radical scavenging activity - a comprehensive kinetic DFT study.","authors":"Žiko Milanović,Svetlana Jeremić,Marko Antonijević,Dušan Dimić,Đura Nakarada,Edina Avdović,Zoran Marković","doi":"10.1080/10715762.2024.2400674","DOIUrl":"https://doi.org/10.1080/10715762.2024.2400674","url":null,"abstract":"This study examined the antiradical activity of three synthesized coumarin derivatives: (E)-3-(1-((2-hydroxyphenyl)amino)ethylidene)-2,4-dioxochroman-7-yl acetate (A1-OH), (E)-3-(1-((3-hydroxyphenyl)amino)ethylidene)-2,4-dioxochroman-7-yl acetate (A2-OH), and (E)-3-(1-((4-hydroxyphenyl)amino)ethylidene)-2,4-dioxochroman-7-yl acetate (A3-OH) against HOO•/O2•- radical species. The investigation included electron spin resonance (ESR) measurements and a DFT kinetic study. Thermodynamic and kinetic parameters of antiradical mechanisms-Formal Hydrogen Atom Transfer (f-HAT), Radical Adduct Formation (RAF), Sequential Proton Loss followed by Electron Transfer (SPLET), and Single-Electron Transfer followed by Proton Transfer (SET-PT)-were evaluated using the Quantum Mechanics-based test for Overall Free Radical Scavenging Activity (QM-ORSA) under physiological conditions. ESR results indicated antiradical activity decreased in the sequence A1-OH (58.7%) > A2-OH (57.5%) > A3-OH (53.1%). Kinetic analysis revealed the f-HAT mechanism dominated HOO• inactivation. A newly formulated Sequential Proton Loss followed by Radical Adduct Formation (SPL-RAF) mechanism described interactions with O2•-. The activity toward O2•- was A2-OH (1.26 × 106 M-1s-1) > A3-OH (7.71 × 105 M-1s-1) > A1-OH (4.22 × 105 M-1s-1). Molecular docking and dynamics studies tested inhibitory capability against enzymes producing reactive species: Lipoxygenase (LOX), Myeloperoxidase (MPO), NAD(P)H oxidase (NOX), and Xanthine Oxidase (XOD). Affinity to enzymes decreased in the order: XOD > LOX > NOX > MPO.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142219710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EP4 receptor agonist CAY10598 upregulates ROS-dependent Hsp90 cleavage in colorectal cancer cells. EP4受体激动剂CAY10598能上调结直肠癌细胞中依赖于ROS的Hsp90裂解。

IF 3.3 3区生物学

Free Radical Research Pub Date : 2024-09-11 DOI: 10.1080/10715762.2024.2396909

In Gyung Chae,Joohee Jung,Do-Hee Kim,Joon-Seok Choi,Kyung-Soo Chun

{"title":"EP4 receptor agonist CAY10598 upregulates ROS-dependent Hsp90 cleavage in colorectal cancer cells.","authors":"In Gyung Chae,Joohee Jung,Do-Hee Kim,Joon-Seok Choi,Kyung-Soo Chun","doi":"10.1080/10715762.2024.2396909","DOIUrl":"https://doi.org/10.1080/10715762.2024.2396909","url":null,"abstract":"Prostaglandin E2 (PGE2) interacts with four specific G protein-coupled receptors, namely EP1, EP2, EP3, and EP4, playing a pivotal role in determining the fate of cells. Our previous findings highlighted that stimulating the EP4 receptor with its agonist, CAY10598, triggers apoptosis in colon cancer HCT116 cells via the production of reactive oxygen species (ROS). This process also reduces the phosphorylation of the oncogenic protein JAK2 and leads to its degradation in these cells. In this study, our goal was to explore the pathways through which CAY10598 leads to JAK2 degradation. We focused on Hsp90, a heat shock protein family member known for its role as a molecular chaperone maintaining the stability of several key proteins including EGFR, MET, Akt, and JAK2. Our results show that CAY10598 decreases the levels of client proteins of Hsp90 in HCT116 cells, an effect reversible by pretreatment with the ROS scavenger N-acetyl cysteine (NAC) or the proteasome inhibitor MG132, indicating that the degradation is likely driven by ROS. Furthermore, we observed that CAY10598 cleaves both α and β isoforms of Hsp90, the process inhibited by NAC. Inhibition of EP4 with the antagonist GW627368x not only prevented the degradation of Hsp90 client proteins but also the cleavage of Hsp90 itself in CAY10598-treated HCT116 cells. Additionally, CAY10598 suppressed the growth of HCT116 cells implanted in mice. Our findings reveal that CAY10598 induces apoptosis in cancer cells by a novel mechanism involving the ROS-dependent cleavage of Hsp90, thereby inhibiting the function of crucial Hsp90 client proteins.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142219711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Low density lipoprotein oxidized under lysosomal conditions decreases arterial vasodilatation. 在溶酶体条件下氧化的低密度脂蛋白会降低动脉血管舒张功能。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-08-01 Epub Date: 2024-09-13 DOI: 10.1080/10715762.2024.2403038

Hadeel K M Alboaklah, Alister J McNeish, David S Leake

{"title":"Low density lipoprotein oxidized under lysosomal conditions decreases arterial vasodilatation.","authors":"Hadeel K M Alboaklah, Alister J McNeish, David S Leake","doi":"10.1080/10715762.2024.2403038","DOIUrl":"10.1080/10715762.2024.2403038","url":null,"abstract":"Endothelial dysfunction is a risk factor for atherosclerosis and includes impaired endothelium-dependent vasodilatation. We have shown previously that low density lipoprotein (LDL) can be oxidized by iron in the lysosomes of macrophages. Macrophage lysis in atherosclerotic lesions might expose endothelial cells to this oxidized LDL and adversely affect their function. LDL was oxidized by ferrous sulfate (5 µM) for 24 h at pH 4.5 at 37 °C. Aortas from male Wistar rats were cut into rings and subjected to wire myography for isometric tension recording. The rings were incubated with or without oxidized LDL (50 µg protein/ml) for one hour, constricted with 100 nM phenylephrine and relaxation to acetylcholine (1 nM - 3 µM) was measured. There was about 50% less relaxation in the presence of this oxidized LDL. Endothelial-independent vasodilatation induced by sodium nitroprusside was less affected by oxidized LDL. Oxidized LDL increased the formation of reactive oxygen species by the aortic rings and by cultured human aortic and dermal microvascular endothelial cells, which might have inactivated nitric oxide. Acetylcholine increased the activatory phosphorylation of eNOS (ser-1177), but oxidized LDL had little effect on this activation in cultured human aortic endothelial cells. These findings raise the possibility that LDL oxidized in lysosomes and released from lysed macrophages might decrease vasodilatation in atherosclerotic arteries.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The effect of hypochlorous acid inhalation on the activity of antioxidant system enzymes in rats of different ages. 吸入次氯酸对不同年龄大鼠抗氧化系统酶活性的影响。

IF 3.6 3区生物学

Free Radical Research Pub Date : 2024-08-01 DOI: 10.1080/10715762.2024.2386688

Bohdan Murashevych, Hanna Maslak, Dmitry Girenko, Olha Abraimova, Olha Netronina, Volodymyr Shvets

{"title":"The effect of hypochlorous acid inhalation on the activity of antioxidant system enzymes in rats of different ages.","authors":"Bohdan Murashevych, Hanna Maslak, Dmitry Girenko, Olha Abraimova, Olha Netronina, Volodymyr Shvets","doi":"10.1080/10715762.2024.2386688","DOIUrl":"10.1080/10715762.2024.2386688","url":null,"abstract":"Hypochlorous acid HOCl is an effective disinfectant with a broad spectrum and high rate of microbicidal action. Its use for air treatment can be an effective tool for the prevention and therapy of infectious diseases. In this work, the in vivo study was conducted on 110 Wistar Han rats (12 and 72 weeks old) on the effect of a single inhalation of air containing gaseous HOCl on the activity of antioxidant system enzymes. For this, a special installation was designed to uniformly maintain the concentration of HOCl in the air and regulate it over a wide range. Inhalation exposure was carried out for 4 h at total chlorine concentrations in the air of approximately 2.0 mg/m3 and 5.0 mg/m3, after which the animals were observed for 14 days. The effect of inhalation on the antioxidant system activity varied significantly in animals of different ages. Catalase activity in young rats increased approximately 2-fold on days 1-2 after inhalation, regardless of the HOCl concentration, while in old animals a sharp dose-dependent decrease was initially observed. The glutathione peroxidase activity in animals of both ages increased upon inhalation of air with 5.0 mg/m3 HOCl, and in old animals this was more pronounced; when the HOCl concentration decreased to 2.0 mg/m3, this indicator increased slightly in old rats and remained virtually unchanged in young ones. The glutathione reductase activity when exposed to 2.0 mg/m3 HOCl did not change for both age groups, and with increasing HOCl concentration it increased by 1.5-2.0 times in all animals.","PeriodicalId":12411,"journal":{"name":"Free Radical Research","volume":null,"pages":null},"PeriodicalIF":3.6,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0