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Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe最新文献

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Evaluation of salivary total antioxidant capacity in cigarette smokers versus water pipe smokers among dental students in Sulaimani city 苏莱曼尼市牙科学生中吸烟者与水烟吸烟者唾液总抗氧化能力的评价
Darya Khalid Mahmood

Background

Tobacco use, whether through cigarettes or waterpipes, has been associated with the development of oxidative stress and a reduction in antioxidant defense. There is dearth of information on the impact of smoking frequency and duration among individuals of close age brackets. This study therefore aimed to assess salivary Total Antioxidant Capacity (TAOc) concentration among male dental students of different narrow age range with different smoking habits, including non-smokers, cigarette smokers, waterpipe users, and dual users.

Methods

In this cross-sectional study, 89 male dental students aged approximately 21.3 years were divided into four groups: non-smokers (n=14), cigarette smokers (n = 39), waterpipe users (n=11), and dual users (n=25). Smoking frequency and duration were recorded, and TAOc levels were measured. Data were analyzed using one-way ANOVA and post hoc Tukey tests.

Results

A significant difference in TAOc levels was observed among the four groups (P < 0.05). Non-smokers exhibited the highest antioxidant levels (27.93±3.79 U/ml), followed by waterpipe smokers (17.40±6.02 U/ml), cigarette smokers (15.59±7.45 U/ml), and dual users (9.68±6.89 U/ml). Post hoc analysis revealed that non-smokers had significantly higher TAOc levels compared to all smoking groups (P ≤ 0.001). Additionally, dual users had significantly lower TAOc than both single-type smokers. Smoking duration and frequency also influenced antioxidant levels, with a significant reduction observed in those with longer durations of use or higher frequency of smoking consumption.

Conclusion

Smoking, particularly dual use of cigarettes and waterpipes, is associated with a significant decline in salivary antioxidant capacity. Longer smoking duration and higher frequency further exacerbate this decline, highlighting the potential oxidative damage associated with tobacco use in young adults.
烟草的使用,无论是通过香烟还是水烟,都与氧化应激的发展和抗氧化防御能力的降低有关。缺乏关于吸烟频率和持续时间对接近年龄组的人的影响的资料。因此,本研究旨在评估不同年龄范围、不同吸烟习惯的男性牙科学生的唾液总抗氧化能力(TAOc)浓度,包括不吸烟者、吸烟者、水烟使用者和双重吸烟者。方法将89名年龄约21.3岁的男性牙科学生分为4组:不吸烟者(n=14)、吸烟者(n= 39)、烟斗使用者(n=11)和双重使用者(n=25)。记录吸烟频率和持续时间,并测量TAOc水平。数据分析采用单因素方差分析和事后Tukey检验。结果四组患者TAOc水平差异有统计学意义(P < 0.05)。非吸烟者抗氧化水平最高(27.93±3.79 U/ml),其次是吸烟(17.40±6.02 U/ml)、吸烟(15.59±7.45 U/ml)和双重吸烟者(9.68±6.89 U/ml)。事后分析显示,与所有吸烟组相比,非吸烟者的TAOc水平明显更高(P≤0.001)。此外,双吸烟者的TAOc含量明显低于单吸烟者。吸烟时间和频率也会影响抗氧化水平,吸烟时间越长或吸烟频率越高的人抗氧化水平显著降低。结论吸烟,特别是香烟和水烟的双重使用,与唾液抗氧化能力的显著下降有关。更长的吸烟时间和更高的吸烟频率进一步加剧了这种下降,突出了与年轻人使用烟草相关的潜在氧化损伤。
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引用次数: 0
Influence of pteridines and statins on cancer: A therapeutic strategy targeting nitric oxide synthase (NOS) pathway 翼状吡啶和他汀类药物对癌症的影响:一种针对一氧化氮合酶(NOS)途径的治疗策略
Jerimon Johnson , Monisha Krishnan , Sasireka Manikandan , Nivetha Shanmuganathan , Martinahingis Kennedy , Kris Santhiya Yeasuraj , Sridhar Muthusami , Angayarkanni Jayaraman
A family of enzymes known as nitric oxide synthases (NOS) produces nitric oxide (NO), a tiny, unstable, and potentially hazardous gas that is highly diffusible across cell membranes. NO and NO metabolites, such as nitrite, nitrate, S-nitrosothiols, nitrosamines, and peroxynitrite, mediate a variety of cytotoxic and genotoxic effects, such as inhibition of mitochondrial respiration, protein and DNA damage that leads to gene mutation, loss of protein function, necrosis, and apoptosis. Through a variety of apoptotic mechanisms, abnormally elevated NO generation by NOS II/iNOS may cause cytotoxicity of cancer cells. Tetrahydrobiopterin (BH4) is required by all NOS isoforms for NO production. Another way mammalian cells can create BH4 is by the "salvage pathway," which uses sepiapterin reductase and dihydrofolate reductase to convert sepiapterin to BH4. Better apoptotic effects on cancer cells may result from boosting BH4 levels by treating cells with sepiapterin, 7-8-dihydropterin, or pterin derivatives, which work in concert to improve NO levels. Another common medication used to treat and prevent hypercholesterolaemia and related cardiovascular disorders is statins, which lower serum cholesterol. They are competitive inhibitors of 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase, the enzyme that limits the rate at which cholesterol is produced. Statins also improve cardiovascular and endothelial function by increasing the generation of nitric oxide (NO) by endothelial cells. They also have an impact on a variety of molecules and signaling pathways that govern the synthesis of apoptotic proteins and raise nitric oxide (NO) levels. Therefore, the NO-mediated route may be used to induce apoptosis due to the synergistic potency of statins and pterin derivatives. This review focusses on the effectiveness of statins and pterin derivatives, as well as their ability to influence the production of nitric oxide, which intensifies the effect on cancer cells.
一氧化氮合成酶(NOS)产生一氧化氮(NO),这是一种微小的、不稳定的、有潜在危险的气体,可以在细胞膜上高度扩散。NO和NO代谢物,如亚硝酸盐、硝酸盐、s -亚硝基硫醇、亚硝胺和过氧亚硝酸盐,介导多种细胞毒性和基因毒性作用,如线粒体呼吸抑制、蛋白质和DNA损伤导致基因突变、蛋白质功能丧失、坏死和细胞凋亡。通过多种凋亡机制,NOS II/iNOS产生的NO异常升高可引起癌细胞的细胞毒性。所有NOS异构体都需要四氢生物蝶呤(BH4)来产生NO。哺乳动物细胞产生BH4的另一种方式是通过“补救途径”,它使用七叶黄素还原酶和二氢叶酸还原酶将七叶黄素转化为BH4。通过用七蝶呤、7-8-二氢蝶呤或蝶呤衍生物处理细胞,可以提高BH4水平,从而提高NO水平,从而对癌细胞产生更好的凋亡作用。另一种用于治疗和预防高胆固醇血症及相关心血管疾病的常用药物是他汀类药物,它可以降低血清胆固醇。它们是3-羟基-3-甲基戊二酰辅酶a (HMG-CoA)还原酶的竞争性抑制剂,这种酶限制胆固醇的产生速度。他汀类药物还通过增加内皮细胞产生一氧化氮(NO)来改善心血管和内皮功能。它们还对控制凋亡蛋白合成和提高一氧化氮(NO)水平的各种分子和信号通路产生影响。因此,由于他汀类药物和蝶呤衍生物的协同作用,no介导的途径可能用于诱导细胞凋亡。这篇综述的重点是他汀类药物和蝶呤衍生物的有效性,以及它们影响一氧化氮产生的能力,一氧化氮增强了对癌细胞的作用。
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引用次数: 0
Targeting the AGE-RAGE axis in acute lung injury: Mechanistic insights and redox-modulatory strategies 针对急性肺损伤的AGE-RAGE轴:机制见解和氧化还原调节策略
Changchang Zhang , Xiao Yu , Peiji Li , Xiangmei Li , Jingwen Chen , Huan Wang , Mengying Yao
Acute Respiratory Distress Syndrome (ARDS) is a serious respiratory condition characterized by a rapid onset of severe inflammation in the lungs. This inflammation results from various causes. The syndrome is marked by widespread damage to the alveolar epithelial cells and capillary endothelial cells. It represents a critical stage of acute lung injury (ALI), a prevalent clinical issue associated with a high mortality rate. The underlying mechanisms of ALI are intricate and primarily driven by an uncontrolled inflammatory response. Given this complexity, there has been growing interest recently in the role of advanced glycation end-products (AGEs) and their receptor, the receptor for advanced glycation end-products (RAGE), in the development of ALI. The AGE-RAGE signaling pathway is pivotal in the initiation and progression of ALI, influencing several processes, including inflammation and apoptosis. However, the detailed mechanisms by which this signaling pathway contributes to ALI are still being investigated. This review aims to summarize recent advancements in understanding the molecular mechanisms, regulation of inflammatory responses, and apoptosis associated with the AGE-RAGE signaling pathway in ALI. It focuses on analyzing how various traditional Chinese medicine formulas and their active components can modulate this pathway to alleviate ALI. Additionally, by integrating network pharmacology, molecular docking, and experimental validation, this review examines the interactions between the AGE-RAGE signaling pathway and significant downstream pathways such as NF-κB and PI3K/AKT, highlighting their potential therapeutic implications. Therefore, this work provides a foundational understanding of the pathogenesis of ALI and paves the way for the development of innovative therapeutic approaches.
急性呼吸窘迫综合征(ARDS)是一种严重的呼吸系统疾病,其特征是肺部迅速发生严重炎症。这种炎症是由多种原因引起的。该综合征的特点是肺泡上皮细胞和毛细血管内皮细胞的广泛损伤。它代表了急性肺损伤(ALI)的关键阶段,这是一个与高死亡率相关的普遍临床问题。ALI的潜在机制是复杂的,主要由不受控制的炎症反应驱动。鉴于这种复杂性,最近人们对晚期糖基化终产物(AGEs)及其受体,晚期糖基化终产物受体(RAGE)在ALI发展中的作用越来越感兴趣。AGE-RAGE信号通路在ALI的发生和发展中起关键作用,影响包括炎症和细胞凋亡在内的几个过程。然而,该信号通路导致ALI的详细机制仍在研究中。本文综述了ALI中AGE-RAGE信号通路相关的分子机制、炎症反应调控和细胞凋亡的最新进展。重点分析各种中药配方及其有效成分如何调节这一通路,从而缓解ALI。此外,通过整合网络药理学、分子对接和实验验证,本综述探讨了AGE-RAGE信号通路与NF-κB和PI3K/AKT等重要下游通路之间的相互作用,强调了它们潜在的治疗意义。因此,这项工作为了解ALI的发病机制提供了基础,并为创新治疗方法的发展铺平了道路。
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引用次数: 0
The effect of atorvastatin on inflammatory markers, lipid profile, and renal function in kidney diseases: a systematic review and meta-analysis of randomized controlled trials 阿托伐他汀对肾脏疾病患者炎症标志物、血脂和肾功能的影响:随机对照试验的系统回顾和荟萃分析
Iman Mohammadi , Behzad Einollahi , Mina Alimohammadi , Seyedeh Mahdieh Khoshnazar , Hoda Sadeghi , Ali Zahiri , Haniye Najafzadeh , Kiavash Hushmandi

Background

Chronic and acute kidney disorders (CKD, AKI) afflict millions globally, leading to increased morbidity and death, especially from cardiovascular consequences. Atorvastatin, a popular statin, offers lipid-lowering, anti-inflammatory, and antioxidant qualities that may assist kidney disease patients in terms of renal and cardiovascular health. This meta-analysis assesses atorvastatin's effectiveness and safety in terms of lipid profiles, inflammatory biomarkers, and renal function in patients with kidney disorders.

Methods

A thorough search of Scopus, Cochrane, Embase, Web of Science, Google Scholar, and PubMed until January 2025 revealed randomized controlled trials (RCTs) evaluating atorvastatin in CKD, diabetic nephropathy, hemodialysis, and other renal diseases. The outcomes included lipid parameters (HDL, LDL, total cholesterol, triglycerides), inflammatory markers (hsCRP, IL-6, MDA), and renal function indices. Random-effects models were used to pool weighted mean differences (WMDs) and 95 % confidence intervals (CIs). Subgroup analyses were performed based on dosage, duration, disease type, and treatment type. The risk of bias and publication bias was evaluated.

Results

Twelve RCTs with 18 trials and sample sizes ranging from 21 to 156 participants were included. As expected, atorvastatin significantly improved HDL cholesterol (WMD: 2.74 mg/dL; 95 % CI: 0.57 to 4.91; p < 0.001) while dramatically decreasing LDL cholesterol (WMD: -13.09 mg/dL; 95 % CI: -21.17 to -5.00; p < 0.001) and total cholesterol (WMD: -15.28 mg/dL; 95 % CI: -24.58 to -5.98; p < 0.001) at lower dosages of ≤10 mg/day and longer treatment periods. More notably, it also reduced MDA (WMD: -2.80; 95 % CI: -3.62 to -1.97; p < 0.001) and showed anti-inflammatory effects by reducing hsCRP in CKD patients receiving a ≤ 10 mg/day dosage.

Conclusions

Atorvastatin medication improves lipid profiles and lowers oxidative stress indicators in renal disease patients, with some indications of decreased inflammation in select subgroups, indicating a possible function as an adjuvant treatment to reduce cardiovascular risk. Future large-scale RCTs are needed to determine the appropriate dose and long-term kidney results.
慢性和急性肾脏疾病(CKD, AKI)折磨着全球数百万人,导致发病率和死亡率增加,特别是心血管后果。阿托伐他汀是一种流行的他汀类药物,具有降脂、抗炎和抗氧化的特性,可能有助于肾脏疾病患者的肾脏和心血管健康。本荟萃分析评估了阿托伐他汀在肾脏疾病患者的脂质谱、炎症生物标志物和肾功能方面的有效性和安全性。方法全面检索Scopus、Cochrane、Embase、Web of Science、b谷歌Scholar和PubMed,直到2025年1月,发现了评价阿托伐他汀治疗CKD、糖尿病肾病、血液透析和其他肾脏疾病的随机对照试验(RCTs)。结果包括脂质参数(HDL、LDL、总胆固醇、甘油三酯)、炎症标志物(hsCRP、IL-6、MDA)和肾功能指标。随机效应模型用于合并加权平均差(wmd)和95%置信区间(ci)。根据剂量、持续时间、疾病类型和治疗方式进行亚组分析。评估偏倚和发表偏倚风险。结果纳入12项随机对照试验,共18项试验,样本量为21 ~ 156人。正如预期的那样,阿托伐他汀显著改善了高密度脂蛋白胆固醇(WMD: 2.74 mg/dL; 95% CI: 0.57至4.91;p < 0.001),同时显著降低了低密度脂蛋白胆固醇(WMD: -13.09 mg/dL; 95% CI: -21.17至-5.00;p < 0.001)和总胆固醇(WMD: -15.28 mg/dL; 95% CI: -24.58至-5.98;p < 0.001),剂量≤10 mg/天且疗程较长。更值得注意的是,它还降低了丙二醛(WMD: -2.80; 95% CI: -3.62至-1.97;p < 0.001),并通过降低≤10mg /天剂量的CKD患者的hsCRP显示出抗炎作用。结论托伐他汀可改善肾脏疾病患者的脂质谱,降低氧化应激指标,在某些亚组中有炎症减少的迹象,表明托伐他汀可能具有降低心血管风险的辅助治疗功能。未来需要大规模随机对照试验来确定合适的剂量和长期肾脏结果。
{"title":"The effect of atorvastatin on inflammatory markers, lipid profile, and renal function in kidney diseases: a systematic review and meta-analysis of randomized controlled trials","authors":"Iman Mohammadi ,&nbsp;Behzad Einollahi ,&nbsp;Mina Alimohammadi ,&nbsp;Seyedeh Mahdieh Khoshnazar ,&nbsp;Hoda Sadeghi ,&nbsp;Ali Zahiri ,&nbsp;Haniye Najafzadeh ,&nbsp;Kiavash Hushmandi","doi":"10.1016/j.arres.2026.100150","DOIUrl":"10.1016/j.arres.2026.100150","url":null,"abstract":"<div><h3>Background</h3><div>Chronic and acute kidney disorders (CKD, AKI) afflict millions globally, leading to increased morbidity and death, especially from cardiovascular consequences. Atorvastatin, a popular statin, offers lipid-lowering, anti-inflammatory, and antioxidant qualities that may assist kidney disease patients in terms of renal and cardiovascular health. This meta-analysis assesses atorvastatin's effectiveness and safety in terms of lipid profiles, inflammatory biomarkers, and renal function in patients with kidney disorders.</div></div><div><h3>Methods</h3><div>A thorough search of Scopus, Cochrane, Embase, Web of Science, Google Scholar, and PubMed until January 2025 revealed randomized controlled trials (RCTs) evaluating atorvastatin in CKD, diabetic nephropathy, hemodialysis, and other renal diseases. The outcomes included lipid parameters (HDL, LDL, total cholesterol, triglycerides), inflammatory markers (hsCRP, IL-6, MDA), and renal function indices. Random-effects models were used to pool weighted mean differences (WMDs) and 95 % confidence intervals (CIs). Subgroup analyses were performed based on dosage, duration, disease type, and treatment type. The risk of bias and publication bias was evaluated.</div></div><div><h3>Results</h3><div>Twelve RCTs with 18 trials and sample sizes ranging from 21 to 156 participants were included. As expected, atorvastatin significantly improved HDL cholesterol (WMD: 2.74 mg/dL; 95 % CI: 0.57 to 4.91; <em>p</em> &lt; 0.001) while dramatically decreasing LDL cholesterol (WMD: -13.09 mg/dL; 95 % CI: -21.17 to -5.00; <em>p</em> &lt; 0.001) and total cholesterol (WMD: -15.28 mg/dL; 95 % CI: -24.58 to -5.98; <em>p</em> &lt; 0.001) at lower dosages of ≤10 mg/day and longer treatment periods. More notably, it also reduced MDA (WMD: -2.80; 95 % CI: -3.62 to -1.97; <em>p</em> &lt; 0.001) and showed anti-inflammatory effects by reducing hsCRP in CKD patients receiving <em>a</em> ≤ 10 mg/day dosage.</div></div><div><h3>Conclusions</h3><div>Atorvastatin medication improves lipid profiles and lowers oxidative stress indicators in renal disease patients, with some indications of decreased inflammation in select subgroups, indicating a possible function as an adjuvant treatment to reduce cardiovascular risk. Future large-scale RCTs are needed to determine the appropriate dose and long-term kidney results.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100150"},"PeriodicalIF":2.7,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Role of L-carnitine in exercise training: Anti-inflammatory, antioxidant, and metabolic interactions 左旋肉碱在运动训练中的作用:抗炎、抗氧化和代谢的相互作用
Soheil Aminizadeh , Aliasghar Zarezadehmehrizi , Maedeh Amiri Deh-Ahmadi , Beydolah Shahouzehi
L-carnitine is a mitochondria-targeted compound that plays a pivotal role in lipid metabolism, redox balance, and inflammatory regulation, particularly under conditions of elevated metabolic demands such as exercise. This review explores the multifaceted functions of L-carnitine in modulating oxidative stress and inflammation, emphasizing its relevance to exercise physiology and clinical health. By facilitating the transport of long-chain fatty acids into mitochondria, L-carnitine enhances β-oxidation and energy production while buffering excess acetyl-CoA to maintain metabolic flexibility. Its antioxidant properties, mediated through the upregulation of SOD, GPx, and catalase, help mitigate reactive oxygen species (ROS) and preserve mitochondrial integrity. Concurrently, L-carnitine suppresses cytokines such as TNF-α and IL-6, interrupting the feedback loop between oxidative stress and chronic inflammation. These mechanisms are particularly beneficial during and after exercise, where L-carnitine supplementation has shown potential to improve endurance, reduce muscle damage, and accelerate recovery in some studies, although findings across the literature are not entirely consistent. Clinical evidence also supports its therapeutic potential in conditions like cardiovascular disease, non-alcoholic fatty liver disease, and neuroinflammation. The review integrates mechanistic insights with performance outcomes, highlighting L-carnitine’s role as both a metabolic modulator and an ergogenic aid. Understanding these complex interactions provides a foundation for optimizing L-carnitine use, yet further research is warranted to clarify the optimal form (e.g., LCLT, ALCAR), dosage, duration, and target populations to maximize its therapeutic and ergogenic potential.
左旋肉碱是一种线粒体靶向化合物,在脂质代谢、氧化还原平衡和炎症调节中起着关键作用,特别是在代谢需求升高的情况下,如运动。本文综述了左旋肉碱在调节氧化应激和炎症中的多方面功能,强调了其与运动生理学和临床健康的相关性。通过促进长链脂肪酸向线粒体的运输,左旋肉碱增强β-氧化和能量产生,同时缓冲过量的乙酰辅酶a以保持代谢灵活性。其抗氧化特性通过上调SOD、GPx和过氧化氢酶介导,有助于减轻活性氧(ROS)并保持线粒体完整性。同时,左旋肉碱抑制细胞因子如TNF-α和IL-6,中断氧化应激和慢性炎症之间的反馈回路。这些机制在运动期间和运动后特别有益,在一些研究中,补充左旋肉碱已显示出提高耐力、减少肌肉损伤和加速恢复的潜力,尽管文献中的发现并不完全一致。临床证据也支持它在心血管疾病、非酒精性脂肪肝和神经炎症等疾病中的治疗潜力。该综述将机制见解与性能结果结合起来,强调了左旋肉碱作为代谢调节剂和促氧剂的作用。了解这些复杂的相互作用为优化左旋肉碱的使用提供了基础,但需要进一步的研究来阐明最佳形式(例如LCLT, ALCAR),剂量,持续时间和目标人群,以最大限度地发挥其治疗和人体作用潜力。
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引用次数: 0
A concise review on health benefits of alkaline reduced water 碱性还原水对健康的益处综述
Maninder Meenu , Mradula , Kiran Khandare , Shradha Duggal , Vasudha Bansal , Manorma Negi , Baojun Xu
Alkaline reduced water (ARW), produced through electrolysis, has emerged as a health-promoting beverage due to its elevated pH and reduced oxidation–reduction potential (ORP). This type of water offers several notable health benefits. ARW effectively neutralizes excess body acidity, promoting a balanced internal pH, which is beneficial in counteracting the effects of an acid-heavy diet. Its smaller molecular clusters enhance cellular absorption, improving hydration and nutrient uptake, which is particularly advantageous for athletes and physically active individuals. The antioxidant properties of ARW, attributed to its negative ORP, play a crucial role in reducing oxidative stress, thereby protecting cells from damage and potentially lowering the risk of chronic diseases such as cancer, cardiovascular diseases, and neurodegenerative disorders. ARW also supports digestive health by promoting a balanced gut environment and reducing harmful bacterial load. It also enhances the solubility and bioavailability of nutrients, improving their utilization in the body. Regular consumption of ARW has been linked to a lower incidence of chronic diseases and reduced fatigue, further enhancing energy levels. Overall ARW is a valuable addition to a health-conscious lifestyle, offering comprehensive benefits by enhancing hydration and preventing diseases. However, further research is needed to fully elucidate the long-term effects of ARW.
电解生产的碱性还原水(ARW)由于其pH值升高和氧化还原电位(ORP)降低而成为一种促进健康的饮料。这种水有几个显著的健康益处。ARW有效地中和体内多余的酸度,促进体内pH平衡,这对抵消高酸性饮食的影响是有益的。其较小的分子簇增强细胞吸收,改善水合作用和营养吸收,这对运动员和身体活跃的个人特别有利。ARW的抗氧化特性,归因于其负ORP,在减少氧化应激中起着至关重要的作用,从而保护细胞免受损伤,并可能降低慢性疾病(如癌症、心血管疾病和神经退行性疾病)的风险。ARW还通过促进平衡的肠道环境和减少有害细菌负荷来支持消化系统健康。它还提高了营养物质的溶解度和生物利用度,提高了它们在体内的利用率。经常食用ARW与慢性病发病率降低和疲劳减轻有关,进一步提高了能量水平。总的来说,ARW是对注重健康的生活方式的宝贵补充,通过增强水合作用和预防疾病提供全面的好处。然而,需要进一步的研究来充分阐明ARW的长期影响。
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引用次数: 0
EROS protein: Decoding its pivotal role in redox homeostasis and disease pathogenesis EROS蛋白:解码其在氧化还原稳态和疾病发病机制中的关键作用
Shiyu Liang , Youli Zhou , Wenfeng Ren , Yang Xu , Ming Tang , Yuxi Su , Li Li , Mei Gao
The Essential for Reactive Oxygen Species (EROS) protein, a critical molecular chaperone for NADPH oxidase 2 (NOX2/gp91phox), has emerged as a central regulator of redox signaling and immune defense. Recent structural and functional studies reveal that EROS orchestrates NOX2 maturation, prevents spontaneous activation, and regulates reactive oxygen species (ROS) production. Dysfunction of EROS is implicated in chronic granulomatous disease (CGD), cancers and vascular pathologies. This review integrates structural insights into EROS-NOX2 interactions, discusses its dual roles in maintaining redox equilibrium and triggering oxidative stress, and explores therapeutic strategies targeting EROS-dependent pathways.
活性氧必需蛋白(EROS)是NADPH氧化酶2 (NOX2/gp91phox)的关键分子伴侣,是氧化还原信号和免疫防御的中心调节因子。最近的结构和功能研究表明,EROS协调NOX2成熟,阻止自发激活,并调节活性氧(ROS)的产生。EROS功能障碍与慢性肉芽肿病(CGD)、癌症和血管病变有关。这篇综述整合了EROS-NOX2相互作用的结构见解,讨论了其在维持氧化还原平衡和触发氧化应激中的双重作用,并探讨了针对eros依赖途径的治疗策略。
{"title":"EROS protein: Decoding its pivotal role in redox homeostasis and disease pathogenesis","authors":"Shiyu Liang ,&nbsp;Youli Zhou ,&nbsp;Wenfeng Ren ,&nbsp;Yang Xu ,&nbsp;Ming Tang ,&nbsp;Yuxi Su ,&nbsp;Li Li ,&nbsp;Mei Gao","doi":"10.1016/j.arres.2025.100147","DOIUrl":"10.1016/j.arres.2025.100147","url":null,"abstract":"<div><div>The Essential for Reactive Oxygen Species (EROS) protein, a critical molecular chaperone for NADPH oxidase 2 (NOX2/gp91<sup>phox</sup>), has emerged as a central regulator of redox signaling and immune defense. Recent structural and functional studies reveal that EROS orchestrates NOX2 maturation, prevents spontaneous activation, and regulates reactive oxygen species (ROS) production. Dysfunction of EROS is implicated in chronic granulomatous disease (CGD), cancers and vascular pathologies. This review integrates structural insights into EROS-NOX2 interactions, discusses its dual roles in maintaining redox equilibrium and triggering oxidative stress, and explores therapeutic strategies targeting EROS-dependent pathways.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"18 ","pages":"Article 100147"},"PeriodicalIF":2.7,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145738770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Methylglyoxal in cancer: Bidirectional regulatory networks and precision intervention—From metabolic reprogramming to cross-disease synergistic targeting 甲基乙二醛在癌症中的作用:双向调控网络和精确干预——从代谢重编程到跨疾病协同靶向
Ji ZeZhao
Methylglyoxal (MG), a core byproduct of glycolysis, exerts a dual role in cancer via a "dose-dependent hormesis effect". At low concentrations, it promotes tumor proliferation and metastasis by regulating polyamine metabolism, epigenetic modifications, and the immune microenvironment. In contrast, high concentrations of MG trigger tumor cell apoptosis through inducing DNA damage and protein glycation. Unlike traditional reviews that focus solely on "MG toxicity" or "GLO1 as a single target", this review takes "metabolic network-signal crosstalk-cross-disease association" as the core context. It systematically dissects the bidirectional regulatory mechanisms of MG in cancer, highlights emerging pathways such as non-coding RNA-mediated GLO1 regulation, MG-polyamine metabolism crosstalk, and immunometabolic reprogramming, and integrates the MG regulatory network in cross-disease scenarios including diabetes, HIV infection, and occupational exposure. Finally, a "stratified targeting + synergistic intervention" precision therapeutic strategy is proposed, providing a novel perspective for basic research and clinical translation of MG-related cancers.
甲基乙二醛(MG)是糖酵解的核心副产物,通过“剂量依赖性激效效应”在癌症中发挥双重作用。在低浓度下,它通过调节多胺代谢、表观遗传修饰和免疫微环境来促进肿瘤增殖和转移。相反,高浓度MG通过诱导DNA损伤和蛋白糖基化触发肿瘤细胞凋亡。与传统文献仅关注“MG毒性”或“GLO1作为单一靶点”不同,本文以“代谢网络信号串扰-跨疾病关联”为核心背景。系统剖析了MG在癌症中的双向调控机制,重点介绍了非编码rna介导的GLO1调控、MG-多胺代谢串扰和免疫代谢重编程等新兴途径,并整合了MG在糖尿病、HIV感染和职业暴露等跨疾病情景中的调控网络。最后,提出了“分层靶向+协同干预”的精准治疗策略,为mg相关肿瘤的基础研究和临床转化提供了新的视角。
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引用次数: 0
Effect of ozone therapy on oxidative stress indices in chronic inflammatory diseases: A systematic review and meta-analysis of randomized clinical trials 臭氧治疗对慢性炎症性疾病氧化应激指标的影响:随机临床试验的系统回顾和荟萃分析
Mina Alimohammadi , Seyedeh Mahdieh Khoshnazar , Hamid Khajehpour , Morteza Izadi , Behzad Einollahi , Kiavash Hushmandi

Background

Chronic inflammatory diseases (CIDs) are defined by prolonged inflammation and oxidative stress (OS), both of which are associated with disease progression and consequences. Ozone (O3) therapy is recognized as a promising complementary therapy for regulating OS indicators. The purpose of this systematic review and meta-analysis is to investigate the effect of O3 therapy on OS parameters in patients with CID.

Methods

A comprehensive literature search was conducted across multiple databases, including PubMed, Cochrane Library, Google Scholar, and Scopus, for randomized controlled trials (RCTs) published up to October 2024. Studies were selected if they investigated the effect of ozone therapy on OS parameters, including malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), glutathione peroxidase (GPx), total hydroperoxides (TH), advanced oxidation protein products (AOPP), and protein peroxidation (PP) in CID patients. Fixed- or Random-effects models were used in the meta-analysis to determine weighted mean differences (WMD) and 95 % confidence intervals (CIs).

Results

12 RCTs with 846 participants included in the current study. Our findings showed that O3 therapy had no significant difference in OS parameters when compared to control groups. According to subgroup analysis, O3 therapy significantly increased SOD activity in patients with T2D (WMD = 7.59, 95 % CI [2.98 to 12.19], I² = 97.75 %, p = <0.001) and arthritis (WMD = 9.21, 95 % CI [6.02 to 12.40], I² = 66.96 %, p = 0.08). In addition, the rectal method showed a statistically significant effect on GPx activity (WMD = 20.00, 95 % CI [0.55 to 39.45], I² = 92.42 %, p = <0.001). O3 therapy also significantly reduced AOPP levels at doses of ≥20 µg/ml and treatment durations of both <30 days (WMD = −5.15, 95 % CI [−7.90 to −2.40], I² = 96.03 %, p = <0.001).

Conclusion

Ozone therapy could improve OS markers in individuals with CIDs, mostly by lowering AOPP and strengthening antioxidant defense systems. More large-scale RCTs are required to validate these outcomes and better comprehend the fundamental mechanisms of action.
慢性炎症性疾病(chronic inflammatory diseases, cid)被定义为长期炎症和氧化应激(oxidative stress, OS),两者都与疾病进展和后果相关。臭氧(O3)疗法被认为是一种很有前景的调节OS指标的补充疗法。本系统综述和荟萃分析的目的是研究O3治疗对CID患者OS参数的影响。方法综合检索PubMed、Cochrane Library、谷歌Scholar、Scopus等数据库,检索截至2024年10月发表的随机对照试验(rct)。如果研究臭氧治疗对OS参数的影响,包括丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GPx)、总氢过氧化物(TH)、晚期氧化蛋白产物(AOPP)和蛋白质过氧化(PP),则选择研究。在荟萃分析中使用固定或随机效应模型来确定加权平均差异(WMD)和95%置信区间(ci)。结果本研究纳入12项随机对照试验,共846名受试者。我们的研究结果显示,与对照组相比,O3治疗在OS参数上没有显著差异。根据亚组分析,O3治疗显著提高T2D (WMD = 7.59, 95% CI [2.98 ~ 12.19], I²= 97.75%,p = <0.001)和关节炎(WMD = 9.21, 95% CI [6.02 ~ 12.40], I²= 66.96%,p = 0.08)患者的SOD活性。此外,直肠法对GPx活性的影响具有统计学意义(WMD = 20.00, 95% CI [0.55 ~ 39.45], I²= 92.42%,p = <0.001)。O3治疗在剂量≥20 μ g/ml和治疗时间均为30天时也显著降低AOPP水平(WMD = - 5.15, 95% CI[- 7.90至- 2.40],I²= 96.03%,p = <0.001)。结论臭氧治疗可改善CIDs患者的OS指标,主要通过降低AOPP和增强抗氧化防御系统来改善。需要更多的大规模随机对照试验来验证这些结果并更好地理解作用的基本机制。
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引用次数: 0
Dietary metal chelator, phytochelatin 2, increases selenium and alters metal homeostasis and associated lipid metabolism in the liver 膳食中的金属螯合剂植物螯合素2可增加硒并改变肝脏中金属稳态和相关的脂质代谢
Zachery R. Jarrell, Ho Young Lee, Choon-Myung Lee, Michael L. Orr, Dean P. Jones, Young-Mi Go
Biological systems have evolved highly regulated systems to ensure homeostatic levels of trace minerals, such as selenium (Se), which are important to metabolic function and signaling. Much of the understanding of these systems is limited to endogenous proteins and small molecules used for trafficking of minerals. Phytochelatins, a class of plant-derived metal chelating peptides with the general structure, (γ-Glu-Cys)n-Gly, are ubiquitous in the diet and were recently found associated with Se and other metals in human urine. These findings suggest that diet-derived phytochelatins could influence metal homeostasis alongside known endogenous metal-binding compounds. In the present study, we investigated the impact of long-term, oral phytochelatin supplementation on metal homeostasis in a murine model. Phytochelatin supplementation increased Se, zinc and cobalt in the liver and increased urinary Se. Integrative analysis of liver metal profiles with untargeted, high-resolution liver metabolomics revealed dynamic metallome interaction with lipid and carbohydrate metabolism. These results highlight an active role of dietary phytochelatins in modulating mammalian metal homeostasis and associated metabolism. Such dietary components could play a pivotal role in regulating trace metal homeostasis and metal-driven pathophysiology.
生物系统已经进化出高度调节的系统,以确保微量矿物质的稳态水平,如硒(Se),这对代谢功能和信号传导很重要。对这些系统的了解大多局限于内源性蛋白质和用于矿物运输的小分子。植物螯合素(Phytochelatins)是一类由植物衍生的金属螯合肽,其一般结构为(γ-Glu-Cys)n-Gly,普遍存在于饮食中,最近发现与人体尿液中的硒和其他金属有关。这些发现表明,饮食来源的植物螯合素可以与已知的内源性金属结合化合物一起影响金属稳态。在本研究中,我们研究了长期口服植物螯合素对小鼠模型金属稳态的影响。补充植物螯合素增加了肝脏中的硒、锌和钴,并增加了尿硒。肝脏金属谱与非靶向、高分辨率肝脏代谢组学的综合分析揭示了金属组与脂质和碳水化合物代谢的动态相互作用。这些结果强调了膳食植物螯合素在调节哺乳动物金属稳态和相关代谢中的积极作用。这些膳食成分可能在调节微量金属稳态和金属驱动的病理生理中起关键作用。
{"title":"Dietary metal chelator, phytochelatin 2, increases selenium and alters metal homeostasis and associated lipid metabolism in the liver","authors":"Zachery R. Jarrell,&nbsp;Ho Young Lee,&nbsp;Choon-Myung Lee,&nbsp;Michael L. Orr,&nbsp;Dean P. Jones,&nbsp;Young-Mi Go","doi":"10.1016/j.arres.2025.100144","DOIUrl":"10.1016/j.arres.2025.100144","url":null,"abstract":"<div><div>Biological systems have evolved highly regulated systems to ensure homeostatic levels of trace minerals, such as selenium (Se), which are important to metabolic function and signaling. Much of the understanding of these systems is limited to endogenous proteins and small molecules used for trafficking of minerals. Phytochelatins, a class of plant-derived metal chelating peptides with the general structure, (γ-Glu-Cys)<sub>n</sub>-Gly, are ubiquitous in the diet and were recently found associated with Se and other metals in human urine. These findings suggest that diet-derived phytochelatins could influence metal homeostasis alongside known endogenous metal-binding compounds. In the present study, we investigated the impact of long-term, oral phytochelatin supplementation on metal homeostasis in a murine model. Phytochelatin supplementation increased Se, zinc and cobalt in the liver and increased urinary Se. Integrative analysis of liver metal profiles with untargeted, high-resolution liver metabolomics revealed dynamic metallome interaction with lipid and carbohydrate metabolism. These results highlight an active role of dietary phytochelatins in modulating mammalian metal homeostasis and associated metabolism. Such dietary components could play a pivotal role in regulating trace metal homeostasis and metal-driven pathophysiology.</div></div>","PeriodicalId":72106,"journal":{"name":"Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe","volume":"17 ","pages":"Article 100144"},"PeriodicalIF":2.7,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145624034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Advances in redox research : an official journal of the Society for Redox Biology and Medicine and the Society for Free Radical Research-Europe
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