• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

氧化应激参数作为一氧化碳中毒潜在生物标志物的关键性评估。

The Critical Assessment of Oxidative Stress Parameters as Potential Biomarkers of Carbon Monoxide Poisoning.

机构信息

Toxicology Clinical Department, University Hospital, Jagiellonian University Medical College, 31-008 Kraków, Poland.

Institute of Health, State Higher Vocational School, 33-320 Nowy Sącz, Poland.

出版信息

Int J Mol Sci. 2023 Jun 28;24(13):10784. doi: 10.3390/ijms241310784.

DOI:10.3390/ijms241310784
PMID:37445969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10341785/
Abstract

In conventional clinical toxicology practice, the blood level of carboxyhemoglobin is a biomarker of carbon monoxide (CO) poisoning but does not correspond to the complete clinical picture and the severity of the poisoning. Taking into account articles suggesting the relationship between oxidative stress parameters and CO poisoning, it seems reasonable to consider this topic more broadly, including experimental biochemical data (oxidative stress parameters) and patients poisoned with CO. This article aimed to critically assess oxidative-stress-related parameters as potential biomarkers to evaluate the severity of CO poisoning and their possible role in the decision to treat. The critically set parameters were antioxidative, including catalase, 2,2-diphenyl-1-picryl-hydrazyl, glutathione, thiol and carbonyl groups. Our preliminary studies involved patients ( = 82) admitted to the Toxicology Clinical Department of the University Hospital of Jagiellonian University Medical College (Kraków, Poland) during 2015-2020. The poisoning was diagnosed based on medical history, clinical symptoms, and carboxyhemoglobin blood level. Blood samples for carboxyhemoglobin and antioxidative parameters were collected immediately after admission to the emergency department. To evaluate the severity of the poisoning, the Pach scale was applied. The final analysis included a significant decrease in catalase activity and a reduction in glutathione level in all poisoned patients based on the severity of the Pach scale: I°-III° compared to the control group. It follows from the experimental data that the poisoned patients had a significant increase in level due to thiol groups and the 2,2-diphenyl-1-picryl-hydrazyl radical, with no significant differences according to the severity of poisoning. The catalase-to-glutathione and thiol-to-glutathione ratios showed the most important differences between the poisoned patients and the control group, with a significant increase in the poisoned group. The ratios did not differentiate the severity of the poisoning. The carbonyl level was highest in the control group compared to the poisoned group but was not statistically significant. Our critical assessment shows that using oxidative-stress-related parameters to evaluate the severity of CO poisoning, the outcome, and treatment options is challenging.

摘要

在传统的临床毒理学实践中,血液中碳氧血红蛋白的水平是一氧化碳(CO)中毒的生物标志物,但与完整的临床情况和中毒的严重程度并不对应。考虑到一些文章表明氧化应激参数与 CO 中毒之间存在关系,因此似乎有理由更广泛地考虑这个问题,包括实验生化数据(氧化应激参数)和 CO 中毒的患者。本文旨在批判性地评估与氧化应激相关的参数作为评估 CO 中毒严重程度的潜在生物标志物,并探讨其在治疗决策中的可能作用。本文批判性地设定了抗氧化参数,包括过氧化氢酶、2,2-二苯基-1-苦肼基、谷胱甘肽、硫醇和羰基。我们的初步研究涉及 2015 年至 2020 年期间在雅盖隆大学医学院毒理学临床科就诊的患者(=82)。根据病史、临床症状和血液中碳氧血红蛋白水平诊断中毒。在急诊科就诊时立即采集血液样本用于检测碳氧血红蛋白和抗氧化参数。应用 Pach 量表评估中毒的严重程度。根据 Pach 量表的严重程度(I°-III°),对所有中毒患者进行了分析,发现过氧化氢酶活性显著降低,谷胱甘肽水平降低。根据实验数据,中毒患者的巯基和 2,2-二苯基-1-苦肼基自由基水平显著升高,与中毒严重程度无关。过氧化氢酶/谷胱甘肽和硫醇/谷胱甘肽比值在中毒患者和对照组之间表现出最重要的差异,中毒组显著升高。这些比值并不能区分中毒的严重程度。与中毒组相比,对照组的羰基水平最高,但无统计学差异。我们的批判性评估表明,使用与氧化应激相关的参数来评估 CO 中毒的严重程度、结果和治疗选择具有挑战性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/b0d734a96c74/ijms-24-10784-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/db730c49ff46/ijms-24-10784-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/a9b1175601f4/ijms-24-10784-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/fa31bf24d0d7/ijms-24-10784-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/9aaaafd637cd/ijms-24-10784-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/b0d734a96c74/ijms-24-10784-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/db730c49ff46/ijms-24-10784-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/a9b1175601f4/ijms-24-10784-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/fa31bf24d0d7/ijms-24-10784-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/9aaaafd637cd/ijms-24-10784-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8382/10341785/b0d734a96c74/ijms-24-10784-g005.jpg

相似文献

1
The Critical Assessment of Oxidative Stress Parameters as Potential Biomarkers of Carbon Monoxide Poisoning.氧化应激参数作为一氧化碳中毒潜在生物标志物的关键性评估。
Int J Mol Sci. 2023 Jun 28;24(13):10784. doi: 10.3390/ijms241310784.
2
Initial blood lactate correlates with carboxyhemoglobin and clinical severity in carbon monoxide poisoned patients.一氧化碳中毒患者的初始血乳酸水平与碳氧血红蛋白及临床严重程度相关。
Clin Biochem. 2014 Dec;47(18):298-301. doi: 10.1016/j.clinbiochem.2014.09.016. Epub 2014 Sep 28.
3
Evaluation of oxidative stress and antioxidant parameters in children with carbon monoxide poisoning.评价一氧化碳中毒患儿的氧化应激和抗氧化参数。
Hum Exp Toxicol. 2019 Nov;38(11):1235-1243. doi: 10.1177/0960327119867751. Epub 2019 Aug 18.
4
Asymmetric dimethylarginine and heart-type fatty acid-binding protein 3 are risk markers of cardiotoxicity in carbon monoxide poisoning cases in Zagazig university hospitals.不对称二甲基精氨酸和心脏型脂肪酸结合蛋白3是扎加齐格大学医院一氧化碳中毒病例中心脏毒性的风险标志物。
Hum Exp Toxicol. 2017 Mar;36(3):247-255. doi: 10.1177/0960327116646621. Epub 2016 Jul 11.
5
Carboxyhemoglobin: a primer for clinicians.碳氧血红蛋白:临床医生入门指南。
Undersea Hyperb Med. 2018 Mar-Apr;45(2):165-171.
6
Oxidative stress increases in carbon monoxide poisoning patients.一氧化碳中毒患者的氧化应激增加。
Hum Exp Toxicol. 2011 Feb;30(2):160-4. doi: 10.1177/0960327110388539. Epub 2010 Nov 1.
7
Veno-venous extracorporeal blood phototherapy increases the rate of carbon monoxide (CO) elimination in CO-poisoned pigs.静脉-静脉体外血液光疗可提高一氧化碳(CO)中毒猪 CO 的消除率。
Lasers Surg Med. 2022 Feb;54(2):256-267. doi: 10.1002/lsm.23462. Epub 2021 Aug 5.
8
[Estimation of carbon monoxide poisonings frequency, based on carboxyhemoglobin determinations performed in Toxicology Laboratory in Krakow in years 2002-2010].[基于2002年至2010年在克拉科夫毒理学实验室进行的碳氧血红蛋白测定对一氧化碳中毒频率的估算]
Przegl Lek. 2011;68(8):413-6.
9
Emergency department management of suspected carbon monoxide poisoning: role of pulse CO-oximetry.急诊疑似一氧化碳中毒的管理:脉搏 CO-血氧仪的作用。
Respir Care. 2013 Oct;58(10):1614-20. doi: 10.4187/respcare.02313. Epub 2013 Mar 19.
10
Clinical and scintigraphic (99mTc-MIBI SPECT) heart evaluation in young acutely carbon monoxide poisoned patients.年轻急性一氧化碳中毒患者的临床及闪烁扫描(99mTc-MIBI单光子发射计算机断层扫描)心脏评估
Przegl Lek. 2003;60(4):226-32.

引用本文的文献

1
Metallic nanoparticles: a promising novel therapeutic tool against antimicrobial resistance and spread of superbugs.金属纳米颗粒:一种对抗抗菌素耐药性和超级细菌传播的有前景的新型治疗工具。
Biometals. 2025 Feb;38(1):55-88. doi: 10.1007/s10534-024-00647-5. Epub 2024 Oct 24.
2
Impact of smokeless tobacco on psychological and oxidative stress in unemployed indian youth.无烟烟草对失业印度青年心理和氧化应激的影响。
Amino Acids. 2024 Oct 12;56(1):59. doi: 10.1007/s00726-024-03416-3.
3
Advances in nephroprotection: the therapeutic role of selenium, silver, and gold nanoparticles in renal health.

本文引用的文献

1
Polymorphisms in Genes Encoding VDR, CALCR and Antioxidant Enzymes as Predictors of Bone Tissue Condition in Young, Healthy Men.维生素 D 受体、钙敏感受体和抗氧化酶基因多态性作为年轻健康男性骨组织状况预测因子的研究。
Int J Mol Sci. 2023 Feb 8;24(4):3373. doi: 10.3390/ijms24043373.
2
Carbon monoxide neurotoxicity is triggered by oxidative stress induced by ROS production from three distinct cellular sources.一氧化碳神经毒性是由三种不同细胞来源的 ROS 产生引起的氧化应激所触发的。
Redox Biol. 2023 Apr;60:102598. doi: 10.1016/j.redox.2022.102598. Epub 2023 Jan 7.
3
Antioxidant Activity of Quercetin in a HO-Induced Oxidative Stress Model in Red Blood Cells: Functional Role of Band 3 Protein.
肾保护的进展:硒、银和金纳米颗粒在肾脏健康中的治疗作用
Int Urol Nephrol. 2025 Feb;57(2):479-510. doi: 10.1007/s11255-024-04212-4. Epub 2024 Sep 23.
4
Diagnostic challenge in a 2-year-old boy poisoned with carbon monoxide: A case report.一名2岁一氧化碳中毒男孩的诊断挑战:病例报告
Clin Case Rep. 2024 Feb 7;12(2):e8470. doi: 10.1002/ccr3.8470. eCollection 2024 Feb.
5
Cellular and Molecular Mechanisms in Oxidative Stress-Related Diseases 2.0/3.0.氧化应激相关疾病的细胞和分子机制 2.0/3.0
Int J Mol Sci. 2023 Nov 6;24(21):16018. doi: 10.3390/ijms242116018.
槲皮素在 HO 诱导的红细胞氧化应激模型中的抗氧化活性:膜蛋白 3 的功能作用。
Int J Mol Sci. 2022 Sep 20;23(19):10991. doi: 10.3390/ijms231910991.
4
Açaì () Extract Protects Human Erythrocytes from Age-Related Oxidative Stress.阿萨伊()提取物可保护人红细胞免受与年龄相关的氧化应激。
Cells. 2022 Aug 3;11(15):2391. doi: 10.3390/cells11152391.
5
Oxidation Stress as a Mechanism of Aging in Human Erythrocytes: Protective Effect of Quercetin.氧化应激作为人类红细胞衰老的机制:槲皮素的保护作用。
Int J Mol Sci. 2022 Jul 14;23(14):7781. doi: 10.3390/ijms23147781.
6
Impact of Drying Conditions on Antioxidant Activity of Red Clover (), Sweet Violet () and Elderberry Flowers ().干燥条件对红三叶草、香堇和接骨木花抗氧化活性的影响
Materials (Basel). 2022 May 5;15(9):3317. doi: 10.3390/ma15093317.
7
The Influence of Organic Vanadium Complexes on an Antioxidant Profile in Adipose Tissue in Wistar Rats.有机钒配合物对Wistar大鼠脂肪组织抗氧化特性的影响。
Materials (Basel). 2022 Mar 6;15(5):1952. doi: 10.3390/ma15051952.
8
Values of Selected Strength Parameters of Miscanthus × Giganteus Stalk Depending on Water Content and Internode Number.根据含水量和节数的芒草×巨芒草茎所选强度参数的值
Materials (Basel). 2022 Feb 16;15(4):1480. doi: 10.3390/ma15041480.
9
d-Galactose Decreases Anion Exchange Capability through Band 3 Protein in Human Erythrocytes.d-半乳糖通过人红细胞中的带3蛋白降低阴离子交换能力。
Antioxidants (Basel). 2020 Aug 2;9(8):689. doi: 10.3390/antiox9080689.
10
Carbon monoxide reverses the metabolic adaptation of microglia cells to an inflammatory stimulus.一氧化碳可逆转小胶质细胞对炎症刺激的代谢适应性。
Free Radic Biol Med. 2017 Mar;104:311-323. doi: 10.1016/j.freeradbiomed.2017.01.022. Epub 2017 Jan 18.