Horhat Florin G, Rogobete Alexandru F, Papurica Marius, Sandesc Dorel, Tanasescu Sonia, Dumitrascu Victor, Licker Monica, Nitu Razvan, Cradigati Carmen A, Sarandan Mirela, Boruga Ovidiu, Crisan Ciprian D, Ungureanu Emil, Popa Daniela M, Popovici Sonia E, Bedreag Ovidiu H
Clin Lab. 2016 Sep 1;62(9):1601-1607. doi: 10.7754/Clin.Lab.2016.160306.
The critically ill polytrauma patient, apart from the primary, traumatic injuries and the secondary, port-traumatic injuries, presents with a series of molecular disasters. Dysfunctions of the biochemical pathways and molecular damage add to the worsening of the clinical status of these patients, one of the most well-known molecular phenomena being oxidative stress (OS), responsible for an escalation of the inflammatory status, multiple infections, and multiple organ dysfunction syndrome (MODS).
For this study was analysed the literature available on PubMed and Scopus. The key words used in the search were "oxidative stress", "lipid peroxidation", "critically ill", "polytrauma patients", and "biomarkers oxidative stress".
For the study we selected 47 science articles. The oxidative attack on lipids is responsible for the biosynthesis of an increased quantity of free radicals (FR), which further intensifies and aggravates the redox status in these patients.
One of the most aggressive redox mechanisms related to lipid molecules is known as lipid peroxidation (LPOX).
危重症多发伤患者除了有原发性创伤损伤和继发性创伤后损伤外，还会出现一系列分子层面的损害。生化途径功能障碍和分子损伤会加重这些患者的临床状况恶化，其中最广为人知的分子现象之一是氧化应激（OS），它会导致炎症状态升级、多重感染和多器官功能障碍综合征（MODS）。
本研究分析了在PubMed和Scopus上可获取的文献。搜索使用的关键词为“氧化应激”“脂质过氧化”“危重症”“多发伤患者”以及“氧化应激生物标志物”。
本研究选取了47篇科学文章。对脂质的氧化攻击会导致大量自由基（FR）的生物合成增加，这进一步加剧并恶化了这些患者的氧化还原状态。
与脂质分子相关的最具侵袭性的氧化还原机制之一被称为脂质过氧化（LPOX）。
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