Prasad Ankush, Balukova Anastasiia, Pospíšil Pavel
Department of Biophysics, Centre of the Region Haná for Biotechnological and Agricultural Research, Faculty of Science, Palacký University, Olomouc, Czechia.
Front Physiol. 2018 Aug 15;9:1109. doi: 10.3389/fphys.2018.01109. eCollection 2018.
The skin is the largest organ in the body and is consistently exposed to aggressive environmental attacks (biological/physical/chemical, etc.). Reactive oxygen species (ROS) are formed during the normal oxidative metabolism which enhances to a lethal level under stress conditions referred to as oxidative stress. While, under normal conditions, cells are capable of dealing with ROS using non-enzymatic and enzymatic defense system, it can lead to a critical damage to cell system via the oxidation of cellular components under stress condition. Lipid peroxidation is a well-established mechanism of cellular injury in all kinds of organisms and it is often used as an indicator of oxidative stress in cells and tissues. In the presence of metal ions, ROS such as hydrogen peroxide (HO) produces highly reactive hydroxyl radical (HO) via Fenton reaction. In the current study, we have used the porcine skin (intact pig ear/skin biopsies) as an / model system to represent human skin. Experimental results have been presented on the participation of HO in the initiation of lipid peroxidation and thereby leading to the formation of reactive intermediates and the formation of electronically excited species eventually leading to ultra-weak photon emission (UPE). To understand the participation of different electronically excited species in the overall UPE, the effect of a scavenger of singlet oxygen (O) on photon emission in the visible and near-infrared region of the spectrum was measured which showed its contribution. In addition, measurement with interference filter with a transmission in the range of 340-540 nm reflected a substantial contribution of triplet carbonyls (L=O) in the photon emission. Thus, it is concluded that during the oxidative radical reactions, the UPE is contributed by the formation of both L=O and O. The method used in the current study is claimed to be a potential tool for non-invasive determination of the physiological and pathological state of human skin in dermatological research.
皮肤是人体最大的器官,持续暴露于具有侵袭性的环境攻击(生物/物理/化学等)之下。活性氧(ROS)在正常氧化代谢过程中形成,在被称为氧化应激的应激条件下会增强至致死水平。虽然在正常情况下,细胞能够利用非酶和酶防御系统处理ROS,但在应激条件下,ROS会通过氧化细胞成分对细胞系统造成严重损害。脂质过氧化是各类生物体中公认的细胞损伤机制,常被用作细胞和组织氧化应激的指标。在金属离子存在的情况下,过氧化氢(HO)等ROS通过芬顿反应产生高活性羟基自由基(HO)。在本研究中,我们使用猪皮肤(完整猪耳/皮肤活检)作为代表人类皮肤的模型系统。实验结果表明了HO在脂质过氧化起始过程中的参与,进而导致反应中间体的形成以及电子激发态物种的形成,最终导致超微弱光子发射(UPE)。为了了解不同电子激发态物种在整体UPE中的参与情况,我们测量了单线态氧(O)清除剂对光谱可见和近红外区域光子发射的影响,结果显示了其贡献。此外,使用透射范围在340 - 540 nm的干涉滤光片进行测量,结果表明三线态羰基(L=O)对光子发射有显著贡献。因此,可以得出结论,在氧化自由基反应过程中,UPE是由L=O和O的形成共同导致的。本研究中使用的方法据称是皮肤病学研究中用于非侵入性测定人类皮肤生理和病理状态的潜在工具。