Metabolic Signatures of Oxidative Stress in the Red Blood Cells: Editorial Commentary

E. Nwose
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Abstract

This issue of the journal contains an interesting article—“Metabolic Signatures of Oxidative Stress and their Relationship with Erythrocyte Membrane Surface Roughness among Workers of Manual Material Handling (MMH)”. Oxidative stress has been a longtime research interest that is yet to be assessed by a clinical laboratory for evidence-based practice, because it is perceived to be implicated in virtually every disease or condition. The report surely has backing from the literature. For instance, oxidative stress has known metabolic signatures,[1,2] which is hallmarked by glutathione (GSH), as well as reactive oxygen species.[3] The concept of erythrocyte oxidative stress (EOS) further denotes that the biomarkers vis-a-vis metabolic signatures are detectable in red blood cells. Indeed, cardiovascular complications in diabetes represent a major health problem worldwide, but knowledge of progression and degree of risk in prediabetes is limited. Significant changes in biomarkers of EOS and indicators of related macrovascular events that may underlie the development of diabetic macrovascular complications, have been consistently reported. The biomarkers are speculated to be emerging risk indicators, namely, (1) indices of EOS, including erythrocyte-reduced GSH, malondialdehyde, and associated enzymes; (2) indices of vasculopathy, including plasma D-dimer, homocysteine, and whole blood viscosity; and (3) indices of dyslipidemia, namely, total cholesterol (TC), high-density lipoprotein (HDL), and TC/HDL ratio. Thus, there has been the recognition of a spectrum of metabolic profile[3] that should be narrowed down to a useful panel of tests to improve early identification and intervention.[4] The present article highlights the significant impact of EOS on the surface of the blood cell membranes. While this effect may be known,[5] it is probably yet to be appreciated that apparently healthy individuals may suffer oxidative damage as occupational hazard. The authors have attempted to develop a linear model to demonstrate how individual oxidative stress marker is related to surface roughness of the erythrocyte membrane. It will be interesting to see corroborative reports that will exemplify and validate the speculated model. Further, the authors have, albeit passively, also mentioned a phenomenon that the carriage of oxygen inside the blood and/or body must be assessed by means of biochemical parameters and the nanoscale levels of changes in the surface roughness of the erythrocyte membrane. This may follow the concept of EOS being associated with hypoxia — e.g., oxidative stress can induce hyperviscosity that in turn leads to the sequence of reduced blood flow, less oxygen supply, and tissue hypoxia. The phenomenon may follow the concept of oxidative stress-inducing anemia or exacerbating iron-deficiency anemia as well. It would be interesting to see corroborative reports that will expatiate on this phenomenon.
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红细胞氧化应激的代谢特征:编辑评论
本期杂志刊登了一篇有趣的文章——“手工物料搬运工人氧化应激的代谢特征及其与红细胞膜表面粗糙度的关系”。氧化应激一直是一个长期的研究兴趣,但临床实验室尚未对其进行基于证据的实践评估,因为它被认为与几乎所有疾病或病症有关。这份报告肯定有文献支持。例如,氧化应激具有已知的代谢特征[1,2],其特征是谷胱甘肽(GSH)和活性氧[3]。红细胞氧化应激(EOS)的概念进一步表明,在红细胞中可以检测到相对于代谢特征的生物标志物。事实上,糖尿病的心血管并发症是世界范围内的一个主要健康问题,但对前驱糖尿病的进展和风险程度的了解有限。EOS生物标志物和相关大血管事件指标的显著变化可能是糖尿病大血管并发症发展的基础,一直有报道。推测生物标志物是新兴的风险指标,即:(1)EOS指标,包括红细胞还原性谷胱甘肽、丙二醛和相关酶;(2)血管病变指标,包括血浆d -二聚体、同型半胱氨酸、全血粘度;(3)血脂异常指标,即总胆固醇(TC)、高密度脂蛋白(HDL)、TC/HDL比值。因此,人们已经认识到代谢谱[3]应该缩小到一个有用的测试小组,以提高早期识别和干预[4]。本文强调了EOS对血液细胞膜表面的重要影响。虽然这种影响可能是已知的[5],但可能尚未认识到,表面上健康的个体可能遭受氧化损伤作为职业危害。作者试图建立一个线性模型来证明个体氧化应激标志物与红细胞膜表面粗糙度的关系。看到将例证和验证推测模型的确证报告将是有趣的。此外,作者还被动地提到了一种现象,即血液和/或体内的氧气运输必须通过生化参数和红细胞膜表面粗糙度的纳米级变化来评估。这可能遵循EOS与缺氧相关的概念-例如,氧化应激可诱导高粘度,进而导致血流量减少,氧气供应减少和组织缺氧。这种现象可能遵循氧化应激诱导贫血或加重缺铁性贫血的概念。看到详细阐述这一现象的确证报告将是很有趣的。
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