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吸烟者红细胞增多与抗氧化状态及C反应蛋白水平有关。

Increased eryptosis in smokers is associated with the antioxidant status and C-reactive protein levels.

作者信息

Attanzio Alessandro, Frazzitta Anna, Vasto Sonya, Tesoriere Luisa, Pintaudi Anna Maria, Livrea Maria Antonia, Cilla Antonio, Allegra Mario

机构信息

Department of Biological, Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, Via Archirafi 28, 90123, Palermo, Italy.

Nutrition and Food Science Area, Faculty of Pharmacy, University of Valencia, Avda. Vicente Andrés Estellés s/n, 46100, Burjassot (Valencia), Spain.

出版信息

Toxicology. 2019 Jan 1;411:43-48. doi: 10.1016/j.tox.2018.10.019. Epub 2018 Oct 29.

Abstract

Cigarette smoking has been linked with oxidative stress and inflammation. In turn, eryptosis, the suicidal erythrocyte death similar to apoptosis that can be triggered by oxidative stress, has been associated with chronic inflammatory diseases including atherosclerosis. However, the link between smoking and eryptosis has not been explored so far. The aim of the present study was to determine the level of eryptotic erythrocytes in healthy male smokers (n = 21) compared to non-smokers (n = 21) and assess its relationship with systemic inflammation (CRP) as well as with antioxidant defense (GSH) and their resistance to ex-vivo induced hemolysis. Smoking caused an increase in phosphatidylserine translocation outside the erythrocyte membrane (hallmark of eryptosis), significantly correlated to the plasma level of CRP (r = 0.546) and GSH concentration in erythrocytes (r=-0.475). With respect to non-smokers, smokers show a marginal increase of total leucocytes and erythrocyte volume, no modifications of the RBC resistance to oxidative stress-induced hemolysis and hematological and lipid parameters unvaried. We conclude that the inflammatory status (high CRP levels) and RBC oxidative stress (low GSH levels) caused by cigarette smoking are associated with an increase of eryptotic erythrocytes, a yet unknown relationship potentially involved with atherosclerosis and cardiovascular disease in smokers.

摘要

吸烟与氧化应激和炎症有关。反过来,红细胞凋亡(eryptosis),即类似于凋亡的自杀性红细胞死亡,可由氧化应激触发,已与包括动脉粥样硬化在内的慢性炎症性疾病相关联。然而,吸烟与红细胞凋亡之间的联系迄今尚未得到探讨。本研究的目的是确定健康男性吸烟者(n = 21)与非吸烟者(n = 21)相比红细胞凋亡水平,并评估其与全身炎症(CRP)以及抗氧化防御(GSH)的关系及其对体外诱导溶血的抵抗力。吸烟导致红细胞膜外磷脂酰丝氨酸易位增加(红细胞凋亡的标志),与血浆CRP水平(r = 0.546)和红细胞内GSH浓度(r = -0.475)显著相关。与非吸烟者相比,吸烟者的总白细胞和红细胞体积略有增加,红细胞对氧化应激诱导溶血的抵抗力无变化,血液学和脂质参数不变。我们得出结论,吸烟引起的炎症状态(高CRP水平)和红细胞氧化应激(低GSH水平)与红细胞凋亡增加有关,这一尚未明确的关系可能与吸烟者的动脉粥样硬化和心血管疾病有关。

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