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砷中毒的血液流变学观点。

Arsenic intoxication, a hemorheologic view.

机构信息

Cátedra de Física Biológica, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Rosario, Santa Fe, Argentina.

出版信息

Clin Hemorheol Microcirc. 2010;44(1):3-17. doi: 10.3233/CH-2010-1246.

Abstract

Arsenic (As) is a toxic semi-metal of wide distribution in nature. People living in regions where drinking water contains large quantities of arsenic, have an unusually high likelihood of developing blood-vessel diseases, but little is known about the mechanisms involved, i.e. the blood rheologic alterations that would contribute to the circulatory obstruction. Erythrocytes are the main target cells for arsenic compounds systemically absorbed and their cell membrane is the first place against the toxic. In this paper we have examined the in vitro effect of arsenic (As(V)) on the rheologic properties of human erythrocytes in relation with membrane fluidity and internal microviscosity. According to our present results, As(V) treatment produces oxidative degradation of membrane lipids and alteration of internal microviscosity. These red blood cells (RBCs) membrane and cytoplasmic structural damage consequently alters RBCs rheologic properties: an alteration of the RBCs discoid shape to stomatocytes, a diminution of erythrocyte deformability and an enhancement of osmotic fragility and cell aggregability. These effects impaired blood fluid behaviour that contribute to obstruct peripheral circulation and provides anemia, both clinic evidences typical of arsenic cronic intoxication.

摘要

砷(As)是一种广泛分布于自然界中的有毒半金属。生活在饮用水中含有大量砷的地区的人们,患有血管疾病的可能性异常高,但人们对相关机制知之甚少,即导致循环阻塞的血液流变学改变。红细胞是全身吸收的砷化合物的主要靶细胞,其细胞膜是对抗毒性的第一场所。在本文中,我们研究了砷(As(V))对人红细胞流变特性的体外影响,以及与膜流动性和内部微粘度的关系。根据我们目前的结果,As(V)处理会导致膜脂质的氧化降解和内部微粘度的改变。这些红细胞(RBC)膜和细胞质结构的损伤继而改变 RBC 的流变特性:RBC 从盘状变为口形细胞,红细胞变形能力降低,渗透性脆性和细胞聚集性增强。这些影响会损害血液的流动特性,导致外周循环阻塞,并导致贫血,这两种临床证据都是砷慢性中毒的典型表现。

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