Authors: Wu, Qingzhi; Huang, Kaixun

Source: Biological Trace Element Research, Volume 112, Number 3, September 2006 , pp. 273-282(10)

Publisher: Humana Press

Abstract:

Wistar rats were fed Se-deficient (0.017±0.002 mg Se/kg) and Seadequate (0.32±0.045 Se mg/kg) diets for 12 mo and then were given 5 mg/kg of cholestane-3β,tα,6β-triol (3-triol), intravenously. Se compounds (Na₂SeO₃ and ebselen) were supplemented in different doses and times to the Se-deficient rats. Twenty-four hours after 3-triol infusion, the changes in ultrastructures of rat aorta were examined by scanning electron micrography (SEM) and transmission electron micrography (TEM). SEM examinations showed that 3-triol induced diffused injuries on arterial endothelial urfaces of long-term Se-deficient rat, and a large number of holes or craterlike defects were observed. TEM examinations further showed that 3-triol induced swelling, necrosis, and shedding of endothelial cells, which resulted in the destruction of endothelial integrity. Mean-while, smooth muscle cells proliferated and migrated toward intimae; the breakage of internal elastic lamina benefited the migration of smooth muscle cells. Supplemented with Na₂SeO₃ (40 μg/kg, 10 d per continuum) and ebselen (20 mg/kg), respectively, exhibited significant protection from damages induced by 3-triol. It seems that protecting mechanisms were different between Na₂SeO₃ and ebselen. The present investigation gave visual evidence that both injuries induced by cholesterol oxides and the Se nutritional status contributed to the development of atherosclerosis.

Keywords: Selenium; arterial wall; cholesterol oxides; scanning electron microscopy; transmission electron microscopy; ebselen; atherosclerosis

Document Type: Research article

DOI: http://dx.doi.org/10.1385/BTER:112:3:273

Affiliations: 1: Department of Chemistry, Huazhong University of Science and Technology, Wuhan, Hubei 430074, People's Republic of China,

Publication date: 2006-09-01

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