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1.
Journal of Pharmaceutical Analysis ; (6): 108-112,172, 2000.
Article in Chinese | WPRIM | ID: wpr-686815

ABSTRACT

Objective According to the distribution of low selenium areas, low nutrition state of the residents and the affecting cartilage growth and articular cartilage of Kashin-Beck Disease(KBD),the chondrocyte differentia- tion and differential expression of collagen types Ⅰ , Ⅱ and Ⅹ in articular cartilage from Chinese mini-pigs treated with low selenium were investigated in order to gain insight into the effects of these conditions on chondrocyte differ- entiation in KBD cartilage. Mothods Eleven male juvenile mini-pigs, aged from 4 weeks to 6 weeks after birth, were divided into 3 groups. The Se content in the diet of the “low Se” group was 0. 035mg/kg diet, and 0. 175 mg/kg diet in the control. For Se-supplemented group 0. 390mg /kg diet was added. The content of Se in blood was assayed at the beginning and at the end of each experiment. Samples of articular cartilage were taken from the right femur condylus, and collagen types Ⅰ , Ⅱ and Ⅹ in articular cartilage were analyzed by immunohistochemistry and in situ hybridization. Results①All cartilage samples from juvenile mini-pigs fed with low selenium diet revealed a re- duction in type Ⅹ collagen mRNA expression in the hypertrophic chondrocytes as shown by in situ hybridization, and reduced type Ⅹ collagen deposition in the lower hypertrophic zone as shown by immunohistochemistry. ②Addition of selenium to the diet restored the type Ⅹ collagen to normal level. ③Type Ⅱ collagen was evenly distributed over the entire articular cartilage in all experimental and control groups. Type Ⅱ collagen mRNA signals were most prominent in the upper articular layer as well as in the hypertrophic zone in all groups. Type Ⅱ collagen expression was restrict- ed to the zone of endochondral ossification in all experimental groups and the control. Conclusion Low selenium has an down-regulatory role on the synthesis and deposition of collagen type Ⅹ in hypertrophic chondrocytes in articular cartilage of mini-pigs. Supplement of the low Se diet with additional Se restored the signals of collagen type Ⅹ to nor- mal levels. These findings indicate that selenium deficiency may disturb chondrocyte differentiation to hypertrophic cells in the growth plate,and worthy to be investigated further.

2.
Journal of Pharmaceutical Analysis ; (6): 1-7, 1999.
Article in Chinese | WPRIM | ID: wpr-621896

ABSTRACT

The relationship of cause-result between low selenium (Se) and Kashin-Beck disease (KBD) was probed by the prospective study of epidemiological method with regarding low-Se as an exposure factor in this paper. 597 healthy children lived in KBD areas with low, middle and high prevalence were divided into the low-Se exposed group and the non-low-Se exposed group according to their Se content in hair. The low-Se exposed group was divided into three subgroups, such as Se content in hair≤110 ng/g, 110 ng/g<Se content in hair≤150 ng/g and 150 ng/g<Se content in hair≤200 ng/g, respectively. Six new cases of the total with KBD (incidence was 0.574% person-year) were found in the low-Se exposed group during three years period of the investigation. No new case was found in the non low-Se exposed group . KBD incidence was not significantly different between those two groups. Two new cases were found in children with Se content in hair kept below 110 ng/g during three years (incidence: 1.21% person-year). SMR in each group indicated that the new cases observed in the low-Se exposed group was remarkable lower than the new cases expected. It was not observed that the dose-response relationship between low-Se and KBD, and was not supported that the low-Se was a predominant factor to cause KBD.

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