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Extracellular superoxide dismutase a...

Regan, Elizabeth Anne.

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Extracellular superoxide dismutase and oxidant stress in osteoarthritis.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Extracellular superoxide dismutase and oxidant stress in osteoarthritis./
作者:	Regan, Elizabeth Anne.
面頁冊數:	128 p.
附註:	Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 3054.
Contained By:	Dissertation Abstracts International67-06B.
標題:	Chemistry, Biochemistry. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3219959
ISBN:	9780542734052

Extracellular superoxide dismutase and oxidant stress in osteoarthritis.
Regan, Elizabeth Anne.

Extracellular superoxide dismutase and oxidant stress in osteoarthritis. - 128 p.

Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 3054.

Thesis (Ph.D.)--University of Colorado Health Sciences Center, 2006.

Osteoarthritis (OA) is a disabling disease of the joints of unknown etiology, in which the articular cartilage is destroyed. We hypothesized that the extracellular isoform of superoxide dismutase would be a constituent of cartilage and that its deficiency could be associated with the characteristic degeneration of osteoarthritis. We studied extracellular superoxide dismutase (EC-SOD) in osteoarthritis by measuring the enzyme in human cartilage and joint fluid, and comparing samples from subjects with and without OA. Joint fluid was also studied for levels of important antioxidants, as well as IL-6 and TGF-beta. We studied the STR/ort mouse, a spontaneous model of OA, for EC-SOD concentration in cartilage and nitrotyrosine formation. We also looked at human chondrocytes in cell culture to define further define chondrocytes are the source of ECSOD in cartilage.

ISBN: 9780542734052Subjects--Topical Terms:

1017722
Chemistry, Biochemistry.

Extracellular superoxide dismutase and oxidant stress in osteoarthritis.
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100 1 $a Regan, Elizabeth Anne. $3 1920638
245 1 0 $a Extracellular superoxide dismutase and oxidant stress in osteoarthritis.
300 $a 128 p.
500 $a Source: Dissertation Abstracts International, Volume: 67-06, Section: B, page: 3054.
500 $a Adviser: James D. Crapo.
502 $a Thesis (Ph.D.)--University of Colorado Health Sciences Center, 2006.
520 $a Osteoarthritis (OA) is a disabling disease of the joints of unknown etiology, in which the articular cartilage is destroyed. We hypothesized that the extracellular isoform of superoxide dismutase would be a constituent of cartilage and that its deficiency could be associated with the characteristic degeneration of osteoarthritis. We studied extracellular superoxide dismutase (EC-SOD) in osteoarthritis by measuring the enzyme in human cartilage and joint fluid, and comparing samples from subjects with and without OA. Joint fluid was also studied for levels of important antioxidants, as well as IL-6 and TGF-beta. We studied the STR/ort mouse, a spontaneous model of OA, for EC-SOD concentration in cartilage and nitrotyrosine formation. We also looked at human chondrocytes in cell culture to define further define chondrocytes are the source of ECSOD in cartilage.
520 $a EC-SOD was measured by ELISA, and immunohistochemistry. Total SOD activity was measured using the cytochrome C method. Real time RT PCR was used to quantitate changes in mRNA for EC-SOD, nNOS, iNOS, COL2, COL10, and Aggrecan. Urate and ascorbate were measured with HPLC; and IL-6 and TGF-beta were measured with ELISA. GSH/GSSG and trolox in joint fluid were measured with colorimetric techniques.
520 $a Our results show that EC-SOD is highly expressed in cartilage and secreted by chondrocytes when they were grown in alginate bead culture. Immunohistochemistry identified EC-SOD in the cartilage matrix and chondrocytes. Osteoarthritic cartilage was deficient in EC-SOD with a four-fold reduction in EC-SOD per microgram of protein. Osteoarthritic joint fluid was deficient in EC-SOD and had decreases in ascorbate and glutathione. mRNA for EC-SOD and nNOS was significantly increased in the osteoarthritis cartilage samples.
520 $a The STR/ort mouse model of osteoarthritis showed a dramatic deficiency of EC-SOD in 5 week old pre-lesional tibial cartilages, with evidence of progressive oxidative stress marked by 3-nitrotyrosine formation in the cartilage. Although the 15 and 25 week mice demonstrated increases in cartilage EC-SOD levels in response to oxidative stress, they were not adequate to control the oxidant damage.
520 $a Human chondrocytes produced EC-SOD protein and mRNA when grown in alginate gel but not when grown in monolayer. The human tissue, cell culture, joint fluid and mouse model data suggest that EC-SOD deficiency and oxidant stress play a role in of osteoarthritis.
590 $a School code: 0831.
650 4 $a Chemistry, Biochemistry. $3 1017722
650 4 $a Health Sciences, Medicine and Surgery. $3 1017756
690 $a 0487
690 $a 0564
710 2 0 $a University of Colorado Health Sciences Center. $3 1023815
773 0 $t Dissertation Abstracts International $g 67-06B.
790 1 0 $a Crapo, James D., $e advisor
790 $a 0831
791 $a Ph.D.
792 $a 2006
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3219959