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11. |
Effect of Santoquin on humoral immune function in mice: lack of interference with selenium utilization |
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Australian Journal of Experimental Biology and Medical Science,
Volume 67,
Issue 1,
1989,
Page 83-84
JC Travis,
S Thornton,
L Daignault,
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摘要:
SummarySantoquin (0·25% by weight) in the diets of mice receiving adequate dietary selenium (1·0 parts/106) reduced the humoral immune response, as monitored by the plaque‐forming cell assay, to levels exhibited by mice maintained on selenium‐deficient diets (0·005 parts/106). Mice exhibiting this suppression of immunity had levels of blood glutathione peroxidase, serum selenium, and liver DNA, RNA and protein similar to mice receiving selenium only. Therefore, it was concluded that Santoquin is not immunosuppressive by interfering with selenium metabolism or general tissue function, but by other unknown mechanisms.
ISSN:0004-945X
DOI:10.1038/icb.1989.11
出版商:Nature Publishing Group
年代:1989
数据来源: WILEY
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12. |
Involvement of O2radicals in ‘autoimmune’ diabetes |
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Australian Journal of Experimental Biology and Medical Science,
Volume 67,
Issue 1,
1989,
Page 85-87
IN Nomikos,
Y Wang,
KJ Lafferty,
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PDF (892KB)
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摘要:
SummarySpontaneous diabetes in the non‐obese diabetic (NOD) mice is a CD4 T cell‐dependent process. We have suggested that specific β cell destruction results from free radical production at the site of islet inflammation; oxygen radicals are produced by activated inflammatory cells. We reported here thatin vivotreatment of spontaneously diabetic NOD mice with the enzyme superoxide dismutase (2000 U for seven injections) and catalase (40 000 U for seven injections) protects islet tissue from disease recurrence following transplantation into spontaneously diabetic mice. Similar results were obtained when animals were treated with either enzyme alone. This effect was dose‐dependent and little protection was observed when the dose of enzyme was reduced four‐fold. These results indicate that oxygen metabolites, specially superoxide and hydrogen peroxide, are directly involved in the pathogenesis of immunology mediated diabetes.
ISSN:0004-945X
DOI:10.1038/icb.1989.12
出版商:Nature Publishing Group
年代:1989
数据来源: WILEY
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