Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1990-4-17
pubmed:abstractText
The mechanisms by which bone resorbing osteoclasts form and are activated by hormones are poorly understood. We show here that the generation of oxygen-derived free radicals in cultured bone is associated with the formation of new osteoclasts and enhanced bone resorption, identical to the effects seen when bones are treated with hormones such as parathyroid hormone (PTH) and interleukin 1 (IL-1). When free oxygen radicals were generated adjacent to bone surfaces in vivo, osteoclasts were also formed. PTH and IL-1-stimulated bone resorption was inhibited by both natural and recombinant superoxide dismutase, an enzyme that depletes tissues of superoxide anions. We used the marker nitroblue tetrazolium (NBT) to identify the cells that were responsible for free radical production in resorbing bones. NBT staining was detected only in osteoclasts in cultures of resorbing bones. NBT staining in osteoclasts was decreased in bones coincubated with calcitonin, an inhibitor of bone resorption. We also found that isolated avian osteoclasts stained positively for NBT. NBT staining in isolated osteoclasts was increased when the cells were incubated with bone particles, to which they attach. We confirmed the formation of superoxide anion in isolated avian osteoclasts using ferricytochrome c reduction as a method of detection. The reduction of ferricytochrome c in isolated osteoclasts was inhibited by superoxide dismutase. Our results suggest that oxygen-derived free radicals, and particularly the superoxide anion, are intermediaries in the formation and activation of osteoclasts.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-14254246, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3016093, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3081643, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3260671, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3343349, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3489738, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3543052, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3805716, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3828129, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-3928762, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-4972775, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-5496991, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-5634987, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6214564, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6256463, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6283263, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6304190, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6323522, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-6386073, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-7158821, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-7347492, http://linkedlifedata.com/resource/pubmed/commentcorrection/2312718-7391600
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0021-9738
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
632-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Oxygen-derived free radicals stimulate osteoclastic bone resorption in rodent bone in vitro and in vivo.
pubmed:affiliation
Department of Medicine/Endocrinology and Metabolism, University of Texas Health Science Center, San Antonio 78284-7877.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't