{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T04:16:37Z","timestamp":1791087397513,"version":"4.1.0"},"reference-count":46,"publisher":"Portland Press Ltd.","issue":"2","content-domain":{"domain":["portlandpress.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2005,7,15]]},"abstract":"<jats:p>IL-1 (interleukin-1) acts as a key mediator of the degeneration of articular cartilage in RA (rheumatoid arthritis) and OA (osteoarthritis), where chondrocyte death is observed. It is still controversial, however, whether IL-1 induces chondrocyte death. In the present study, the viability of mouse chondrocyte-like ATDC5 cells was reduced by the treatment with IL-1\u03b2 for 48\u00a0h or longer. IL-1\u03b2 augmented the expression of the catalytic gp91 subunit of NADPH oxidase, gp91phox, as well as inducible NO synthase in ATDC5 cells. Generation of nitrated guanosine and tyrosine suggested the formation of reactive nitrogen species including ONOO\u2212 (peroxynitrite), a reaction product of NO and O2\u2212, in ATDC5 cells and rat primary chondrocytes treated with IL-1\u03b2. Death of ATDC5 cells after IL-1\u03b2 treatment was prevented by an NADPH-oxidase inhibitor, AEBSF [4-(2-aminoethyl)benzenesulphonyl fluoride], an NO synthase inhibitor, L-NAME (NG-nitro-L-arginine methyl ester), and a ONOO\u2212 scavenger, uric acid. The viability of ATDC5 cells was reduced by the ONOO\u2212-generator 3-(4-morpholinyl)sydnonimine hydrochloride, but not by either the NO-donor 1-hydroxy-2-oxo-3-(N-methyl-2-aminopropyl)-3-methyl-1-triazene or S-nitrosoglutathione. Disruption of mitochondrial membrane potential and ATP deprivation were observed in IL-1\u03b2-treated ATDC5 cells, both of which were restored by L-NAME, AEBSF or uric acid. On the other hand, no morphological or biochemical signs indicating apoptosis were observed in these cells. These results suggest that the death of chondrocyte-like ATDC5 cells was mediated at least in part by mitochondrial dysfunction and energy depletion through ONOO\u2212 formation after IL-1\u03b2 treatment.<\/jats:p>","DOI":"10.1042\/bj20041996","type":"journal-article","created":{"date-parts":[[2005,7,12]],"date-time":"2005-07-12T14:35:21Z","timestamp":1121178921000},"page":"315-323","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":93,"title":["Interleukin-1\u03b2 induces death in chondrocyte-like ATDC5 cells through mitochondrial dysfunction and energy depletion in a reactive nitrogen and oxygen species-dependent manner"],"prefix":"10.1042","volume":"389","author":[{"given":"Rika","family":"Yasuhara","sequence":"first","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoichi","family":"Miyamoto","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takaaki","family":"Akaike","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teruo","family":"Akuta","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masanori","family":"Nakamura","sequence":"additional","affiliation":[{"name":"Department of Oral Anatomy and Developmental Biology, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masamichi","family":"Takami","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Naoko","family":"Morimura","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kayoko","family":"Yasu","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ryutaro","family":"Kamijo","sequence":"additional","affiliation":[{"name":"Department of Biochemistry, Showa University School of Dentistry, Tokyo 142-8555, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"288","published-online":{"date-parts":[[2005,7,5]]},"reference":[{"key":"2021112217464822100_B1","doi-asserted-by":"crossref","first-page":"34","DOI":"10.1159\/000070573","article-title":"Pathophysiological mechanisms in osteoarthritis lead to novel therapeutic strategies","volume":"174","author":"Malemud","year":"2003","journal-title":"Cells Tissues Organs"},{"key":"2021112217464822100_B2","doi-asserted-by":"crossref","first-page":"617","DOI":"10.1038\/nm1054","article-title":"Selective inhibition of NF-\u03baB blocks osteoclastogenesis and prevents inflammatory bone destruction in vivo","volume":"10","author":"Jimi","year":"2004","journal-title":"Nat. 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