{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T19:29:01Z","timestamp":1777922941341,"version":"3.51.4"},"reference-count":41,"publisher":"SAGE Publications","issue":"8","license":[{"start":{"date-parts":[[2008,9,1]],"date-time":"2008-09-01T00:00:00Z","timestamp":1220227200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Toxicol Ind Health"],"published-print":{"date-parts":[[2008,9]]},"abstract":"<jats:p>\n                    Mercury is a global pollutant considered to be a persistent bioaccumulative and toxic chemical. Humans may be exposed to organic forms of mercury by either inhalation, oral, or dermal routes. Methylmercury is more toxic to living organisms than the inorganic forms. In this study, we attempted to elucidate the altered functions of alveolar macrophage including nitric oxide production after methylmercury exposure. Treatment of 7\u00a0\u03bcM methylmercury for 24\u00a0h inhibited lipopolysaccharide-induced nitric oxide and nitric oxide synthase production of alveolar macrophages. The addition of H-89 (PKA inhibitor) significantly decreased the methylmercury inhibition of lipopolysaccharide-mediated nitric oxide production. We found the cell had a calcium-dependent adenylate cyclase, and MeHg could inhibit the phosphorylation of extracellular-signal regulated kinase (ERK). Because methylmercury could increase the intracellular calcium ion concentration, it might activate the adenylate cyclase by increasing [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    . Though the interaction of methylmercury with the immune system has been studied by several investigators, the actual mechanisms underlying these interactions are still poorly understood. We discovered that methylmercury could activate protein kinase A, which in turn would inhibit the activation of Raf-1-ERK and so inhibit the release of nitric oxide.\n                  <\/jats:p>","DOI":"10.1177\/0748233708098122","type":"journal-article","created":{"date-parts":[[2008,11,27]],"date-time":"2008-11-27T09:53:57Z","timestamp":1227779637000},"page":"531-538","source":"Crossref","is-referenced-by-count":8,"title":["The influence of methylmercury on the nitric oxide production of alveolar macrophages"],"prefix":"10.1177","volume":"24","author":[{"given":"TC","family":"Kuo","sequence":"first","affiliation":[{"name":"Department of Cosmetic Science, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2008,9,1]]},"reference":[{"key":"atypb1","doi-asserted-by":"publisher","DOI":"10.1677\/joe.1.07079"},{"key":"atypb2","doi-asserted-by":"publisher","DOI":"10.1016\/j.tox.2004.11.035"},{"key":"atypb3","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.bi.63.070194.001135"},{"key":"atypb4","doi-asserted-by":"publisher","DOI":"10.1006\/bbrc.1993.2162"},{"key":"atypb5","doi-asserted-by":"crossref","first-page":"12190","DOI":"10.1016\/S0021-9258(17)32700-X","volume":"269","author":"Cali JJ","year":"1994","journal-title":"J Biol 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