{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T19:08:36Z","timestamp":1789067316262,"version":"build-2803163510"},"reference-count":30,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":89,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,11]]},"abstract":"<jats:sec><jats:title>Background and purpose:<\/jats:title><jats:p>Hydrogen sulphide (H<jats:sub>2<\/jats:sub>S) has been involved in cardiovascular homoeostasis but data about its role in animal models of diabetic pathology are still lacking. Here, we have analysed H<jats:sub>2<\/jats:sub>S signalling in a genetic model of diabetes, the non\u2010obese diabetic (NOD) mice.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental approach:<\/jats:title><jats:p>NOD mice exhibit a progressive endothelial dysfunction characterized by a reduced reactivity of blood vessels as diabetes develops. NOD mice were divided into three groups according to different glycosuria values: NOD I, NOD II and NOD III. Age\u2010matched non\u2010obese resistant (NOR) mice were used as controls. H<jats:sub>2<\/jats:sub>S levels in plasma and aortic tissue were measured. Functional studies in aorta were carried out in isolated organ baths using both an exogenous source of H<jats:sub>2<\/jats:sub>S (NaHS) and the metabolic precursor (<jats:sc>L<\/jats:sc>\u2010cysteine). Real time PCR and western blot analysis were also carried out on aortic tissues.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key results:<\/jats:title><jats:p>NOD mice exhibited a progressive reduction of H<jats:sub>2<\/jats:sub>S plasma levels, which paralleled disease severity. <jats:sc>L<\/jats:sc>\u2010cysteine\u2010induced H<jats:sub>2<\/jats:sub>S production by aortic tissues was also progressively reduced. <jats:sc>L<\/jats:sc>\u2010cysteine\u2010induced vasorelaxation was significantly reduced in NOD mice while NaHS\u2010induced relaxation was unaffected. ODQ (guanylate cyclase inhibitor), <jats:sc>L<\/jats:sc>\u2010NAME (NO synthase inhibitor) or PAG, an inhibitor of cystathionine\u2010\u03b3\u2010lyase (CSE) inhibited H<jats:sub>2<\/jats:sub>S production induced by <jats:sc>L<\/jats:sc>\u2010cysteine.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and implications:<\/jats:title><jats:p>In NOD mice, endogenous H<jats:sub>2<\/jats:sub>S production is significantly impaired. Also, the ability of isolated aorta to respond to exogenous H<jats:sub>2<\/jats:sub>S is enhanced and endothelium\u2010derived NO appears to be involved in the enzymatic conversion of <jats:sc>L<\/jats:sc>\u2010cysteine into H<jats:sub>2<\/jats:sub>S.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>155<\/jats:bold>, 673\u2013680; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"fn1\">fn1<\/jats:ext-link>; published online 21 July 2008<\/jats:p><\/jats:sec>","DOI":"10.1038\/bjp.2008.296","type":"journal-article","created":{"date-parts":[[2008,7,21]],"date-time":"2008-07-21T10:06:17Z","timestamp":1216634777000},"page":"673-680","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":152,"title":["Biosynthesis of H<sub>2<\/sub>S is impaired in non\u2010obese diabetic (NOD) 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