{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T00:57:45Z","timestamp":1760576265896,"version":"build-2065373602"},"reference-count":40,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2006,1,11]],"date-time":"2006-01-11T00:00:00Z","timestamp":1136937600000},"content-version":"vor","delay-in-days":6616,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Applied Toxicology"],"published-print":{"date-parts":[[1987,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Arterial blood gases and the pulmonary uptake of putrescine and 5\u2010hydroxytryptamine (5\u2010HT) were studied between 6 h and 18 days after the administration to rats of an oral <jats:sc>LD<\/jats:sc><jats:sub>50<\/jats:sub>\u2010dose of the pneumotoxin, <jats:italic>O<\/jats:italic>,<jats:italic>S<\/jats:italic>,<jats:italic>S<\/jats:italic>\u2010trimethyl phophorodithioate (OSSMe), a potential impurity in several organophosphorus insecticides.<\/jats:p><jats:p>Aortic blood was sampled under pentobarbitone anaesthesia for measurements of arterial pH, and partial pressures of oxygen (<jats:italic>Pa<\/jats:italic>O<jats:sub>2<\/jats:sub>) and carbon dioxide (<jats:italic>Pa<\/jats:italic>CO<jats:sub>2<\/jats:sub>). <jats:italic>Pa<\/jats:italic>O<jats:sub>2<\/jats:sub> was significantly decreased 4 days after OSSMe administration, i.e. at the time of maximum lethality and increases in wet lung weight. This was accompanied by a significant increase in <jats:italic>Pa<\/jats:italic>CO<jats:sub>2<\/jats:sub> and acidosis. These results are compatible with an impairment of gas exchange due to diffuse lung damage. For reasons that are unclear, <jats:italic>Pa<\/jats:italic>CO<jats:sub>2<\/jats:sub> was slightly increased 2, 6 and 12 days after dosing.<\/jats:p><jats:p>The uptake of putrescine (1,4\u2010diaminobutane) and of 5\u2010HT was measured by incubating lung slices with several concentrations of [<jats:sup>3<\/jats:sup>H]\u2010putrescine and [<jats:sup>14<\/jats:sup>C]\u22125\u2010HT, so as to estimate the apparent kinetic parameters of uptake, <jats:italic>V<\/jats:italic><jats:sub>max<\/jats:sub> and <jats:italic>K<\/jats:italic><jats:sub>m<\/jats:sub>. The <jats:italic>V<\/jats:italic><jats:sub>max<\/jats:sub> for putrescine\u2010uptake was significantly decreased 1,2,4,6 and 12 days after the administration of OSSMe. The <jats:italic>V<\/jats:italic><jats:sub>max<\/jats:sub> for 5\u2010HT\u2010uptake was significantly increased 1 day and significantly decreased 4 days after OSSMe administration.<\/jats:p><jats:p>The uptake of 5\u2010HT is an endothelial function, and the decrease in 5\u2010HT\u2010uptake at 4 days may reflect injury to the pulmonary vascular endothelium at this time. The uptake of putrescine probably reflects the function of the pulmonary (mainly alveolar) epithelium. Alveolar type I cells are the cellular targets for the toxic action of OSSMe, and their destruction is followed by type II cell proliferation. The early and prolonged decrease in putrescine\u2010uptake, therefore, suggests that this function is different in proliferating type II cells as opposed to quiescent type II cells.<\/jats:p>","DOI":"10.1002\/jat.2550070608","type":"journal-article","created":{"date-parts":[[2006,10,14]],"date-time":"2006-10-14T11:46:21Z","timestamp":1160826381000},"page":"391-396","source":"Crossref","is-referenced-by-count":1,"title":["Respiratory and non\u2010respiratory lung function indices during the development and resolution of <i>O<\/i>,<i>S<\/i>,<i>S<\/i>\u2010trimethyl phosphorodithioate\u2010induced lung damage in the rat. A chemical model of adult respiratory distress syndrome"],"prefix":"10.1002","volume":"7","author":[{"given":"Beno\u00edt","family":"Nemery","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,1,11]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0272-0590(84)90155-6"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0272-0590(85)90114-9"},{"volume-title":"Selectivity and molecular mechanisms of toxicity","year":"1986","author":"Aldridge W. 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