{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T10:56:44Z","timestamp":1702378604691},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2006,6,8]],"date-time":"2006-06-08T00:00:00Z","timestamp":1149724800000},"content-version":"vor","delay-in-days":4937,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J. Biochem. Toxicol."],"published-print":{"date-parts":[[1992,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The acute hepatotoxicity and response of hepatic cytochrome P450 to treatment with the three isomers of dichlorobenzene (DCB) have been investigated. The objectives were to estimate the onset of toxicity and to further elucidate the role of cytochrome P450 in the metabolism and toxicity of these compounds. In a study design employing one animal per dose level, Fischer\u2010344 rats were gavaged with up to 25 different dosages, then evaluated 24 h later. Hepatic necrosis, serum alanine aminotransferase, and serum aspartate aminotransferase exhibited similar patterns demonstrating that <jats:italic>ortho<\/jats:italic>\u2010DCB (<jats:italic>O<\/jats:italic>\u2010DCB) was the most toxic in terms of both earliest onset and degree of response at higher dosages. For these three end\u2010points, <jats:italic>meta<\/jats:italic>\u2010DCB (<jats:italic>m<\/jats:italic>\u2010DCB) exhibited a lesser toxicity. <jats:italic>Para<\/jats:italic>\u2010DCB (<jats:italic>p<\/jats:italic>\u2010DCB) did not cause changes in these three endpoints, but hepatic degenerative changes were found. Total hepatic cytochrome P450 responses were also different after treatment with each isomer. The <jats:italic>o<\/jats:italic>\u2010DCB produced a dose\u2010dependent decrease in P450 beginning at dosages lower than the onset of necrosis and appeared to be a suicide substrate for P450. The <jats:italic>m<\/jats:italic>\u2010DCB treatment increased P450 at dosages below the onset of necrosis and decreased P450 at higher dosages, with the decline preceding the onset of hepatocyte death. Treatment with <jats:italic>p<\/jats:italic>\u2010DCB increased P450 beginning at 380 mg\/kg. The combination of toxicity and P450 profiles has provided a framework for interpreting literature data on the metabolism and toxicity of the DCBs in rats. It is also noteworthy that <jats:italic>o<\/jats:italic>\u2010DCB and <jats:italic>p<\/jats:italic>\u2010DCB were administered at dosages several times the oral rat LD\u201050 (RTECS) without any lethality.<\/jats:p>","DOI":"10.1002\/jbt.2570070409","type":"journal-article","created":{"date-parts":[[2006,10,18]],"date-time":"2006-10-18T01:49:05Z","timestamp":1161136145000},"page":"257-264","source":"Crossref","is-referenced-by-count":15,"title":["The differential hepatotoxicity and cytochrome P450 responses of fischer\u2010344 rats to the three isomers of dichlorobenzene"],"prefix":"10.1002","volume":"7","author":[{"given":"John W.","family":"Allis","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane Ellen","family":"Simmons","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dennis E.","family":"House","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Barbara L.","family":"Robinson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ezra","family":"Berman","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,6,8]]},"reference":[{"key":"e_1_2_1_2_2","unstructured":"US EPA(1985).Health Assessment Document for Chlorinated Benzenes Final Report January US Environmental Protection Agency Washington DC EPA 600\/8\u201384\u2013015F."},{"key":"e_1_2_1_3_2","unstructured":"US EPA(1991).Drinking Water Regulations and Health Advisories April Office of Water US Environmental Protection Agency Washington DC."},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/path.1700440203"},{"key":"e_1_2_1_5_2","doi-asserted-by":"publisher","DOI":"10.1002\/jps.3030380304"},{"key":"e_1_2_1_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(91)90010-C"},{"key":"e_1_2_1_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/0006-2952(71)90359-5"},{"key":"e_1_2_1_8_2","doi-asserted-by":"publisher","DOI":"10.1248\/cpb.23.824"},{"key":"e_1_2_1_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(85)90293-5"},{"key":"e_1_2_1_10_2","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(76)90016-8"},{"key":"e_1_2_1_11_2","doi-asserted-by":"publisher","DOI":"10.1016\/0041-008X(83)90317-4"},{"key":"e_1_2_1_12_2","doi-asserted-by":"publisher","DOI":"10.1042\/bj0590415"},{"key":"e_1_2_1_13_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.68.1.160"},{"key":"e_1_2_1_14_2","first-page":"62","volume-title":"Pharmacology and the Future of Man","author":"Reid W. 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