{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:42:32Z","timestamp":1786977752774,"version":"build-2736575974"},"reference-count":51,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":9619,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1989,5]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Both human porphyria cutanea tarda and experimental hexachlorobenzene-induced porphyria are associated with hepatic injury and are potentiated by excess hepatic iron. The mechanisms whereby cellular injury occurs and the synergistic role of iron overload are unknown. In the present experiments, we studied hepatic mitochondrial function and lipid peroxidation in rats with hexachlorobenzene-induced porphyria in which iron loading was achieved by dietary carbonyl iron supplementation. Female rats were treated for 8 weeks, receiving a chow diet supplemented with hexachlorobenzene (0.2%, w\/w), carbonyl iron (1.0%, w\/w) or hexachlorobenzene + iron. Hepatic total porphyrins were increased 100-fold in rats receiving hexachlorobenzene (hexachlorobenzene alone and hexachlorobenzene + Fe), and total hepatic iron was increased approximately 10-fold in rats receiving iron supplementation (Fe alone and hexachlorobenzene + Fe). There was a significant increase in mitochondrial lipid peroxidation in rats treated with hexachlorobenzene alone and hexachlorobenzene + Fe. A significant reduction in mitochondrial respiratory control ratios and in oxidative phosphorylation (ADP\/O ratios) using glutamate and succinate as substrates was demonstrated when rats were treated with hexachlorobenzene + iron. The reductions in respiratory control ratios were due to a combination of an inhibitory defect in electron transport as evidenced by an irreversible decrease in State 3 respiration and an uncoupling effect as evidenced by an increase in State 4 respiration. These findings suggest that lipid peroxidation and mitochondrial dysfunction may contribute to the hepatotoxicity seen in hexachlorobenzene-induced porphyria.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hep.1840090505","type":"journal-article","created":{"date-parts":[[2007,3,3]],"date-time":"2007-03-03T18:11:16Z","timestamp":1172945476000},"page":"686-692","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":18,"title":["Hepatic mitochondrial oxidative metabolism and lipid peroxidation in experimental hexachlorobenzene-induced porphyria with dietary carbonyl iron overload\u2020"],"prefix":"10.1097","volume":"9","author":[{"given":"Edward S.","family":"Feldman","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce R.","family":"Bacon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"10.1002\/hep.1840090505-BIB1","first-page":"1301","volume-title":"The metabolic basis of inherited disease","author":"Kappas","year":"1983","unstructured":", . The porphyrias. In: , , et al, eds. The metabolic basis of inherited disease, Ed. 5. New York: McGraw Hill, 1983: 1301\u20131384."},{"key":"10.1002\/hep.1840090505-BIB2","first-page":"351","volume-title":"Hepatology. A textbook of liver disease","author":"Bonkowsky","year":"1982","unstructured":"Porphyrin and heme metabolism and the porphyrias. In: , eds. Hepatology. A textbook of liver disease. Philadelphia: W. B. 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In: , eds. Methods in enzymology, Vol. 10. New York: Academic Press, 1967: 41\u201347."},{"key":"10.1002\/hep.1840090505-BIB24","first-page":"90","volume-title":"Iron","author":"Torrance","year":"1980","unstructured":". Tissue iron stores. In: ed. Iron. 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Lyon: International Agency for Research on Cancer, 1986; 487\u2013491."},{"key":"10.1002\/hep.1840090505-BIB49","doi-asserted-by":"crossref","first-page":"221","DOI":"10.1042\/bj2460221","volume":"246","author":"Smith","year":"1987","journal-title":"Biochem J"},{"key":"10.1002\/hep.1840090505-BIB50","first-page":"1160","volume":"6","author":"Loveless","year":"1986","journal-title":"Hepatology"},{"key":"10.1002\/hep.1840090505-BIB51","doi-asserted-by":"crossref","first-page":"671","DOI":"10.1042\/bj2350671","volume":"235","author":"Tangeras","year":"1986","journal-title":"Biochem J"}],"container-title":["Hepatology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1002%2Fhep.1840090505","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.lww.com\/01515467-198905000-00004","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,2,7]],"date-time":"2025-02-07T10:19:20Z","timestamp":1738923560000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.lww.com\/01515467-198905000-00004"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1989,5]]},"references-count":51,"journal-issue":{"issue":"5","published-print":{"date-parts":[[1989]]}},"URL":"https:\/\/doi.org\/10.1002\/hep.1840090505","relation":{},"ISSN":["0270-9139"],"issn-type":[{"value":"0270-9139","type":"print"}],"subject":[],"published":{"date-parts":[[1989,5]]}}}