Regular ArticleProtection of the Cyp1a2(−/−) Null Mouse against Uroporphyria and Hepatic Injury Following Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin
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2017, Toxicology and Applied PharmacologyCitation Excerpt :Porphyria cutanea tarda (PCT), the most common human porphyria, is a photosensitive skin disease caused by over-production of hepatic porphyrins, resulting in high urinary concentrations. Biochemically, PCT is characterized by a UROD deficiency that causes uroporphyrinogen III accumulation, although nutritional and/or environmental interactions, such as exposure to AhR agonists, are typically required for disease expression (Smith et al., 2001). In the presence of Fe and CYP1A2, uroporphyrinogen III is oxidized to uroporphomethene, a UROD inhibitor, and finally, uroporphyrin III, a urinary metabolite identified in rodent porphyria models and PCT patients.
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