coproporphyrin/nekrosis

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Excretion of coproporphyrin in rats developing acute massive hepatic necrosis.

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Phototoxicity of coproporphyrin as a novel photodynamic therapy was enhanced by liposomalization.

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This study attempted the liposomalization of coproporphyrin I (CPI) with hydrophobic properties. Liposomalization of CPI was not successful at any pH when using lactate buffer. In contrast, when using 9% sucrose/10mM phosphate buffer (pH 7.8), CPI liposomes (Lipo-CPI) and polyethyleneglycol (PEG)

Transient porphyrinemia in a liver transplant recipient.

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We report a case of acquired porphyrinemia in a liver transplant recipient. Thrombosis of the portal vein and hepatic artery led to massive necrosis of the patient's first donor liver, necessitating its removal. After an 18-hour anhepatic period, a second donor liver was transplanted. During this

Accumulation of porphyrins in plasma and tissues of dogs after delta-aminolevulinic acid administration: implications for photodynamic therapy.

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Protoporphyrin accumulates in tissues after administration of delta-aminolevulinic acid, and can be used as a photosensitizer for photodynamic therapy. To determine the distribution of porphyrins in a large animal model after administration of this porphyrin precursor, delta-aminolevulinic acid was

Reduction of coproporphyrinogen oxidase level by antisense RNA synthesis leads to deregulated gene expression of plastid proteins and affects the oxidative defense system.

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A full-length cDNA sequence encoding coproporphyrinogen oxidase was inserted in inverse orientation behind a CaMV promoter and transferred to tobacco (Nicotiana tabacum) by standard transformation techniques. Transformants showed reduced coproporphyrinogen oxidase activity and accumulation of

Hepatic porphyrin concentration and uroporphyrinogen decarboxylase activity in hepatitis C virus infection.

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Previous studies have shown a high prevalence of hepatitis C virus (HCV) infection in patients with porphyria cutanea tarda (PCT). The aim of this study was to assess hepatic porphyrin concentrations (HPC) and hepatic uroporphyrinogen decarboxylase (UROD) activity in HCV-infected patients free of

Feline congenital erythropoietic porphyria associated with severe anemia and renal disease. Clinical, morphologic, and biochemical studies.

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A feline erythropoietic porphyria was studied in an affected female Siamese cat and 2 male offspring. The principal elevated porphyrins were Type I isomers of uroporphyrin and coproporphyrin; the porphyrin precursors, porphobilinogen and sigma-aminolevulinic acid, were also detected. Porphyrins were

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