Disease relevance of DICARBETHOXYDIHYDROCOLLIDINE

• PK 11195 aggravates 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced hepatic porphyria in rats [1].
• Studies on the mechanism of experimental porphyria produced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine. Role of a porphyrin-like inhibitor of protohaem ferro-lyase [2].
• Atypical ductular proliferation and its inhibition by transforming growth factor beta1 in the 3,5-diethoxycarbonyl-1,4-dihydrocollidine mouse model for chronic alcoholic liver disease [3].
• The MM 120-1 antigen was present in murine MBs induced by griseofulvin or 3,5-diethoxycarbonyl-1,4-dihydrocollidine feeding and also in human MBs in livers of patients with alcoholic hepatitis [4].

High impact information on DICARBETHOXYDIHYDROCOLLIDINE

• Oval cell expansion induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) was significantly reduced in Fn14-null mice as well as in adult wild-type mice with a blocking anti-TWEAK mAb [5].
• METHODS: Liver fibrosis was induced either by feeding mice with the 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet or by injecting them with carbon tetrachloride [6].
• Male Swiss albino mice were fed a powdered standard diet containing 2.5% of 3,5-diethoxycarbonyl-1,4-dihydrocollidine up to 95 days [7].
• To study the origin and properties of this cell population, oval cell proliferation was induced in adult mouse liver by 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) and a method for their isolation was developed [8].
• A detailed study on the expression of p62 and its relationship to MB formation in the 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-treated mouse liver is reported based on immunohistochemical, immunoblot, and Northern blot analyses [9].

Chemical compound and disease context of DICARBETHOXYDIHYDROCOLLIDINE

• This was achieved by studying putrescine, spermidine and spermine levels in a model of acute porphyria, i.e. 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-induced porphyria, and in a model of non-acute porphyria, i.e. hexachlorobenzene (HCB)-induced porphyria [10].

Anatomical context of DICARBETHOXYDIHYDROCOLLIDINE

• Maintenance of microsomal hemoprotein concentrations following inhibition of ferrochelatase activity by 3,5-diethoxycarbonyl-1,4-dihydrocollidine in chick embryo liver [11].
• Cytoskeletal alterations of hepatocytes were studied in mice fed 3,5-diethoxycarbonyl-1,4-dihydrocollidine from the onset of the experiment to the time when Mallory bodies were induced, using immunofluorescent microscopy and a method which we devised in order to visualize the cytoskeletal framework of hepatocytes [12].
• 1. A porphyrinogenic drug, 3,5-diethoxycarbonyl-1,4-dihydrocollidine, caused a decrease in the proportion of single ("run off") ribosomes, and an increase in the number of polyribosomes, in the livers of treated animals [13].
• BACKGROUND/AIMS: Chronic intoxication of mice with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) or griseofulvin (GF) results in appearance of Mallory bodies (MBs) and alterations of the keratin cytoskeleton, which are reversible upon drug withdrawal but recur after readministration within 2-3 days [14].
• The ferrochelatase inhibitor dihydropyridine 3,5-diethoxycarbonyl-1,4-dihydrocollidine reduced the accumulation of PpIX in both cell lines [15].

Associations of DICARBETHOXYDIHYDROCOLLIDINE with other chemical compounds

• Evidence that 2-allyl-2-isopropylacetamide, phenobarbital and 3,5-diethoxycarbonyl-1,4-dihydrocollidine induce the same cytochrome P450 mRNA in chick embryo liver [16].
• To address this data gap, we exposed small mammals to tralkoxydim, to 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC; a known porphyrinogenic chemical), or to sunflower oil alone [17].
• Furthermore marked porphyrin accumulation was not seen with many drugs that induce delta-aminolevulinate synthase and cytochrome P-450 but was more characteristic of compounds that reduced the metabolism of protoporphyrin to heme, such as 1,4-dihydro-3,5-dicarbethoxycollidine (DDC) and high doese of hydralazine [18].

Gene context of DICARBETHOXYDIHYDROCOLLIDINE

• We tested the effect of the transglutaminase-2 (TG2) inhibitor KCC009 on MB formation in a mouse model fed 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) [19].
• When the ferrochelatase-inhibited drug, 3,5-dicarbethoxy-1,4-dihydrocollidine (DDC) is used, a 6 and 28 fold induction of liver apo A-IV mRNA is observed in male and female mice, respectively [20].
• These studies show directly that treatment of chick embryos with 2-allyl-2-isopropylacetamide or 3,5-diethoxycarbonyl-1,4-dihydrocollidine caused increased levels of cytochrome P-450 mRNA and suggest that this involved increased transcription of the gene [21].
• Hepatic 5-aminolevulinate synthase was induced in chick embryos by administration of the porphyrinogenic drugs 2-allyl-2-isopropylacetamide and 3,5-diethoxycarbonyl-1,4-dihydrocollidine [22].
• Effects of hemin on the synthesis and intracellular translocation of delta-aminolevulinate synthase in the liver of rats treated with 3,5-dicarbethoxy-1,4-dihydrocollidine [23].

Analytical, diagnostic and therapeutic context of DICARBETHOXYDIHYDROCOLLIDINE

• This porphyrin resembles closely in chromatographic and spectral properties the inhibitory pigment isolated after treatment with 3,5-diethoxycarbonyl-1,4-dihydrocollidine, but differs from other green pigments that do not inhibit protohaem ferro-lyase [24].

References