Inhibition of chick embryo hepatic uroporphyrinogen decarboxylase by components of xenobiotic-treated chick embryo hepatocytes in culture. II.

1992 ◽  
Vol 70 (7) ◽  
pp. 939-942 ◽  
Author(s):  
R. P. Green-Thompson ◽  
S. M. Kimmett ◽  
G. S. Marks
Keyword(s):  
Chick Embryo ◽  
Enzyme Inhibition ◽  
Culture System ◽  
Hepatocyte Culture ◽  
Uroporphyrinogen Decarboxylase ◽  
Soluble Component ◽  
Sodium Phenobarbital

A variety of xenobiotics, viz., 3,3′,4,4′-tetrachlorobiphenyl (TCBP), sodium phenobarbital (PB), 3,5-diethoxycarbonyl-2,4,6-trimethylpyridine (OX-DDC), and nifedipine, cause a decrease in uroporphyrinogen decarboxylase (UROG-D) activity, accompanied by uroporphyrin accumulation, in chick embryo hepatocytes in culture. In this study the activity of 17-day-old chick embryo hepatic UROG-D was determined by measuring the conversion of pentacarboxylporphyrinogen I to coproporphyrinogen I, and it was shown that a UROG-D inhibitor, previously reported to accumulate in TCBP-treated and PB-treated chick embryo hepatocytes in culture, also accumulates in OX-DDC-treated and nifedipine-treated chick embryo hepatocytes in culture. It was concluded that the accumulation of a UROG-D inhibitor provides an explanation for the UROG-D inhibition observed in this culture system with xenobiotics that cause uroporphyrin accumulation. Studies of the UROG-D inhibitory fraction isolated from the 10 000 × g, 40 000 × g, and 100 000 × g supernatant fractions of cultured chick embryo hepatocyte homogenate led to the conclusion that the UROG-D inhibitor is derived from a soluble component of the homogenate.Key words: uroporphyrinogen decarboxylase, chick embryo hepatocyte culture, nifedipine, 3,5-diethoxycarbonyl-2,4,6-trimethylpyridine, enzyme inhibition.

Inhibition of chick embryo hepatic uroporphyrinogen decarboxylase by components of xenobiotic-treated chick embryo hepatocytes in culture

1989 ◽  
Vol 67 (3) ◽  
pp. 246-249 ◽  
Author(s):  
C. A. James ◽  
G. S. Marks
Keyword(s):  
Chick Embryo ◽  
Protein Concentration ◽  
Enzyme Assay ◽  
Uroporphyrinogen Decarboxylase ◽  
Optimum Ph ◽  
Embryo Liver ◽  
Liver Homogenates ◽  
Previous Demonstration ◽  
Sodium Phenobarbital ◽  
Cytochrome P 450

Uroporphyrinogen decarboxylase (UROG-D) activity in the 10 000 g supernatant of 17-day-old chick embryo liver homogenates was determined by measuring the conversion of pentacarboxylporphyrinogen I to coproporphyrinogen I. The optimum pH of the enzyme was found to be approximately 6.0 and enzyme activity was found to be linear with protein concentrations ranging from 0.3 to 2.0 mg/mL. At a protein concentration of 1.2 mg/mL and pH 6.0, the activity was found to be linear for a reaction time of 50 min and to be approximately 10 pmol/(mg protein∙min). This enzyme assay was used to demonstrate that a UROG-D inhibitor, previously reported to accumulate in rodent liver, also accumulates in 3,3′4,4′-tretrachlorobiphenyl (TCBP) and sodium phenobarbital (PB) treated chick embryo hepatocytes in culture. This result accords with the previous demonstration of a TCBP- and PB-induced decrease in UROG-D activity in this system. Uroporphyrin accumulation in chick embryo hepatocyte culture is interpreted as resulting from a combination of two mechanisms, viz., inhibition of UROG-D activity and uroporphyrinogen oxidation to uroporphyrin catalyzed by a cytochrome P-450 isozyme.Key words: uroporphyrinogen decarboxylase, enzyme inhibition, chick embryo hepatocytes, tetrachlorobiphenyl, porphyria.

scholarly journals Uroporphyrin accumulation produced by halogenated biphenyls in chick-embryo hepatocytes. Reversal of the accumulation by piperonyl butoxide

1986 ◽  
Vol 237 (1) ◽  
pp. 63-71 ◽  
Author(s):  
P R Sinclair ◽  
W J Bement ◽  
H L Bonkovsky ◽  
R W Lambrecht ◽  
J E Frezza ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Chick Embryo ◽  
De Novo ◽  
Covalent Binding ◽  
Piperonyl Butoxide ◽  
Uroporphyrinogen Decarboxylase ◽  
Drug Induced ◽  
Cytochrome P 450 ◽  
Inhibition Of Metabolism ◽  
Methylenedioxyphenyl Compounds

Cultures of chick-embryo hepatocytes were used to study the mechanism by which 3,4,3′,4′-tetrachlorobiphenyl and 2,4,5,3′,4′-pentabromobiphenyl cause accumulation of uroporphyrin. In a previous paper, an isoenzyme of cytochrome P-450 induced by 3-methylcholanthrene had been implicated in this process [Sinclair, Bement, Bonkovsky & Sinclair (1984) Biochem. J. 222, 737-748]. Cells treated with 3,4,3′,4′-tetrachlorobiphenyl and 5-aminolaevulinate accumulated uroporphyrin and heptacarboxyporphyrin, whereas similarly treated cells accumulated protoporphyrin immediately after piperonyl butoxide was added. Piperonyl butoxide also restored haem synthesis as detected by incorporation of radioactive 5-aminolaevulinate into haem, and decrease in drug-induced 5-aminolaevulinate synthase activity. The restoration of synthesis of protoporphyrin and haem by piperonyl butoxide was not affected by addition of cycloheximide, indicating recovery was probably not due to protein synthesis de novo. Piperonyl butoxide also reversed uroporphyrin accumulation caused by 3,4,5,3′,4′,5′-hexachlorobiphenyl, mixtures of other halogenated biphenyls, lindane, parathion, nifedipine and verapamil. The effect of piperonyl butoxide was probably not due to inhibition of metabolism of these compounds, since the hexachlorobiphenyl was scarcely metabolized. Other methylenedioxyphenyl compounds, as well as ellipticine and acetylaminofluorene, also reversed the uroporphyrin accumulation caused by 3,4,3′,4′-tetrachlorobiphenyl. SKF-525A (2-dimethylaminoethyl-2,2-diphenyl valerate) did not reverse the uroporphyrin accumulation caused by the halogenated biphenyls, but did reverse that caused by phenobarbital and propylisopropylacetamide. We conclude that the mechanism of the uroporphyrin accumulation cannot be due to covalent binding of activated metabolites of halogenated compounds to uroporphyrinogen decarboxylase.

The porphyrogenic effects of calcium channel blocking drugs

1985 ◽  
Vol 69 (5) ◽  
pp. 581-586 ◽  
Author(s):  
N. Schoenfeld ◽  
J. Aelion ◽  
Y. Beigel ◽  
O. Epstein ◽  
A. Atsmon
Keyword(s):  
Chick Embryo ◽  
Calcium Channels ◽  
Calcium Channel ◽  
Decarboxylase Activity ◽  
Blocking Drug ◽  
Slight Effect ◽  
Uroporphyrinogen Decarboxylase ◽  
Channel Blocking

1. Treatment of monolayers of chick embryo hepatocytes with the calcium channel blocking drugs nifedipine and verapamil resulted in a decrease in the activity of uroporphyrinogen decarboxylase, an increase in the activity of δ-aminolaevulinate synthase and accumulation of porphyrins with uroporphyrin and heptacarboxylic porphyrin predominating. 2. Diltiazem, another calcium channel blocking drug, did not affect uroporphyrinogen decarboxylase activity and had a slight effect only on the accumulation of porphyrins. 3. Experiments with nifedipine and verapamil in the presence of various concentrations of calcium indicate that the porphyrogenic effect is apparently not related to blocking of calcium channels.

scholarly journals ID: 1088 Experimental culturing of chick embryo in shell-less culture system – the first research in Vietnam

2017 ◽  
Vol 4 (S) ◽  
pp. 176
Author(s):  
Quy Xuan Nguyen ◽  
Long Thanh Dang
Keyword(s):  
Chick Embryo ◽  
Traditional Method ◽  
Culture System ◽  
Lethal Effect ◽  
Calcium Lactate ◽  
High Rate ◽  
Chick Embryos ◽  
Ideal Model ◽  
Significant Difference ◽  
First Time

Chick embryo is an ideal model with numerous applications in biomedical research. Among a variety of methods have been carried out for culturing chick embryos, shell-less culture system has a large number of advantages on accessibility, observation and manipulation. In this study, chick embryos were transferred to the shell-less culture system and the development of the chick embryos were assessed. Correlation between the diameter of sinus terminalis on the surface of yolk sac and viability of the embryos would be evaluated. In addition, calcium lactate was added to the culture system in order to find out the optimal amount. After the experiments, results showed that there was no difference between embryos in shell-less culture system and traditional method during incubation period. Secondly, the proportion of live chick embryos until embryonic day 17 reached the highest rate at 87,5% when the diameter of sinus terminalis was between 16 and 21 mm. At last, there was no significant difference between the group with 250 mg calcium lactate supplemented as compared to no supplemented group. Calcium lactate had a lethal effect on chick embryos when the supplemented content was 550 mg. In conclusion, the shell-less culture system could be able to allow the survival of chick embryos until day 21, with high rate in day 17. Besides, this has been the very first time the shell-less culture system was performed in Vietnam.

A Microfluidic 3D Hepatocyte Culture System -HepaChip®- For Drug And Toxicity Investigations

2012 ◽  
Vol 50 (01) ◽  
Author(s):  
J Böttger ◽  
J Schütte ◽  
K Benz ◽  
C Freudigmann ◽  
B Hagmeyer ◽  
...  
Keyword(s):  
Culture System ◽  
Hepatocyte Culture
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