Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Liver Extracts”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1999

31P and 1H NMR spectroscopic studies of liver extracts of carbon tetrachloride-treated rats.

NMR spectroscopy was used to examine hepatic metabolism in cirrhosis with a particular focus on markers of functional cellular hypoxia. (31)P and (1)H NMR spectra were obtained from liver extracts from control rats and from rats with carbon tetrachloride-induced cirrhosis. A decrease of 34% in total phosphorus content was observed in cirrhotic rats, parallelling a reduction of 40% in hepatocyte mass as determined by morphometric analysis. Hypoxia appeared to be present in cirrhotic rats, as evidenced by increased inorganic phosphate levels, decreased ATP levels, decreased ATP:ADP ratios (1.72 +/- 0.40 vs 2.48 +/- 0.50, p < 0.01), and increased inorganic phosphate:ATP ratios (2.77 +/- 0.48 vs 1.62 +/- 0.24, p < 0.00001). When expressed as a percentage of the total phosphorus content, higher levels of phosphoethanolamine and lower levels of NAD and glycerophosphoethanolamine were detected in cirrhotic rats. Cirrhotic rats also had increased phosphomonoester:phosphodiester ratios (5.73 +/- 2.88 vs 2.53 +/- 0.52, p < 0.01). These findings are indicative of extensive changes in cellular metabolism in the cirrhotic liver, with many findings attributable to the presence of intracellular hypoxia.

Adenosine Diphosphate↗
PubMed1983

Impairment of ascorbic acid synthesis in liver extracts of magnesium-deficient rats.

The effect of feeding a magnesium (Mg)-deficient diet for 9-34 days to weanling and young male rats on urinary and tissue ascorbate levels were studied. The concentrations of ascorbic acid in the liver and kidney were significantly reduced in the rats receiving a Mg-deficient diet as compared to those receiving a Mg-supplemented diet. The response to trichloro-2-methyl-2-propanol stimulation of urinary ascorbic acid was found to be considerably suppressed by dietary deficiency of Mg, suggesting that the decrease was not due to feed intake. In in vitro studies, the enzymatic synthesis of the vitamin from glucuronolactone or gulonolactone by liver extracts from Mg-deficient rats was significantly decreased as compared with Mg-supplemented rats. These results suggest that Mg-deficient rats have a reduced capacity to synthesize ascorbate which in turn produces a decrease in ascorbic acid concentrations in the liver.

Animals↗
PubMed1987

Inhibitory effects of pyrimidine, barbituric acid and pyridine derivatives on 5-fluorouracil degradation in rat liver extracts.

The inhibitory effects of about 30 compounds, mainly pyrimidine and pyridine derivatives, on 5-fluorouracil degradation catalyzed by dihydrouracil dehydrogenase (DHU dehydrogenase) were investigated. The inhibitory activities of 5-substituted uracil derivatives decreased time-dependently during preincubation with liver extracts, indicating that these compounds are substrates of DHU dehydrogenase. During preincubation, 4,6-dihydroxypyrimidine derivatives were found to be converted to barbituric acid derivatives, which have stronger activities. The inhibitory activity of 2,4-dihydroxypyridine (3-deazauracil), which was stronger than that of uracil, did not change during preincubation, indicating that this compound is not a substrate but is an inhibitor of DHU dehydrogenase, and suggesting that 2,6-dihydroxypyridine (1-deazauracil) could be a potent inhibitor. In the light of these findings, we examined various derivatives of barbituric acid, 2,4-dihydroxypyridine and 2,6-dihydroxypyridine. Among these compounds, 3-cyano-2,6-dihydroxypyridine and 5-chloro-2,4-dihydroxypyridine were the strongest inhibitors with Ki values for DHU dehydrogenase of 2.3 X 10(-7) M and 3.6 X 10(-7) M, respectively.

Animals↗
PubMed1990

Selective photochemical treatment of oestrogen receptor in a Xenopus liver extract destroys hormone binding and transcriptional activation but not DNA binding.

Photochemical excitation of a simple derivative of oestradiol using light in the UV-A range totally, permanently and selectively inactivates the oestrogen receptor protein present in a Xenopus liver extract without affecting its overall size. Inactivation of the binding site proceeds to completion with simple, first-order kinetics. Inactivation is prevented by excess oestradiol but not by non-oestrogenic steroids. Using an in vitro transcription system, we show that the treatment eliminates transcription of vitellogenin genes, which are normally oestrogen-responsive, but has no effect on the transcription of albumin genes, which are not. Native receptor binds to the two imperfectly palindromic sequences in the vitellogenin B2 gene which together constitute an oestrogen-response unit. Its affinity for one sequence is greater than its affinity for the other, suggesting that a compulsory binding order operates when receptor interacts with the B2 gene. Photoinactivated receptor still binds to both sequences, but with reduced affinity. We also discuss our findings in the context of the current concern over the effects of UV-A on human tissues.

Animals↗