Effect of cytochrome P450 induction on phosphorus metabolites and proton relaxation times measured by in vivo31P-magnetic resonance spectroscopy and 1H-magnetic resonance relaxometry in human liver
✍ Scribed by W Block; C Reichel; F Traber; T Skodra; R Lamerichs; B Kreft; U Spengler; T Sauerbruch; H Schild
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 438 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0270-9139
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✦ Synopsis
Experimental and clinical studies have led to the hypothesis
The liver is the primary site of oxidative metabolism in humans. Ingestion of ethanol and drugs such as phenobarbi-that the phosphodiester signal obtained by 31 P magnetic resonance (MR) spectroscopy may be a specific marker for the tone 1 or rifampin 2 induce the oxidative metabolism of the liver. This induction is accompanied by hypertrophy of the hepatic induction of oxidative metabolism (P450 induction) by phenobarbitone or ethanol. Systematic studies in humans smooth endoplasmic reticulum. This structure is composed primarily of lipid bilayers that contain the P450 monooxy-are lacking. Therefore, we studied 10 volunteers who received rifampin (600 mg/d) for 6 days, resulting in a documented genase system.
In vivo 31 P magnetic resonance (MR) spectroscopy is a induction of oxidative metabolism as measured by an increase in urinary 6-b-hydroxycortisol output in all volunteers (P Å noninvasive technique that provides information on hepatic energy metabolism, phospholipid substrates, and hepatocyte .0004). 31 P-MR spectroscopy and 1 H-MR relaxometry were performed before and after hepatic P450 induction. As shown lipid bilayers. Experimental studies in rats have shown that treatment with phenobarbitone increased the phosphodiester by 31 P-MR spectroscopy, the median phosphomonoester concentration (PME) relative to nucleoside triphosphate (NTP) (PDE) but not the phosphomonoester (PME) signal obtained by 31 P-MR spectroscopy. Like phenobarbitone, ethanol in-increased by 21% from 0.63 (range, 0.40-0.89) before induction to 0.76 (0.49-1.67) after induction (P Å .0451). The duces hypertrophy of the hepatic endoplasmic reticulum.
Consequently, Menon et al. speculated that an elevation of median level of phosphodiesters (PDE) relative to NTP increased by 28% from 4.82 (3.41-6.67) before induction to the PDE relative to the nucleoside triphosphate (NTP) signal observed in their patients with chronic alcohol abuse may 6.18 (4.63-11.63) after induction (P Å .0091). An increase in the level of inorganic phosphates (Pi) relative to NTP was be the result of an induction of the endoplasmic reticulum.
They further speculated that the elevated PME/NTP ratio also observed, but changes were not significant. As shown by 1 H-MR relaxometry, a nonsignificant trend of the liver paren-observed in their patients may be caused by changes in the hepatic redox potential. However, the influence of hepatic chyma to shorter relaxation times was observed after P-450 induction. In conclusion, both PME/NTP and PDE/NTP ratios P450 induction on 31 P-MR spectroscopy has so far not been studied systematically in humans.
(measured by in vivo 31 P-MR spectroscopy) increased significantly after hepatic induction with rifampin. Further clinical
We selected 10 healthy volunteers to study the effect of short-term rifampin induction on the findings obtained by studies with 31 P-MR spectroscopy must take into account the potential effects of P450-inducing agents. (HEPATOLOGY 31 P-MR spectroscopy. The degree of P450 induction was determined by measurement of urinary output of 6-b-hy-1997;26:1587-1591.) droxycortisol. 7