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PubMedDate not supplied

[Restoration of enzyme induction, reduced as a result of long-term cortisol administration, in rat liver].

Restoration of tyrosinamine transferase (TAT) with cortisol in the rat hepatocytes after the cessation of prolonged (for many days) administration of this hormone was investigated. The effect of the liver regeneration and insulin administration on this process was also studied. In single cortisol administration the TAT activity rose 5-fold; the induction response decreased after 21 days of daily administration. The TAT induction in response to cortisol administration was restored completely only on the 25th--30th day after the cessation of this hormone injection. A three-day insulin administration led to the restoration of TAT induction in response to cortisol administration. The process of the liver regeneration during the first 24 hours after partial hepatectomy induced TAT in the cells of both control animals and those given cortisol for prolonged periods; besides, it aided restoration of the induction response to cortisol administration.

Animals↗
PubMed1993

Effects of soya bean flakes and liquorice root extract on enzyme induction and toxicity in B6C3F1 mice.

Both soya bean flakes (SBF) and liquorice root extract (LRE) have previously been reported to have anticarcinogenic properties, which have been thought to be related to an increased activity of specific enzymes responsible for the detoxification of chemical carcinogens. 30- and 90-day studies were conducted in male B6C3F1 mice to determine which, if any, of several detoxification enzymes are induced by SBF or LRE. Mice fed 8 and 25% LRE showed a variety of adverse clinical signs, poor weight gain and 30% mortality. Significant increases in liver:body weight ratios were observed in both the SBF and LRE groups. No significant treatment-related gross autopsy findings were observed in any of the SBF groups. A number of abnormalities were observed in the LRE groups, including lesions of the kidney, liver, spleen and thymus. Liver samples from the 90-day study were analysed for 7-ethoxycoumarin O-deethylase (7-ECOD), benzo[a]pyrene hydroxylase (BPH), superoxide dismutase (SOD), glutathione S-transferase (GST) and UDP-glucuronyl transferase (UDPGT) at 90 days, and at an interim 30-day autopsy. No treatment-related increases were observed for BPH or SOD. Both SBF and LRE induced modest increases in UDPGT activity. SBF induced modest increases in GST activity, but LRE decreased this activity. 7-ECOD activity was significantly increased by LRE and decreased by SBF. Samples from a 30-day study in which both LRE and SBF were administered at various dose levels were examined for UDPGT activity; all dose groups showed decreases in UDPGT activity relative to controls. The results suggest that both SBF and LRE may alter the activities of specific enzymes involved in the detoxification of chemical carcinogens; however, the combination of these two foodstuffs may not produce an additive effect in B6C3F1 mice.

Administration, Oral↗
PubMed1987

Metabolism of 1-phthalidyl 5-fluorouracil in rat liver and enzyme induction by phenobarbital.

1. When 1-phthalidyl 5-fluorouracil (PH-FU) was incubated with isolated rat hepatocytes, 5-fluorouracil, 2-carboxybenzaldehyde (CBA) and alpha-hydroxymethylbenzoic acid (HMB) were detected as the major metabolites. 2. The enzymes involved in the metabolism of PH-FU, PH-FU hydrolase and CBA reductase are cytosolic and were induced by treating the rats with phenobarbital (PB). Treatment of rats with 3-methylcholanthrene (3-MC) did not affect either enzyme activity. 3. The PB-induced PH-FU hydrolase was inhibited by NADH and several aldehydes, while NAD stimulated the hydrolase and protected it from inactivation by SH reagents. 4. Study in vivo revealed that treatment of rats with PB accelerated the metabolism of PH-FU in the liver and markedly decreased the blood PH-FU after its oral administration to rats, which resulted in reduction of the anti-tumour activity of PH-FU. This activity was not affected by treatment of the rats with 3-MC.

Aldehyde Oxidoreductases↗