PubMed Health⌕ Search

Biomedical subjects

F Horio

Publications and source records attributed to F Horio.

42 records · Page 3Linked to original sources
PubMed1986

Ascorbic acid requirement for the induction of microsomal drug-metabolizing enzymes in a rat mutant unable to synthesize ascorbic acid.

We investigated the requirement of ascorbic acid for the induction by polychlorinated biphenyls (PCB) of hepatic drug-metabolizing enzymes in ODS-od/od rat (OD rat) which is a rat mutant unable to synthesize ascorbic acid. ODS- +/+ rats (+/+ rat), which can synthesize ascorbic acid, were used as controls. In OD rats, the dietary requirement of ascorbic acid to maintain normal growth and prevent any signs of scurvy is about 300 mg of ascorbic acid per kilogram diet. In this study, dietary levels of ascorbic acid tested were 0, 50, 300, 1000 and 3000 mg ascorbic acid per kilogram diet with or without 200 mg of PCB per kilogram diet. Feeding PCB did not affect growth in rats of either genotype. When statistical analysis was done within groups fed diets without PCB, ascorbic acid deficiency caused significant decreases in body weight gain, hepatic activities of drug-metabolizing enzymes and level of hepatic cytochrome P-450. When OD rats were fed a diet without PCB, the supplementation of about 300 mg ascorbic per kilogram diet was sufficient to maintain normal activities of hepatic aminopyrine N-demethylase, aniline hydroxylase, cytochrome c reductase and reduction of cytochrome P-450 and a normal level of hepatic cytochrome P-450. However, when OD rats were fed a diet supplemented with 200 mg PCB per kilogram of diet, significantly higher activities of hepatic aminopyrine N-demethylase and aniline hydroxylase and significantly higher level of hepatic cytochrome P-450 were observed in OD rats fed a diet supplemented with 1000 mg or 3000 mg ascorbic acid per kilogram of diet than in rats fed a diet supplemented with 300 mg of ascorbic acid. It is concluded that the dietary requirement of ascorbic acid is increased severalfold by the administration of xenobiotics, such as PCB, for the maximum induction of hepatic drug metabolism.

Aminopyrine N-Demethylase↗
PubMed1985

Requirement for ascorbic acid in a rat mutant unable to synthesize ascorbic acid.

The activities of several enzymes involved in hepatic ascorbic acid synthesis and the requirement of dietary ascorbic acid were investigated in the OD (osteogenic disorder) rat, which has a hereditary defect in ascorbic acid-synthesizing ability. No activity of hepatic L-gulonolactone oxidase was detected in OD rats. However, OD rats maintained the normal activities of hepatic UDPglucose dehydrogenase, UDPglucuronyl transferase and beta-glucuronidase. Hemorrhage in muscle and leg joints, lower hepatic content of cytochrome P-450 and lower activities of hepatic drug-metabolizing enzymes, higher serum and adrenal levels of corticosterone and lower urinary excretion of hydroxyproline were observed in ascorbic acid-deficient OD rats than in OD rats fed 300 mg ascorbic acid/kilogram diet. Consequently, we conclude that OD rats cannot synthesize ascorbic acid because of the lack of activity of hepatic L-gulonolactone oxidase and that the dietary addition of about 300 mg ascorbic acid (per kilogram diet) is enough to prevent signs of vitamin C deficiency and to achieve maximum growth, and that more than 300 mg ascorbic acid per kilogram diet may be required for the maximum activity of hepatic drug-metabolizing enzymes.

Adrenal Glands↗
PubMed1983

Effect of several xenobiotics on the activities of enzymes affecting ascorbic acid synthesis in rats.

The dietary addition of several xenobiotics, such as PCB, DDT, aminopyrine, chloretone, BHT and BHA, caused significant increases in the ascorbic acid in urine and liver of rats. The administration of all types of xenobiotics used in the present experiments increased the activity of hepatic UDP-glucose dehydrogenase (1.3-2.8-fold), and the administration of PCB, DDT, BHT or BHA significantly increased the activity of hepatic UDP-glucuronyl transferase (2.2-13.1-fold). The activity of beta-glucuronidase was slightly increased with feeding of PCB, DDT, chloretone or aminopyrine. However, the activity of hepatic UDP-glucuronic acid pyrophosphatase, the conversion of D-glucuronic acid or D-glucuronolactone into L-ascorbic acid and the activity of hepatic L-gulonolactone oxidase did not increase with the administration of PCB or DDT. It is suggested that the increases in the activities of UDP-glucose dehydrogenase and UDP-glucuronyl transferase would have a major role in the stimulation of ascorbic acid synthesis in xenobiotic treated rats.

Aminopyrine↗
PubMed1982

Effects of some xenobiotics on ascorbic acid metabolism in rats.

The administration of xenobiotics, PCB, DDT, or aminopyrine to rats causes a marked increase in urinary excretion of ascorbic acid and in various tissue levels of ascorbic acid. When rats were fed diet containing 200 ppm PCB or 500 ppm DDT (14 days), the incorporations from D-(U-14C) glucose into ascorbic acid in liver were significantly increased. The dietary addition of 200 ppm PCB, 500 ppm DDT, 2,000 ppm pentobarbital or 3,000 ppm chloretone caused a significant increase in the activity of hepatic UDPglucose dehydrogenase, but did not affect the activity of hepatic L-gulonolactone oxidase. Good correlation between the liver level of ascorbic acid and the activity of hepatic UDPglucose dehydrogenase was observed. Subsequently, in rats fed the basal diet (30% casein diet) or the diet containing 200 ppm PCB, the specific activities of ascorbic acid in urine and in various tissues were measured 6 hours, 12 hours and 24 hours after the oral administration of L-(l-14C)ascorbic acid. Dietary PCB accelerated the disappearances of radioactivities in ascorbic acid in urine and various tissues, that is, shortened the half lives of radioactivities in ascorbic acid. It is likely that the administration of xenobiotics, such as PCB or DDT, to rats increases the biosynthesis of ascorbic acid and accelerates concomitantly the turnover of ascorbic acid in body.

Aminopyrine↗
PubMed1979

Effect of an amino acid imbalance on intestinal sucrase and leucine aminopeptidase activities in rats.

In order to investigate the relationship between dietary amino acids and protein, as well as the activities of intestinal sucrase and leucine aminopeptidase in rats, the effects of an amino acid imbalance on these enzyme activities were studied. The amino acid imbalance was created by adding 8% of an indispensable amino acid mixture lacking threonine to a 6% casein diet supplemented with 0.3% methionine. The food intake and growth of rats fed the imbalanced diet ad libitum were depressed, and the segmental weights of the small intestine and its sucrase activity were clearly lower than those of rats fed the basal diet. The effect of the imbalanced diet under pair-feeding condition on the sucrase activity was similar to that under an ad libitum feeding condition. The food intake and segmental sucrase activity, that is, sucrase activity per length of the small intestine, of rats injected with cortisol (1 mg/day) and fed the imbalanced diet were not depressed, although administration of insulin (1.5 U/day) had no effect on the food intake or segmental sucrase activity. Force-feeding stimulated growth of rats receiving the imbalanced diet, as well as increasing their segmental sucrase activities. The effects of these different conditions on the leucine aminopeptidase activity of rats receiving the imbalanced diet were obscure. These results suggest that changes in segmental sucrase activity might be mediated by stimulating factors in food intake affected by the composition of ingested amino acids and protein together with sucrose in the gastrointestinal lumen.

Animals↗