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Biomedical subjects

A Aitio

Publications and source records attributed to A Aitio.

At least 91 records · Page 5Linked to original sources
PubMed1981

The effect of enzyme induction on the metabolism of disopyramide in man.

1 The effects of rifampicin, phenytoin, and disopyramide treatments on the metabolism of disopyramide were studied in patients and volunteers. 2 Rifampicin treatment markedly increased the metabolism of disopyramide. 3 Phenytoin had effects similar to those of rifampicin. The effect subsided in 2 weeks after stopping the treatment. 4 The metabolism of disopyramide seemed fastest in the patient group with the higher dose of disopyramide. Both in patients and volunteers a significant increase occurred in the urinary mono-N-dealkyldisopyramide/disopyramide ratio during the first week of disopyramide therapy. This change can partly be due to pharmacokinetic differences between disopyramide and its metabolite. The inducing effect of disopyramide remained uncertain.

Adult↗
PubMed1981

Activation and inhibition of rat hepatic UDP-glucuronyltransferase by mercuric acetate.

1. The effects of mercuric acetate on glucuronide conjugation of bilirubin and 4-methylumbelliferone in vitro represent a new type of modifier of UDP-glucuronyltransferase activity. 2. Bilirubin UDPG-transferase was normally activated (optimally 4-fold), inhibition was seen only at high concn. of Hg2+. 4-Methylumbelliferone UDPG-transferase was normally inhibited by Hg2+, but at high concn. of UDPGA (10 mmol/l) slight activation was seen. 3. Activation of bilirubin conjugation was unaffected by Mg2+ concn., indicating that the mechanism of Hg2+ activation differs from that caused by Mg2+. 4. Glucuronidation of bilirubin in liver microsomes from control rats, or rats treated with phenobarbital, methylcholanthrene or TCDD respond similarly to Hg2+, confirming with phenobarbital, methylcholanthrene or TCDD respond similarly to Hg2+, confirming the view that bilirubin conjugation is not inducible by these inducers.

Animals↗
PubMed1980

Kinetics of the inhibition of styrene oxide and benzo(a)pyrene-4,5-oxide hydration in rat liver microsomes by cadmium.

The kinetics of the inhibition by cadmium of styrene oxide and benzo(a)pyrene-4,5-oxide hydration were studied in a microsomal preparation from rat liver. Cadmium inhibited the hydration of styrene oxide in an apparently noncompetitive manner, whereas the inhibition of benzo(a)pyrene-4,5-oxide hydration showed a competitive mechanism. Styrene oxide inhibited the hydration of benzo(a)pyrene-4,5-oxide competitively and cyclohexene oxide inhibited the hydration of both styrene oxide and benzo(a)pyrene-4,5-oxide competitively. The present data suggest that cadmium is bound near the active centre of the enzyme. Occupation of this site by cadmium inhibits the enzymic hydration of the polycyclic benzo(a)pyrene-4,5-oxide molecule competitively, and that of the smaller monocyclic alkene oxide of styrene noncompetitively. The estimated Ki values were below 10 mu mol for hydration of both substrates indicating that cadmium is a very potent inhibitor of epoxide hydration.

Animals↗
PubMed1980

Effect of metal salts on UDPglucuronosyltransferase activity of various aglycones in rat liver microsomes in vitro.

The effects of aluminium, manganese, ferrous and ferric iron, cobalt, nickel, copper, zinc, cadmium, barium, mercury and lead ions on the rat hepatic UDPglucuronosyltransferase activity with regard to 4-methylumbelliferone, 4-nitrophenol, bilirubin, and 2-aminophenol were investigated in vitro. Conjugation of bilirubin was found to be activated by manganese, cobalt, nickel, cadmium, mercury and lead ions in native microsomes, but not in digitonin-treated microsomes. Aluminum, ferrous iron, cadmium, barium and lead increased the conjugation of 4-nitrophenol in native microsomes and aluminium in digitonin-treated microsomes as well. Lead slightly activated 4-methylumbelliferone conjugation, whereas none of the metal salts studied were found to activate the conjugation of 2-aminophenol. Copper and zinc salts inhibited all conjugations. In digitonin-treated microsomes, the conjugation of 4-nitrophenol was inhibited by cadmium and mercury, that of 4-methylumbelliferone by nickel and lead as well. The sensitivity of 4-methylumbelliferone conjugation to inhibition by mercury was most pronounced in microsomes prepared from rats pretreated with 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Aminophenols↗
PubMed1980

[Dioxins].

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Animals↗
PubMed1979

Immunochemical determination of serum transferrin. Reference values, correlation with serum total iron-binding capacity and value in the diagnosis of iron deficiency anaemia and anaemia of chronic disorders.

Immunologically determined reference values of serum transferrin are presented for adults and children. A good correlation between serum transferrin and total iron-binding capacity values was found. In 2 groups of anaemic patients - 51 patients with iron deficiency anaemia and 45 patients with anaemia of chronic disorders - serum transferrin determination distinguishes the two groups of anaemic patients from normals somewhat better than TIBC determination.

Adolescent↗
PubMed1979

Effects of tetraethyl lead on the activities of drug metabolizing enzymes in different tissues of the rat.

The present study describes the effects of tetraethyl lead on various drug metabolizing enzymes in different tissues of the rat. Tetraethyl lead was administered intraperitoneally to rats (250 mumol/kg) on two consecutive days. The animals were killed on day 3. Tetraethyl lead-treatment decreased the concentration of hepatic cytochrome P-450 (to 45 per cent of the control), the hepatic activity of aryl hydrocarbon hydroxylase (to 41 per cent of the control) and ethoxycoumarin deethylase (to 45 per cent of the control). Epoxide hydratase activity was enhanced in the liver (1.3-fold), kidney (3.3-fold), and small intestinal mucosa (4.7-fold). The activity of glutathione S-transferase decreased in the liver (to 69 per cent of the control) but increased in the kidney (1.5-fold) and small intestinal mucosa (1.7-fold). The glucuronidation of o-aminophenol was enhanced (2.2-fold) in the kidney of tetraethyl lead treated rats. It is concluded that exposure to tetraethyl lead brings about widespread changes in the ability of mammals to detoxify foreign compounds.

Animals↗
PubMed1979

Physiological defence against xenobiotics at their portals of entry to the organism.

The size and relatively high enzyme activity of the liver means that it has the major role in the biotransformation of xenobiotics in mammals. The tissues through which xenobiotics enter the body, lungs, skin, and gastrointestinal tract, have, however, quite a significant capacity for biotransformation, too. Major fractions of small doses of xenobiotics are therefore already metabolized and inactivated before the compounds have penetrated into the body. Most xenobiotics appear in the food and fluid ingested. This emphasises the importance of the gastrointestinal mucous membrane as the first line of defence of body against foreign chemicals. The biotransformation capacity varies with age and environmental chemical exposure, and depends on species and strain.

Age Factors↗
PubMed1979

Induction of disopyramide N-dealkylation by phenobarbital and disopyramide in rat liver.

An in vitro assay for the determination of the activity of disopyramide-N-dealkylation was developed. This reaction was concluded to be catalyzed by the liver microsomal, cytochrome P-450 centered monooxygenase system. Phenobarbital enhanced the N-dealkylation of disopyramide four fold, and disopyramide itself 1.6 fold, whereas methylcholanthrene was without effect. Disopyramide also increased ethoxycoumarin deethylation 1.6 fold, and had a slight increasing effect on the activity of epoxide hydratase, but did not affect the activities of glutathione S-transferase or UDPglucuronosyltransferase.

Animals↗
PubMed1979

Effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the hepatic metabolism of testosterone in the rat.

A dose of 20 micrograms/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was given to adult male rats intragastrically and the metabolism of [4-14C]-testosterone by liver homogenate was examined 1 week later. The overall catabolism of testosterone was significantly reduced by the TCDD treatment. Dihydroxysteroids (intermediate reduced metabolites) were increased, while the production of polar non-conjugated metabolites (end products) was diminished.

Animals↗