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Biomedical subjects

I Nafstad

Publications and source records attributed to I Nafstad.

At least 55 records · Page 3Linked to original sources
PubMed1981

Studies on the biliary excretion and metabolites of hexachlorobenzene in the rat.

1. The biliary excretion of metabolites of hexachlorobenzene (HCB) was studied in rats dosed intragastrically with 14C-HCB. Approx. 80% dose was absorbed from the gastrointestinal tract. An average of 3.6% dose was recovered in the bile of bile-duct-cannulated rats in 48 h. 2. By g.l.c.-mass spectrometry, 2.0 and 1.8% of the 14C excreted in the 24 h bile was shown to be due to unchanged HCB and pentachlorobenzene (PCB), respectively. The major metabolite pentachlorophenol (PCP) accounted for 24.2%. 3. Sulphur-containing metabolites were not identified. However, the hepatic GSH concn. decreased by 50% within 24 h following oral administration of HCB (200 mg/kg).

Animals↗
PubMed1980

Tissue distribution of 14C-lynestrenol in pregnant rats.

The tissue distribution of 4-14C-lynestrenol (17 alpha-ethynyl-oestr-4-en-17 beta-ol) following oral administration to pregnant rats was studied by whole body autoradiography and liquid scintillation counting. Pregnant females were sacrificed on days 10, 12, 14 and 19 of gestation, in each case 5 hours after oral administration of 43 microCi 4-14C-lynestrenol per animal. The isotopelabelled compound was distributed throughout most tissues, including the fetuses. The highest concentrations were found in the liver, while there was lower activity in the fatty tissues and the activity in the fetuses was comparable with that in the brain. The placental transfer was verified by the results of liquid scintillation counting. The concentration of labelled substance in the fetuses increased with the duration of pregnancy.

Administration, Oral↗
PubMed1979

The distribution of 14C-ethoxyquin in rat.

Adult male rats were given the antioxidant 14C-ethoxyquin by oral intubation and were sacrificed at various time intervals from 0.5 hr to 6 days following administration of the drug. The distribution pattern was studied by whole-body autoradiography and liquid scintillation counting. The isotopelabelled antioxidant was distributed throoughout most tissues and the blood at 0.5 hr after administration. The highest radioactivity throughout the experimental period was observed in the liver, the kidney, the gastrointestinal tract and the adipose tissue. No activity was observed in the brain and the central nervous system. Of the dose ingested 2.2 and 0.2% were found in the liver at 0.5 hr and 6 days respectively following dosing. The hepatic peak in radioactivity was measured at 8 hrs and after 6 days 7.5% of this level was still present in the liver. Six days after administration residues of ethoxyquin and metabolites were also present in the kidney cortex, the intestines, the lung, various adipose tissue and blood.

Animals↗
PubMed1978

The modifying effect of multiple generation selection and dietary cadmium on methyl mercury toxicity in Japanese quail.

Japanese quails were exposed to dietary methyl mercury chloride in graded amounts from 2--8 ppm through a series of multiple-generation experiments with the experimental periods lasting from 6--12 weeks, starting with the experimental diets when the birds were 6 weeks old. Cadmium chloride was added to diets with and without mercury and fed to groups in three of the five experiments. Hatchability was depressed at 8 ppm mercury. The mortality of chicks from 8 ppm exposed parents was 100% in the first two generations, while chick mortality at the 4 ppm level in the same experiments was 54--63%. After six generations mortality in chicks hatched in 8 ppm group was reduced to about 50%. Cadmium supplementation at a level of 5 ppm counteracted the mercury-induced toxicity but failed to be effective in preventing the effects of mercury toxicity when added at 15 ppm level. Significant toxic effects of cadmium alone did not occur until the level was raised to 60 ppm. The morphology of mercury-induced encephalopathy was similar to the brain lesions reported in other bird species, with the injuries predominantly being localized to the cerebellar cortex and medulla.

Animals↗
PubMed1978

Interaction of vitamin E and selenium with the hepatotoxic agent dimethylnitrosamine.

Pretreatment of rats with vitamin E, 0.02% w/w of the diet and a sc dose, 200 mg/kg, given 48 hrs. before dimethylnitrosamine, DMNA, was found to ameliorate the acute hepatotoxicity of DMNA (30 mg/kg) as reflected in reduced plasma asparagine-amino-transferase (AspAT) activity. This effect was confirmed by histological evaluation. No significant effect of DMNA on plasma levels of vitamin E was observed, however, DMNA significantly increased the hepatic level of vitamin E supplemented rats. Pretreatment with selenium, 0.5 mg/kg given intraperitoneally 48 hrs. before DMNA, was found to enhance the acute hepatotoxicity of DMNA as reflected in increased elevation of plasma AspAT activity. This effect was not confirmed morphologically. DMNA did not have any effect on the hepatic selenium state in selenium pretreated rats; however, selenium pretreatment tended to decrease hepatic and plasma tocopherol levels. To explain the effects observed in the present investigation, various mechanisms were discussed. If the compounds were acting as antioxidants, then the difference in intracellular localization had to be important. More likely a specific biochemical function involving drug metabolizing enzymes could be involved. Finally vitamin E could protect membranes from damage during the necrotizing action of DMNA.

Animals↗