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Biomedical subjects

G L Plaa

Publications and source records attributed to G L Plaa.

At least 91 records · Page 5Linked to original sources
PubMed1982

Morphological aspects of manganese-bilirubin induced cholestasis.

Small doses of manganese or bilirubin administered alone to rats produce no morphologic alterations in the hepatocytes. However, combination of both treatments produced a rapid and severe decrease in bile flow that was paralleled by the appearance and aggravation of the cholestatic lesion: bile canaliculi progressively lost their microvilli; vacuolization occurred in the pericanalicular area and subsequently in the cytoplasm. When bile flow returned to normal, or when cholestasis was prevented by an injection of sulfobromophthalein or a pretreatment with phalloidin, no cholestatic signs were observed. A close correlation appears to exist between the presence of morphologic alterations and the decrease of bile flow in manganese-bilirubin cholestasis.

Animals↗
PubMed1982

Present status: toxic substances in the environment.

"Environmental toxicology" and "ecotoxicology" are defined and the characteristic components of each discussed. The sources of chemical pollution (production and use of energy sources and industrial chemicals; increased agricultural practices) and their dispersion in the environment are put into perspective. Characteristics of some chemical pollutants are summarized. The problems facing these branches of toxicology as predictive disciplines are briefly presented.

Animals↗
PubMed1981

Biliary excretion of diazepam in rats: influence of the route of administration and dosage.

The biliary excretion of diazepam metabolites was found in rats. Equivalent dosages of diazepam were administered orally and intraperitoneally. The biliary excretion was dose-dependent and was greater following intraperitoneal administration. After intravenous administration, a greater percentage of the diazepam dosage administered was excreted into the bile. Repetitive intravenous administrations yielded results which approached those observed after intraperitoneally administered dosages given as a bolus.

Administration, Oral↗
PubMed1980

Modification of haloalkane-induced hepatotoxicity by exogenous ketones and metabolic ketosis.

A variety of chemicals potentiate haloalkane-induced liver injury, but structure-activity relationships are not apparent. Recent studies have shown that one structural determinant, a carbonyl moiety, is common to several potentiating agents. Thus five ketonic chemicals (acetone, 2-butanone, methyl n-butylketone, 2,5-hexanedione, Kepone) and three chemicals that are metabolized to ketones (isopropranol, 2-butanol, n-hexane) potentiate the liver injury produced by one or more haloalkanes. Potentiation also has been observed when haloalkanes are administered to animals in a state of metabolic ketosis produced by alloxan-induced diabetes or by 1,3-butanediol administration. These observations are consistent with the hypothesis that administration or generation of ketonic substances increases the susceptibility of the liver to the toxic actions of haloalkanes.

Acidosis↗
PubMed1979

Bilirubin excretion pattern in manganese-bilirubin cholestasis.

Impaired bilirubin excretion has been investigated as the possible mechanism for the cholestasis observed following the injection of manganese and bilirubin in rats. We studied the biliary excretion pattern of bilirubin in bile under both cholestatic (manganese plus bilirubin) and noncholestatic (manganese or bilirubin alone; manganese plus bilirubin plus sulfobromophthalein) conditions using a diazotization reaction and this layer chromatography. The accumulation of non-C-1-glucuronides or of nonglucuronoconjugates of bilirubin in bile does not seem to be responsible for the cholestasis. The altered biliary bilirubin metabolic pattern of the azodipyrollic fractions observed during manganese-bilirubin cholestasis appeared to be the result of the cholestasis, rather than its cause.

Animals↗