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Biomedical subjects

M A Collins

Publications and source records attributed to M A Collins.

At least 127 records · Page 7Linked to original sources
PubMed1980

Neuroamine condensations in human subjects.

Non-enzymatic products of neuroamines and endogenous carbonyl compounds are apparent "normal" products in human metabolism, and their levels become increased during pathological conditions. DA condensation products--salsolinol, its O-methylated derivative, and methylated derivatives of 1-carboxyl-THP--are found normally in human urine, and the last TIQ is in human brain. Potential beta-carboline condensation products also occur in (aging) human lens tissue. Chronic drinking in alcoholics causes significant increases in urinary salsolinol and O-methyl-salsolinol, presumably due to the increased AcH which is made available. L-DOPA therapy (in Parkinson's disease) elevates urinary and tissue levels of the carboxylated THP derivatives, as well as of salsolinol and THP itself; hyperphenylalaninemia during PKU also increases tissue levels of a DA/phenylpyruvate-derived TIQ and an imine condensate of phenylethylamine and vitamin B6. These unusual products may interfere with neural dynamic processes, and produce cytotoxic metabolites.

Adult↗
PubMed1979

Dopamine-related tetrahydroisoquinolines: significant urinary excretion by alcoholics after alcohol consumption.

Concentrations of dopamine-related tetrahydroisoquinolines (salsolinol and O-methylated salsolinol) were significantly higher in the daily urine samples of alcoholic subjects admitted for alcohol detoxification than in the daily urine samples of nonalcoholic control subjects. Salsolinol concentrations in alcoholic subjects appeared to drop to trace (control) values 2 to 3 days after admission, following the disappearance of ethanol and its reactive metabolite acetaldehyde from the blood. These results indicate that physiologically active tetrahydroisoquinolines increase in humans during long-term alcohol consumption, presumably because of acetaldehyde's direct condensation with catecholamines. The presence of these or similar condensation products in the urine could be useful as clinical indicators of prior blood acetaldehyde concentrations in chronic alcoholics.

Acetaldehyde↗
PubMed1979

The induction of hepatic and extrahepatic xenobiotic metabolism in the rat and ferret by a polychlorinated biphenyl mixture (Aroclor 1254).

1. The effect of a single i.p. dose (500 mg/kg) of a polychlorinated biphenyl mixture (Aroclor 1254) on hepatic and extrahepatic xenobiotic metabolism in male rat, and male and female ferret, was studied. 2. Aroclor 1254 treatment induced hepatic microsomal N-demethylase activities, and cytochrome P-450 and protein content in both rat and ferret. Liver size and aniline 4-hydroxylase were also increased in rat, but not ferret. The polychlorinated biphenyl mixture appeared to be a mixed-type inducer of hepatic xenobiotic metabolism in both species. 3. Aroclor 1254 treatment produced large increases in activities of benzo(a)pyrene hydroxylase and 7-ethoxycoumarin O-deethylase in whole homogenates of the liver, small intestinal mucosa, kidneys and lungs of both species. Maximal stimulation of xenobiotic metabolism occurred in the kidney of both the rat and ferret. In contrast, UDP-glucuronyltransferase activity was only stimulated in liver, intestine and kidney of the rat and in liver and intestine of the ferret. 4. These results suggest a general species similarity in the response to the polychlorinated biphenyl mixture between the rat and ferret.

Animals↗
PubMed1978

Lack of evidence for sustained blood acetaldehyde concentrations during alcohol detoxification.

Contrary to a published report, blood acetaldehyde concentrations become undetectable in patients 1--2 days following admission for alcohol detoxification. The persistently elevated blood acetaldehydes reported by others probably were due to artifactual formation during analysis. Nevertheless, our admission blood acetaldehyde concentrations are significant enough to support the contention that acetaldehyde has a cytotoxic role in alcoholic disease.

Acetaldehyde↗
PubMed1976

Studies on the effects of pyrogallol and the structurally related dopa decarboxylase inhibitor RO4-4602 on acetaldehyde metabolism.

Microanalytic procedures for the determination of AcH in whole blood from EtOH-intoxicated animals given PG or related drugs should utilize a hemolysis step in 0.5 N PCA in order to inhibit PG-dependent AcH production in vitro. Thiourea may also be included as an added protective measure. RO4-4602, a clinically important drug that contains a PG ring structure, is a moderate in vitro inhibitor of AldDH activity, comparable in potency to PG, chloral hydrate, or diethyldithiocarbamate.

Acetaldehyde↗