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Biomedical subjects

V N Finelli

Publications and source records attributed to V N Finelli.

5 recordsLinked to original sources
PubMed1977

Tyrosinemia with acute intermittent porphyria: aminolevulinic acid dehydratase deficiency related to elevated urinary aminolevulinic acid levels.

A patient who had hereditary tyrosinemia was observed during two illnesses to have characteristics of acute intermittent porphyria with associated hypertension. Metabolic studies revealed elevated levels of urinary aminolevulinic acid but normal levels of porphyrin metabolites associated with, and possibly explained by, decreased red blood cell activity of the zinc-dependent enzyme, aminolevulinic acid dehydratase. Zinc deficiency could not be directly associated with the diminished enzyme activity. The patient's hypertension appeared to be related to increased urinary excretion of catecholamines and to elevated renin activity in peripheral venous blood.

Adolescent↗
PubMed1976

Biologic effects of auto emissions. I. Exhaust from engine with and without catalytic converter.

This paper relates to the efficacy of a catalytic converter in reducing the levels of certain pollutants emitted from an automobile engine and to the reduction and/or elimination of gross biologic damages in animals exposed to emissions from an exhaust system containing such catalysts. Groups of rats were exposed to diluted emissions from an automobile engine with and without catalyst. Concomitantly, a comparative experiment was conducted by exposing a group of rats to carbon monoxide alone (575 mg/m3). The parameters measured included hematocrit, serum LDH, GOT, and lysozyme. An elevation in hematocrit was observed in animals of the experiment run without catalyst and in those exposed to carbon monoxide; the use of the catalyst reduced the carbon monoxide levels in the exposure chambers by more than tenfold and prevented these bioeffects from occurring. Serum LDH activity was elevated in the groups of rats in the experiment conducted without catalyst, but no alternation was observed in the animals from the experiment utilizing the catalyst or in those exposed to carbon monoxide alone. The data obtained in this study showed that acute exposure to noncatalytic emissions caused significant alterations in certain biologic parameters. Conversely, the introduction of an oxidizing catalytic converter into the engine exhaust system reduced or prevented such biologic damage.

Animals↗
PubMedDate not supplied

Lead, zinc, and erythrocyte delta-aminolevulinic acid dehydratase: relationships in lead toxicity.

A lead-intoxicated patient with extremely high blood lead levels and unexpectedly mild symptoms was studied prior to and following treatment with calcium disodium edetate (ethylenediaminetetraacetic acid) and then prior to and following oral administration of zinc sulfate. During chelation therapy, erythrocyte (delta)-aminolevulinic acid dehydratase (ALAD) activity decreased as blood lead levels fell. Urinary excretion of zinc increased and was more than 3.5 times greater than that of lead. The ratio of blood lead to serum zinc was greatest (1.47) when ALAD activity was lowest. Oral administration of zinc sulfate following chelation therapy resulted in a significant increase in mean ALAD activity. In vitro additions of zinc chloride to the patient's erythrocytes resulted in reactivation of ALAD activity. These studies suggest that zinc is an important element in the ALAD system in man. Zinc may play a protective role in lead toxicity, and zinc supplementation may be a useful adjunct to chelation therapy for lead toxicity.

Adult↗