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Biomedical subjects

T Hultin

Publications and source records attributed to T Hultin.

69 records · Page 4Linked to original sources
PubMed1968

The effects of polyuridylic acid on phenylalanine incorporation by subcellular fractions from carbon tetrachloride-poisoned rat liver.

1. Ribosomes and microsomes isolated from the livers of rats that had received carbon tetrachloride 1hr. previously had decreased endogenous capacity to incorporate amino acid. 2. The capacity of the isolated structures to respond to a synthetic messenger, polyuridylic acid, and to incorporate phenylalanine was investigated. 3. It was found that ribosomes from carbon tetrachloride-treated animals, prepared with detergent and at high ionic strength, could be restored to the same specific activity as control particles with polyuridylic acid but that these particles required more Mg(2+) in the incubation mixture. 4. Microsomes could also be stimulated to control activities with polyuridylic acid, but had a narrow optimum range of Mg(2+) concentration. 5. Microsomes prepared from poisoned animals could be preprogrammed with polyuridylic acid to a significantly greater degree than could control particles, and this response was greater with increasing Mg(2+) concentrations. These data suggested that in carbon tetrachloride poisoning the messenger-ribosome interaction had been altered. 6. Attempts to deprogramme particles from control and treated animals resulted in decreased endogenous activity of both particles and a decreased capacity for the treated particles to be restored with the synthetic messenger. 7. It is suggested that two effects are present in carbon tetrachloride poisoning, namely an alteration of the messenger-ribosome interaction and an increased lability of the ribosome, as either separate or related events.

Amino Acids↗
PubMed1967

Alterations in microsomal electron transport, oxidative N-demethylation and azo-dye cleavage in carbon tetrachloride and dimethylnitrosamine-induced liver injury.

The effect of administration of carbon tetrachloride and dimethylnitrosamine in vivo on hepatic microsomal function related to drug metabolism was measured. It was found that the capacity of isolated microsomes to demethylate dimethylaniline was diminished during the first hour after carbon tetrachloride poisoning and during the second hour after dimethylnitrosamine poisoning. Thereafter the microsomes from carbon tetrachloride-poisoned livers showed a continuous decline in activity so that at 24hr. there was little residual capacity to undertake demethylation. Microsomes from dimethylnitrosamine-poisoned animals were not different from controls at 24hr. During the first 3hr. there was a transient rise in the accumulation of the N-oxide intermediate in carbon tetrachloride-poisoned livers, with a subsequent fall to below control values. In dimethylnitrosamine poisoning there was a parallel decrease in N-oxide accumulation with decreased demethylation. In the latter part of the first 24hr. the ratio of N-oxide accumulation to demethylation was increased in both instances. At 2hr. after poisoning with either compound there was no evidence of altered NADPH(2)-dependent neotetrazolium reduction or lipid peroxidation. NADPH(2)-dependent azo-dye cleavage was decreased. There was no difference in microsomal cytochrome b(5) content, but there was a decrease in the amount of cytochrome P-450. This latter change was correlated with the decreased capacity for NADPH(2)-dependent oxidative demethylation. It is suggested that dimethylnitrosamine is associated with a defect in microsomal NADPH(2)-dependent electron transport at the level of cytochrome P-450. In addition to affecting cytochrome P-450, carbon tetrachloride is associated with a second severe block involving the release of formaldehyde from the N-oxide intermediate.

Alkylation↗
PubMed1967

Reversible degradation of polyribosomes in Chang cells cultured in a glutamine-deficient medium.

The effects of temporary glutamine deficiency on the protein and nucleic acid metabolism of Chang's liver cells in suspension cultures have been studied. It was observed that cells maintained in a glutamine-free medium showed a reduced incorporation of labeled precursors into protein and RNA. At the same time, the activity of the ribosomes and the proportion of polyribosomal aggregates in cell extracts diminished. These effects were reversed when the glutamine content of the medium was restored. The restoration of a normal rate of amino acid incorporation by intact cells as well as by cell-free systems was time dependent, and took place within a few hours after glutamine addition without preceding increase in the prevailing low rate of RNA synthesis. The addition of actinomycin D at concentrations that strongly inhibited the RNA metabolism of the cells did not prevent the increase in protein synthesis or the reappearance of polyribosomal aggregates. These facts suggest that the restoration of protein synthesis in the cells after glutamine starvation was not dependent on a production of new messenger RNA. The experimental data are consistent with the hypothesis that previously synthesized messenger RNA, preserved in the cells in a stable form, was brought into action in response to the reestablishment of an adequate cellular environment.

Amino Acids↗