Intoxicated Cells Research Articles

The effects of ascorbic acid on diphtheria toxin and intoxicated hela cells.

Ascorbic acid (vitamin C) prevented diphtheria toxin from inhibiting the incorporation of [U-14C]-alanine into trichloroacetic acid precipitable material in HeLa cells. Ascorbic acid did not exhibit an effect on the adenosine diphosphate-ribosylation of amino acyl transferase II nor did it separate fragment A from fragment B in "nicked" toxin. A non-specific reducing agent, para-methylaminophenol sulfate, exhibited an effect on HeLa cells very similar to the results of ascorbic acid. Citric acid, a tricarboxylic acid, had no effect on HeLa cells.

Mitochondrial swelling induced by diphtheria toxin. The behaviour of citrate in intoxicated cells.

Mitochondrial swelling induced by diphtheria toxin. The behaviour of citrate in intoxicated cells.

An early effect of Staphylococcus alpha-toxin on cells growing in culture: ATP levels in normal and intoxicated cells.

An early effect of Staphylococcus alpha-toxin on cells growing in culture: ATP levels in normal and intoxicated cells.

The response of cultured mammalian cells to diphtheria toxin. I. Amino acid transport, accumulation, and incorporation in normal and intoxicated sensitive cells.

The response to diphtheria toxin of two sensitive cell lines, KB and HeLa, was investigated. Inhibition of the incorporation of radioactively labeled amino acids into protein was the earliest detectable effect of diphtheria toxin. It was observed that, during the period of intoxication, the cell membrane was morphologically intact and retained its semi-permeable character, although it was rendered fragile and more easily disrupted by mechanical manipulations than the normal cell. The transport of amino acids continued even after intoxicated cells had ceased to synthesize protein, and the levels accumulated were equal to those of control cells. It was observed that cultural conditions, age, and handling of cells affected their response to toxin. In early log phase cells subjected to a minimum of handling before application of the toxin, the normally observed latent period preceding detectable effects was reduced to 15 min for KB cells and 30 min for HeLa cells, shorter times than previously reported. The data are consistent with the hypothesis that diphtheria toxin enters susceptible cells, possibly by pinocytosis, and there acts upon cytoplasmic sites of protein synthesis.

Studies of the activity of diphtheria toxin. I. Poliovirus replication in intoxicated HeLa cells.

It has been demonstrated that a saturating dose of diphtheria toxin produced a 90% inhibition of polio-virus replication in HeLa cells. This inhibition was reflected in infectious viral RNA synthesis and in mature virus production. Toxin had no direct effect on virus particles or I-RNA, and poliovirus adsorption and eclipse appeared to be carried out normally in intoxicated cells. When toxin was given at various time intervals after infection, the amount of inhibition depended on the time of toxin addition. Toxin given before or immediately after infection gave maximum inhibition, while toxin given several hours after infection had little effect. The data suggest that toxin inhibits viral replication through its effect on protein synthesis. It is likely that a critical step in the viral replication cycle, the production of poliovirus-induced RNA polymerase, is inhibited, and possibly the synthesis of capsid protein. Ammonium salts and the aliphatic amines, glycamine and prolamine, prevented the inhibition of viral replication by toxin. The kinetics of the protective action of ammonium chloride and diphtheria antitoxin are remarkably similar.

Toxic Substances and the Renal Tubules of the Rat

Minute processes of cell regeneration in rat renal tubules were observed, placing the principal object on the mitochondria in the cells of portio principalis. For this purpose potassium chromate or mercuric chroride was given less than their mortal dosage. Potassium chromate caused characteristic changes in the proximal part of portio principalis, but minor changes in its middle and distal part. Mercuric chroride, on the other hand, caused peculiar changes in the distal part while it caused minor changes in its middle and proximal part.Afterwards certain intoxicated cells became necrotic, while others recovered, and the loss of cells was supplied by mitosis.