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PubMed1993

Long-term effects of the anticholinesterases sarin and soman on latencies of muscle action potentials in mouse diaphragm muscle.

In-vivo administration of the irreversible anticholinesterases sarin and soman has been shown to produce long-term effects on latency and variability of latency of muscle action potentials in in-vitro mouse diaphragm muscle preparations. The maximum observed effects occurred three days post-soman administration and seven days post-sarin administration, and were no longer detectable 28 days later. With both anticholinesterases the increase in latency, and variability of latency, was reduced by pyridostigmine pretreatment. Therapeutic administration of pralidoxime mesylate effectively prevented the sarin-induced effects when given after a delay of 24 h. In contrast, the effectiveness of pralidoxime mesylate declined rapidly when its administration was delayed following soman. These findings are consistent with this action of soman and sarin being a product of acetylcholinesterase inhibition. The results obtained with sarin suggest that a period of acetylcholinesterase inhibition in excess of 24 h is required to trigger the events leading to the production of this long-term effect.

Action Potentials↗
PubMed1979

Expression of simian virus 40 gene A affects tubulin stability.

The stability of tubulins present in crude extracts of untransformed BALB/c-3T3 mouse fibroblasts, Chinese hamster lung cells, and various of their simian virus 40 transformants was assessed by measurement of their individual colchicine-binding decay rates. In all cases studied the decays followed the kinetics of first-order reactions, and rates were reduced at low temperatures and by vinblastine sulfate. Under all assay conditions, including different temperatures and protein concentrations, tubulins of normal cells decayed considerably faster than those of simian virus 40-transformed cells. Experiments performed with a number of Chinese hamster lung cell clones transformed with temperature-sensitive simian virus 40 gene A mutants showed a clear correlation between increased tubulin stability and the expression of gene A function. These results suggest that it is T-antigen, the viral gene A product, that affects tubulin.

Animals↗