Abstract
INHIBITION of protein synthesis seems to be the mechanism of action of diphtheria toxin1,2 at least in cell cultures and in cell free systems. Whether this is the mode of action of the toxin in producing selective damage to Schwann cells is not known3. To clarify this relationship we have investigated the incorporation of 14C-glycine into protein of the normal peripheral nerve of the chicken (Silver Link × Rhode Island Red) and the rat (WAG/C strain) during maturation. The rat shows approximately a 1,000-fold greater resistance to the toxin than the chicken, as assessed by intraneural inoculation of toxin4,5, and in both species the delay period before the onset of paralysis is considerably shorter in immature than in adult animals. It was considered that these differences could well be explained by differences in rates of protein synthetic activity in the two species and by the maturation states of the nerves.
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MATHESON, D., CAVANAGH, J. Protein Synthesis in Peripheral Nerve and Susceptibility to Diphtheritic Neuropathy. Nature 214, 721–722 (1967). https://doi.org/10.1038/214721a0
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DOI: https://doi.org/10.1038/214721a0
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