Statistical fluctuation versus specific mechanism and the origin of the left-handed asymmetry of proteins.

We point out an intrinsic weakness in the reasoning that adduces a statistical fluctuation as the origin of a left-handed, prebiotic stereoisomeric asymmetry which might have been the initial asymmetry that led to the left-handed asymmetry of proteins observed now on Earth. The argument in favor of a statistical fluctuation as the source of the asymmetry depends implicitly on the assumption of a very small number of terrestrial sites at which polymerization leading to protein formation took place. On the other hand, the probability that a left-handed prebiotic asymmetry produced by a specific mechanism was efficacious would have increased linearly with the number of terrestrial sites. Thus, on the basis of the greater likelihood of a large number of possible polymerization sites in the prebiotic era, a random fluctuation is deemed to be a much less probable source of a stereoisomeric asymmetry than a specific mechanism, particularly the mechanism that follows from the parity violating weak interaction.

Chirality of electrons from beta-decay and the left-handed asymmetry of proteins.

A simplified mathematical model of the origin of the left-handed asymmetry of proteins in living matter is presented. The model is based on the hypothesis of Vester and Ulbricht that the chirality of (left-handed) electrons from naturally beta-active elements, e.g. 14C, 40K, etc., was the specific source of the asymmetry; it requires for its application data on interaction of electrons having non-zero chirality with racemic mixtures of amino acids. This interaction is here treated theoretically in an order-of-magnitude calculation. Our analysis yields a very approximate value of the induced steady-state asymmetry in the amino acids at the beginning of protein synthesis and indicates that this asymmetry, though small, may have been sufficient to account for the dominant left-handedness of proteins now observed.