Chemical structure and biological activity 



THE TOXICITY OF PLANT GROWTH REGULATORS 



It seems to be a general rule that highly active anti-auxins which stimulate 

 the growth of wheat or flax roots at very low concentrations also show 

 inhibition at lower concentrations than weak anti-auxins. Such a phe- 

 nomenon could lead to the assumption that the inhibitions exerted by 

 sufficiently high concentrations of all anti-auxins were in some way related 

 to the auxin system. A decrease in the level of active auxin below its optimum 

 value would be a possible explanation, but this is ruled out by the fact that 

 such inhibitions are not relieved by the addition of auxin (Aberg, 1951; 

 1953a). Instead, it has been assumed that the inhibitions are due to accessory 

 toxic effects which have no connection with the auxin system proper (Aberg, 

 1951, 1953a; Burstrom, 1951a,b; Hansen, 1954). 



The nature of such a 'toxicity' is, of course, a problem in itself. It is 

 tempting to assume some connection with a general ability of regulator 

 substances to become bound to enzymes and other proteins, thereby upsetting 

 their physiological functions when present in high concentrations. A certain 

 parallelism between the affinity of the regulators for the specific growth 

 centres and their general 'toxicity' would then be quite natural. In this 

 connection, it is very interesting to find that there are indications of a 

 parallelism between the bactericidal effect of many phenols and the growth- 

 regulating activity of the corresponding phenoxyacetic acids. As a measure 

 of the bactericidal activity, the 'phenol coefficient', giving the relation 

 between the concentration of unsubstituted phenol and the equi-effective 

 concentration of the substance to be characterized, may be used (see Reddish, 

 1954). 



A rise in the phenol coefficient upon /jara-chlorination is apparent for 

 several pairs of phenols related both to auxinic and to anti-auxinic phenoxy- 

 acetic acids. We thus find about a four-fold increase from phenol to 4-Cl- 

 phenol, from 2-Cl- to 2:4-Cl2-phenol, and from thymol to chlorothymol; 

 from 2:6-Cl2- to 2:4:6-Cl3-phenol the increase is approximately two- to 

 three-fold, and from 2-Me- to 2-Me-4-Cl-phenol about five-fold (data 

 obtained from Suter, 1941; McCuUoch, 1945; Wolf and Westveer, 1952; 

 Reddish, 1954). Such a para chlorine effect is also apparent for many pairs 

 of phenols studied by Blackman et al. (1955) in respect to their capacity to 

 induce chlorosis in Lemna minor. In this case the rise in activity from phenol 

 to 4-Cl-phenol is 7-3, from 2-Me- to 2-Me-4-Cl-phenol 10-6, and from the 

 3:5-Me.2-, 2:5-Me2-, 2:6-Me2-, and 3-Me-5-Et-phenols to the corresponding 

 /?ara-chlorinated compounds 7-3, 9-5, 9-2, and 9-0 respectively. 



Hypothetically we may thus assume that /^ara-chlorination of phenols and 

 phenol derivatives increases the affinity of the substance for receptor places in 

 the cytoplasm, thereby conditioning in part the increased activity of several 

 auxins and also leading to increased activity of many anti-auxins, to higher 

 'toxicity' (root-growth-inhibiting activity) of anti-auxins and to increased 

 chlorose-inducing and bactericidal effects of many phenols. The strong 

 increase in the rate of hydrolysis of certain chymotrypsin substrates upon 

 /)flra-chlorination of a phenylalanine residue (see Neurath and Schwert, 

 1950; Aberg, 1953b) is relevant in the present connection in that it indicates 

 a corresponding increase in enzyme-substrate affinity. The presence of a 



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