FREDERICK G. SMITH 1 1? 



uptake; and they found that the extent of inhibition was directly 

 proportional to the oxygen tension indicating that the same systems were 

 hmited by oxygen as inhibited by lAA. They found further that the 

 inhibition by lAA was largely reversed by washing stem slices which is 

 similar to Audus' observation (3) that root growth inhibition by 2,4-D 

 was similarly reversible. Further in vitro studies with these mature tissue 

 slices should provide a valuable link between the classical seedling tissue 

 studies and the herbicidal investigations with intact plants. 



Finally, there have been a few investigations of the in vivo and in vitro 

 effects of growth substances on respiratory enzymes themselves. Berger 

 and Avery (4,5) working with Avena coleoptile homogenates found a 

 marked rise in alcohol dehydrogenase activity after 15 to 24 hours 

 treatment with 10 ppm. lAA but no effect of />2 vitro treatment until 

 inhibitive concentrations were reached between 100 and 1,000 ppm. 

 The Wisconsin workers (21) have failed to find any in vitro effect on the 

 cytochrome, ascorbic acid, catechol, or glycolic acid oxidases by either 

 lAA or 2,4-D in the range of about 2 to 200 ppm. The direct inhibition 

 of oxidases or dehydrogenases seems, at present, an unUkely basis for 

 the toxic action of growth substances. 



Discussion and Conclusions 



The evidence relating toxic action of growth substances with respira- 

 tory metabolism is still rather scattered and fragmentary but some 

 interesting possibilities are apparent. In the relatively simple cases of 

 inhibition of elongation, streaming, and water uptake in Avena coleoptile 

 there seems to be a close parallel. The major evidence, in fact, for a 

 respiratory role of plant growth substances, physiological, or nonphysio- 

 logical is from studies on this classical tissue. With roots the evidence 

 is limited, though it looks as if the inhibition of cell elongation and water 

 uptake may occur at concentrations of growth substances which do not 

 affect over-all respiration. This, of course, should not be considered 

 evidence against any connection with respiratory metabolism since the 

 fraction of total respiration involved in these processes may be small 

 (13) or may not be expressed in terms of gross oxygen uptake or dry 

 weight change. Our greatest need is clearly for a closer examination of the 

 metabolic changes which accompany growth substance treatment. 



In the case of intact plants, seedlings or larger, toxic effects are more 

 varied and complex, and there is no close parallel between respiratory 



