Herbicides 275 



toxic reaction. Having discussed these steps in chapter VI, attention 

 here will be centered on the physiological basis for the toxic reaction 

 itself. 



Possible Mechanisms of Toxic Action 



Once distribution of the auxin through the plant has been ob- 

 tained, some toxic action at the cellular level occurs. The nature 

 of this action is not yet established. There are five major theories to 

 explain the herbicidal action of auxin and most of these are closely 

 related to the theories of auxin action in growth described in chapter 

 VIII. These theories attempt to ascribe the herbicidal action to 

 respiratory depletion, cellular proliferation, the formation of toxic 

 materials, an activation of phosphate metabolism, and lastly the dis- 

 sociation or hydrolysis of proteins. 



The first of these theories, that the herbicidal effects of auxins are 

 caused by respiratory depletion, was suggested by Mitchell and Brown 

 (1945) who found that 2,4-D applied to morning glory at sub-lethal 

 dosages would cause respiratory increases and a depletion of the car- 

 bohydrate reserve of the plant. This action was studied in some detail 

 by Rasmussen (1947) who concluded that the rather large weight 

 losses in dandelion tissue following 2,4-D application would indeed 

 be accounted for by respiratory increases. However, neither the weight 

 loss nor the respiratory changes were proportional to the herbicidal 

 effects observable. The conclusion that the weight loss could not 

 account for the killing action was independently reached by Taylor 

 (1947). 



The possibility that cellular proliferation induced by auxins may 

 be responsible for their herbicidal action was pointed out by Struck- 

 meyer (1951). She suggested that the selectivity of auxins against 

 dicotyledonous plants might be accounted for on the basis that po- 

 tential cambial layers are abundant in the dicotyledonous stem and 

 are generally in a ring-like pattern which passes close to each group 

 of phloem cells in the stem. Presumably proliferation of these weakly 

 differentiated cells would destroy the phloem system of the stem. 

 Eames (1950) has demonstrated that this phloem destruction actually 

 takes place after auxin application. Struckmeyer points out that in 

 contrast to the dicot, the less sensitive monocotyledonous stem does 

 not have potential cambial layers or weakly difEerentiated cells ad- 

 jacent to the phloem, which may account in part for the fact that most 

 monocots are less sensitive to auxin herbicides. 



Van Overbeek et al (1951) suggested that herbicidal killing may 

 be due to the production of toxic substances through abnormal me- 



