The herbicide cinmethylin {exo-1-methyl-4-(1-methylethyl)-2-[(2-methylphenyl)methoxy]-7-oxabicyclo [2.2.1] heptane} inhibited oat (Avena sativa L. ‘Porter’) root growth during the first 6 h of treatment at a concentration of 6.7 × 10-8 M. A concentration of 1 × 10-8 M cinmethylin inhibited root growth within 12 to 18 h. Inhibition of shoot growth was less sensitive, but was inhibited by 36 to 48 h after treatment with 1 × 10-7 M and by 12 to 24 h after treatment with 1 × 10-5 M cinmethylin. Cinmethylin concentrations of 1 × 10-5 M and lower did not inhibit cell elongation in isolated oat coleoptiles during a 24-h exposure. Mitotic frequency in oat root tips was reduced after 12 h of treatment with 1 × 10-7 M cinmethylin. The frequency of all stages of mitosis (prophase, metaphase, and anaphase + telophase) was reduced. Concentrations of 1 × 10-6 M cinmethylin resulted in nearly complete arrest (87% inhibition) of mitosis. These data suggest cinmethylin inhibits growth by inhibiting entry of cells into mitosis. The cause of mitotic arrest is unknown; however, the mechanism appears to be different from other herbicides known to inhibit mitosis.

Dinitroaniline herbicides are absorbed readily by roots and emerging shoots, but shoot exposure is more phytotoxic. Translocation within the plant varies by specific herbicide but commonly is minor. Dinitroaniline herbicides injure plants by binding to tubulin, a dimer protein in the ceil that polymerizes to form microtubules (MTs). MTs form the major part of the mitotic apparatus, including spindle fibers, which enable chromosomes to separate during cell division. Dinitroaniline herbicides prevent tubulin from polymerizing into MTs, thus arresting mitosis. This leads to abnormal cells with more than the normal complement of chromosomes and, frequently, lobed nuclei. MTs also are responsible for orienting cell wall microfibrils in such a way that they prevent lateral enlargement of cells. Treatment with dinitroaniline herbicides leads to disorientation of the microfibrils, leading to one of the common symptoms—spherical cells instead of rectangular ones. Studies on the metabolism of trifluralin in plants have shown that amination, dealkylation, and cyclization all can occur. However, metabolites often amount to a small percentage of the original herbicide. In general, trifluralin seems quite stable within the plant.

The effects of varying concentrations and duration of alachlor [2-chloro-2′,6′diethyl-N-(methoxymethyl)acetanilide] and metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide] treatment on root growth, cell division, and cell enlargement were studied. Peas (Pisum sativum L. ‘Alaska’) and oats (Avena sativa L. ‘Victory’) were treated from 0 to 48 h with concentrations ranging from 1 × 10-8 to 1 × 10-3 M of each herbicide. After 48 h, average growth rates were significantly inhibited at concentrations of 1 × 10-7 M alachlor and 5 × 10−8 M metolachlor, and 5 × 10−7 M alachlor and 1 × 10-6 M metolachlor for peas and oats, respectively. When growth inhibitions were examined across time at concentrations greater than these, the degree of growth inhibition was a function of both concentration and duration of treatment. Often the greatest decrease in growth occurred between 0 and 12 h. Mitotic indices of root tip squashes from pea roots and paraffin sections from oat roots were determined. There was a significant reduction in the mitotic indices of pea roots treated for 48 h with 5 × 10−6 M alachlor or 1 × 10-5 M metolachlor. After a 30-h treatment, the mitotic indices of oat roots were significantly reduced by 1 × 10−7 M metolachlor and 1 × 10−6 M alachlor. Significant inhibition of elongation of etiolated oat coleoptiles were observed at 5 × 10−6 M alachlor (27%) and 5 × 10−5 M metolachlor (30%). Inhibition of pea hypocotyl elongation did not occur at concentrations below 5 × 10−4 M. It was concluded that the growth inhibition of plants caused by alachlor and metolachlor results from both an inhibition of cell division and cell enlargement.