Atrazine metabolism

Excretion of free atrazine in urine is consistent with the pattern of exposure, with maximal excretion rates at the end of the workshift and a rapid decrease after cessation of exposure. This pattern suggests that atrazine does not accumulate in the body (Catenacci et al., 1990). Atrazine metabolism gives rise to bi-dealkylated (80%), deisopropylated (10%), and deethylated (8%) metabolites, which are eliminated in urine over a period slightly longer... 

Egaas, E., J.U. Skaare, N.O. Svendsen, M. Sandvik, J.G. Falls, W.C. Dautennan, T.K. Collier, and J. Netland. 1993. A comparative study of effects of atrazine on xenobiotic metabolizing enzymes in fish and insect, and of the in vitro phase II atrazine metabolism in some fish, insects, mammals and one plant species. Comp. Biochem. Physiol. 106C 141-149. 

Malan, C., J.H. Visser, and H.A. van de Venter. 1987. Atrazine metabolism in field-grown maize and the effect of atrazine phytotoxicity on yield. S. Afr. Jour. Plant Soil 4 7-11. 

Pillai, P, J.D. Weete, A.M. Diner, and D.E. Davis. 1979. Atrazine metabolism in box crabs. Jour. Environ. Qual. 8 277-280. 

Giardina, M.C., Giardi, M.T, and Filacchioni, G. Atrazine metabolism by Nocardia elncidation of initial pathway and synthesis of potential metabolites, Agric. Biol Chem., 46 1439-1445, 1982. 

Shimabukuro, R.H. and H.R. Swanson (1969). Atrazine metabolism, selectivity, and mode of action. J. Agric. Food Chem., 17 199-205. 

Shimabukuro, R.H. (1967b). Atrazine metabolism and herbicidal selectivity. Plant Physiol., 42 1269-1276. 

Behki, R.M. (1995). Activation of atrazine metabolism thiocarbamate herbicides in Rhodococcus TE1. J. Environ. Sci. Health B-Pestic., 30 201-219. 

Sadowsky, M.J., Z. Tong, M. de Souza, and L.P. Wackett (1998). atzC is a new member of the amidohydrolase protein superfamily and is homologous to other atrazine-metabolizing enzymes. J. Bacteriol., 180 152-158. 

At this point, evidence that similar molecules acted as effective antidotes by inducing needed metabolic pathways for herbicide detoxication was at most very speculative. However, another hypothesis emerged. Could early herbicide pretreatments increase crop tolerance to these herbicides by elevating the substrates and enzymes needed for detoxication While not a new concept in animal systems, such an idea has received little attention in plant systems and it certainly has not been exploited in any practical way. The whole idea has seemed much more credible with the study by Jacetta and Radosevich (19) of photosynthetic recovery in corn after treatment with atrazine. More specifically, they showed that inhibition of photosynthesis was reduced and the rate of recovery enhanced in corn plants treated for the second or third time with atrazine compared to "first exposed" plants (Figure 2). Furthermore, the faster recovery was related to enhanced rates of atrazine metabolism in the previously treated plants (Table III). 

Figure 2. Pathway for atrazine metabolism in Pseudomonas strain ADP (Adapted from Reference 60)...

N-Dealkylation also plays a role in the metabolism and selectivity of 5-triazine herbicides such as atrazine," simazine, simetryn, and ter-butryn. In species in which this pathway was prominent, the major products identified were monodealkylated triazines, which retained phytotoxicity. However, in a study of atrazine metabolism in C. album, C. strictum, and Amaranthus ponelli, Khan et al. identified the bound residue from resistant biotypes as N-desethylatrazine and suggested that sequestration of ph3 otoxic metabolites contributed to tolerance to the herbicide. " ... 

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