Previous reports have suggested that bentazon [3-(1-methylethyl)-(1H)-2,1,3,-benzothiadiazin-4(3H)-one 2,2-dioxide] tolerance among soybean genotypes is the result of differential translocation or metabolism. The basis for tolerance was reexamined using susceptible and tolerant genotypes. Tolerant genotypes (''Hill'' or ''Clark 63'') were found to tolerate 100- to 300-fold more bentazon than susceptible genotypes (''L78-3263'', ''Hurrelbrink'', and ''PI 229.342''). Minor differences in absorption and translocation occurred among the genotypes but they did not correlate with tolerance. Tolerant genotypes metabolized 80 to 90% of absorbed bentazon within 24 h, while susceptible genotypes metabolized only 10 to 15%. Two major metabolites, the glycosyl conjugates of 6- and 8-hydroxybentazon, were formed in tolerant genotypes. Susceptible genotypes did not form the hydroxybentazon conjugates but instead produced relatively low level of two unidentified metabolites. It is concluded that differential bentazon tolerance among soybean genotypes is linked to the ability to form both the 6- and 8-hydroxybenatzn conjugates.