Hydroxylation of the aromatic rings of DES and subsequent conjugation of the ethyl side chains accounts for 80 to 90% of DES metabolism, while oxidation accounts for the remaining 10 to 20% and is dominated by conjugation reactions. Conjugation of DES consists of glucuronidation, while oxidation includes dehydrogenation into ("Z","Z")-dienestrol. The medication is also known to produce paroxypropione as a metabolite. DES produces transient quinone-like reactive intermediates that cause cellular and genetic damage, which may help to explain the known carcinogenic effects of DES in humans. However, other research indicates that the toxic effects of DES may simply be due to overactivation of the ERs. In contrast to estradiol, the hydroxyl groups of DES do not undergo oxidation into an estrone-like equivalent.