Diindolylmethane (DIM) Interactions with Oxidation

GENETICS Damage

Injections of POOR in rats for two weeks prior to total body irradiation noted dose-dependent improvements in survival (up to 60% from 75mg/kg), and while 7. 5mg/kg was ineffective when given over this time period a single dose one day before radiation came out to confer 55% success. This protective effect was thought to be credited to activation of ataxia-telangiectasia mutated (ATM), a repair enzyme which increases in activity in answer to genetic damage, seen with 300nM DIM thought to be secondary to suppressing PP2A (MRE11 and BRCA1 also required); PP2A normally complexes with ATM keeping it in a non-active state, and its inhibited allows ATM to become hyperactive in reaction to genetic damage.

Low levels of DIM appear to allow a genetic repair enzyme (ATM) to be more responsive when incubated alongside an oxidative stressor that damages DNA.