Hydroxylated　polybrominated　diphenyl　ethers　(OH-PBDEs)　have　emerged　as　contaminants　of　environmental　concerns　because　they　pose　potential　risks　to　human　and　animal　health.　The　purpose　of　this　study　was　to　investigate　the　in　vitro　metabolism　of　OH-PBDEs　and　their　potential　inhibition　against　17　beta-estradiol　(E2)　metabolism.　Rat　liver　microsomes　were　used　as　a　source　of　P450　enzymes　in　an　in　vitro　metabolism　study　of　OH-PBDEs.　Inhibition　of　E2　metabolism　and　kinetic　study　were　performed　by　incubating　with　rat　liver　microsomes　in　the　presence　of　OH-PBDEs.　The　obtained　data　clearly　demonstrated　that　OH-PBDEs,　especially　those　congeners　with　lower　bromination,　could　be　metabolized　to　bromophenol　and　diOH-PBDEs.　The　less　metabolic　rate　of　OH-PBDEs　was　observed　with　the　increasing　number　of　bromine　substituents.　OH-PBDEs　with　hydroxyl　group　and　bromine　adjacent　to　the　ether　bridge　showed　faster　metabolic　rates.　In　addition,　the　results　showed　non-competitive　inhibition　of　E2　metabolism　by　OH-PBDEs　with　IC50　values　in　the　range　from　13.7　to　55.2　mu　M.　The　most　potent　OH-PBDE　inhibitor　was　found　to　be　3＇-OH-BDE-100.　The　inhibitory　potencies　for　OH-PBDEs　were　significantly　higher　than　those　of　parent　PBDE　and　methoxylated　metabolites,　providing　the　evidence　that　PBDEs　exerted　estrogenic　activity　in　part　by　their　hydroxylated　metabolites.　OH-PBDEs　exhibited　large　differences　in　their　capacity　to　be　metabolized　and　to　inhibit　E2　metabolism　in　rat　liver　microsomes.　The　finding　might　increase　our　understanding　of　healthy　risk　associated　with　PBDEs　in　human　and　wildlife.