Even if it is not a common substrate for metabolism, benzene can be oxidized by both bacteria and eukaryotes. In bacteria, dioxygenase enzyme can add an oxygen to the ring, and the unstable product is immediately reduced (by NADH) to a cyclic diol with two double bonds, breaking the aromaticity. Next, the diol is newly reduced by NADH to catechol. The catechol is then metabolized to acetyl CoA and succinyl CoA, used by organisms mainly in the citric acid cycle for energy production.
The pathway for the metabolism of benzene is complex and begins in the liver.  Several enzymes are involved.  These include cytochrome P450 2E1 (CYP2E1), quinine oxidoreductase (NQ01 or DT-diaphorase or NAD(P)H dehydrogenase (quinone 1)), GSH, and myeloperoxidase (MPO).  CYP2E1 is involved at multiple steps: converting benzene to oxepin (benzene oxide), phenol to hydroquinone, and hydroquinone to both benzenetriol and catechol.  Hydroquinone, benzenetriol and catechol are converted to polyphenols.  In the bone marrow, MPO converts these polyphenols to benzoquinones.  These intermediates and metabolites induce genotoxicity by multiple mechanisms including inhibition of topoisomerase II (which maintains chromosome structure), disruption of microtubules (which maintains cellular structure and organization), generation of oxygen free radicals (unstable species) that may lead to point mutations, increasing oxidative stress, inducing DNA strand breaks, and altering DNA methylation (which can affect gene expression). NQ01 and GSH shift metabolism away from toxicity.  NQ01 metabolizes benzoquinone toward polyphenols (counteracting the effect of MPO).  GSH is involved with the formation of phenylmercapturic acid.
Genetic polymorphisms in these enzymes may induce loss of function or gain of function.  For example, mutations in CYP2E1 increase activity and result in increased generation of toxic metabolites.  NQ01 mutations result in loss of function and may result in decreased detoxification.  Myeloperoxidase mutations result in loss of function and may result in decreased generation of toxic metabolites.  GSH mutations or deletions result in loss of function and result in decreased detoxification. These genes may be targets for genetic screening for susceptibility to benzene toxicity.