Reduced level of serum thiols in patients with a diagnosis of active disease.

Oxidative stress, or the production of oxygen-centered free radicals, has been hypothesized as the major source of DNA damage that in turn can lead to altered genetic expression, disease, and aging of humans. Serum protein thiol levels in blood are a direct measure of the in vivo reduction/oxidation (redox) status in humans, because thiols react readily with oxygen-containing free radicals to form disulfides. Moreover, serum thiols also reflect DNA repair capacity and the possible eventual accumulation of genetic damage, since a key DNA repair enzyme, poly ADP-ribose polymerase (PARP), is thiol/disulfide redox regulated.