Mito­chon­dria and xenobiotics

Mito­chon­dr­ial func­tion are involved in the tox­i­c­ity of many xeno­bi­otic com­pounds (A chem­i­cal com­pounds for­eign to a liv­ing organ­ism). We are increas­ingly exposed to a vari­ety of xeno­bi­otic com­pounds such as drugs, envi­ron­men­tal pol­lu­tants, and even nat­u­rally pro­duced tox­ins. The tox­i­c­ity of many of these com­pounds involves either direct or sec­ondary effects on mito­chon­dr­ial func­tion. Exam­ples of direct effects include inhi­bi­tion of elec­tron trans­port sys­tem com­po­nents that can dis­rupt energy pro­duc­tion and lead to oxida­tive stress. Indi­rect effects can occur through stim­u­la­tion of non-mitochondrial oxida­tive stress that then results in impaired mito­chon­dr­ial func­tion and ampli­fi­ca­tion of the tox­i­c­ity. The acute tox­i­c­ity effects of high dose expo­sures of many com­pounds are well estab­lished. How­ever, the mech­a­nisms by which chronic expo­sure dis­rupts cell and organ­is­mal func­tion and con­tributes to last­ing dys­func­tion are less well known. Our lab is par­tic­u­larly inter­ested in the inter­ac­tion between mito­chon­dr­ial biol­ogy, chronic xeno­bi­otic expo­sure, and dis­ease. We are pur­su­ing this area in col­lab­o­ra­tion with tox­i­col­o­gists and clin­i­cal scientists.