3-Monochloropropane-1,2-diol (3-MCPD) and
3-MCPD fatty acid esters are process contaminants in foodstuff which are generated during thermal treatment. Long-term exposure to
3-MCPD or
3-MCPD esters causes toxicity especially in kidney and testis.
3-MCPD esters are efficiently hydrolyzed in the gastrointestinal tract, suggesting that their toxicity is mediated by free
3-MCPD. Combined exposure to free
3-MCPD and
3-MCPD released from
3-MCPD esters might lead to dietary consumption above the tolerable daily intake of 2 μg/kg
body weight/day. Suspected mechanisms of
3-MCPD toxicity include the inhibition of glycolysis and oxidative stress. Here, a comparative proteomic approach was followed to analyze the effects of
3-MCPD or
3-MCPD dipalmitate in livers from rats exposed to 10 mg/kg
body weight 3-MCPD, an equimolar dose of
3-MCPD dipalmitate, or a 4-fold lower dose of the
ester during a 28-day repeated-dose feeding study. Early cellular changes were monitored in the absence of overt toxicity. A comprehensive view of 3-MCPD- or
3-MCPD dipalmitate-triggered proteomic changes in rat liver links to previously proposed mechanisms of toxicity and substantially extends our knowledge on molecular hepatic effects of
3-MCPD. Organ-independent marker
proteins altered upon
3-MCPD exposure, for example DJ-1/PARK7, were identified by comparison of the proteomic patterns of kidney, testis and liver.