Effects of sub-chronic dietary 2-monochloro-1,3-propanediol on oxidized lipids in rat heart, kidney, serum, and skeletal muscle
Chlorinated propanols are processing induced food contaminants formed in the manufacturing of vegetable oils and hydrolyzed vegetable protein. The 2-monochloro-propanediol (MCPD) isomer has been insufficiently studied for hazard assessment, while the 3-MCPD isomer has received more attention and has been classified as a possible human carcinogen. Xenobiotics and polyunsaturated fatty acids (PUFA) are known to be metabolized by some of the same classes of enzymes, namely cytochrome P450 (CYP), cyclooxygenase (COX), and lipoxygenase (LOX); and previous studies have shown PUFA metabolites to be altered by exposure to toxins. This study investigated the effects of dietary 2-MCPD by profiling PUFA metabolites called oxylipins, which have diverse homeostatic functions, and non-enzymatically produced oxidized phosphatidylcholines (OxPC) and isoprostanes (isoP) as markers of oxidative stress, in the heart, kidney, serum, and skeletal muscle of rats treated with control or 40 mg/kg body weight 2-MCPD for 90-days. It was observed that 2-MCPD treatment decreased n-3 PUFA derived oxylipins in the heart and decreased LOX produced oxylipins in the serum. In the kidney, 2-MCPD treatment altered few oxylipins with no clear grouping by enzyme pathway or PUFA precursor. In the skeletal muscle, there was an absence of oxylipin alterations with 2-MCPD treatment. 2-MCPD treatment did not alter the OxPC or isoP in any of the tissues quantified, indicating oxidative stress did not play a role in the mechanism of action of 2-MCPD. These findings of altered oxylipin profiles add to the weight of the evidence of 2-MCPD toxicity, as well as support the potential use of serum oxylipins as biomarkers of 2-MCPD exposure.
2-monochloro-1,3-propanediol (2-MCPD), Oxylipin, Oxidized phosphatidylcholine, Cardiotoxicity, Food contaminant