Dilinoleoylphosphatidylcholine is responsible for the beneficial effects of polyenylphosphatidylcholine on ethanol-induced mitochondrial injury in rats.

Chronic ethanol consumption depletes phosphatidylcholines (PC) in membranes and hepatic mitochondria are an early target of this toxicity. Our previous studies showed that soybean-derived polyenylphosphatidylcholine (PPC), attenuated mitochondrial liver injury. Since dilinoleoylphosphatidylcholine (DLPC) is the major component of PPC, we assessed whether it is responsible for the protection of PPC. Forty-two male rats were fed the following liquid diets for 8 weeks: Control; Control with DLPC (1.5 g/1000 Calories (Cal); Alcohol (36% of Cal); Alcohol with DLPC (1.5 g/1000 Cal) and Alcohol with PPC (3 g/1000 Cal). As expected, ethanol feeding diminished the capacity of hepatic mitochondria to oxidize glutamate and palmitoyl-1-carnitine, and also decreased the activity of mitochondrial cytochrome oxidase. These effects were equally prevented by either PPC or DLPC. In conclusion, DLPC fully reproduced PPC's protective action and may be effective in the prevention or delay of more severe liver damage.