Effect of dietary di‐2‐ethylhexyl phthalate on oxidation of 14 C‐palmitoyl CoA by mitochondria from mammalian heart and liver

Oxidation of [1‐ 14 C] palmitoyl CoA by heart and liver mitochondria from rats fed dietary di‐2‐ethylhexyl phthalate (DEHP) was investigated in vitro. Oxidation of 14 C‐palmitoyl CoA to 14 CO 2 increased two‐ to threefold in hepatic mitochondria from rats fed 0.1% DEHP for 2 to 3 days; this increase appeared to be a maximum response since similar data were obtained using hepatic mitochondria from rats receiving 0.5% or 1.0% DEHP in the diet. The response of hepatic mitochondria to DEHP was found to continue throughout the duration of 35‐day trials in which 1.0% DEHP was fed. In contrast to hepatic mitochondria, the oxidation of 14 C‐palmitoyl CoA by heart mitochondria decreased ca. 40% upon addition of 0.1% or 0.5% DEHP to the diet; this effect of DEHP on heart mitochondria was not sustained beyond ca. 8 days of DEHP feeding. Limited studies were also performed in rabbits and pigs. Oxidation of 14 C‐palmitoyl CoA was increased ca. twofold in hepatic mitochondria from rabbits fed 1% dietary DEHP for 12 days and in hepatic mitochondria from pigs that received 5 doses of DEHP (0.8g/kg) at 12‐hr intervals; the oxidation 14 C‐palmitoyl CoA by heart mitochondria from these same animals was unchanged in the rabbit but increased an average of 37% in the pig. DEHP feeding to rats was associated with increased yields of hepatic mitochondrial protein; standardized preparations of heart mitochondria were not similarly affected.