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

Abstract

AbstractOxidation of [1‐14C] palmitoyl CoA by heart and liver mitochondria from rats fed dietary di‐2‐ethylhexyl phthalate (DEHP) was investigated in vitro. Oxidation of14C‐palmitoyl CoA to14CO2 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 of14C‐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 of14C‐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 oxidation14C‐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.