FIGURE 5.

Effect on fatty acid metabolism in isolated mouse liver mitochondria. Isolated, previously frozen mouse liver mitochondria were used as enzyme source. (A) Effect on CPT1A activity. Formation of ¹⁴C-palmitoylcarnitine from ¹⁴C-palmitoyl-CoA was assessed after incubation with the toxicants for 10 min. Basal rates of palmitoyl-CoA formation for control incubations (0.1% DMSO) were 3.0 ± 0.25 nmol palmitoyl-CoA × min^-1 × mg protein^-1. (B) Effect on 1-¹⁴C-palmitoylcarnitine metabolism. Mitochondria were treated with the toxicants for 10 min before formation of acid soluble products was determined. Basal rates of palmitoylcarnitine oxidation for control incubations (0.1% DMSO) were 213 ± 22 nmol palmitoylcarnitine × min^-1 × mg protein^-1. (C,D) Effect on long-chain and medium-chain acyl-CoA dehydrogenases. After pretreatment with the toxicants for 3 min, reduction of cytochrome c by FADH produced by the acyl-CoA dehydrogenases was determined spectrophotometrically. Basal rates of cytochrome c oxidation by long- and medium-chain acyl-CoA dehydrogenases in control incubations (0.1% DMSO) were 53.7 ± 2.2 nmol × min^-1 × mg protein^-1 and 32.3 ± 1.2 nmol × min^-1 × mg protein^-1, respectively. Results were normalized to the values obtained in DMSO 0.1% exposed controls and are expressed as mean ± SEM. ^∗p < 0.05 vs. DMSO 0.1% control.