Polycyclic aromatic hydrocarbons (PAHs) reduce hepatic β-oxidation of fatty acids in chick embryos

Abstract

Polycyclic aromatic hydrocarbons (PAHs) are widespread fused-ring contaminants formed during incomplete combustion of almost all kind of organic materials from both natural and anthropogenic sources. Some PAHs have been shown to be carcinogenic to humans, and a wide range of PAHs are found in wildlife all around the globe including avian species. The purpose of this project was to assess the effects of a standard mixture of 16 PAHs (United States Environmental Protection Agency) on the hepatic fatty acid β-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The hepatic β-oxidation was measured using a tritium release assay with [9,10-(3)H]-palmitic acid (16:0) as substrate. Treated groups were divided into groups of 0.05, 0.1, 0.3, 0.5, and 0.8 mg PAHs/kg egg weight. The hepatic β-oxidation was reduced after exposure in ovo to the 16 PAHs mixture compared to control. The mechanisms causing reduced fatty acid oxidation in the present study are unclear, however may be due to deficient membrane structure, the functionality of enzymes controlling the rate of fatty acid entering into the mitochondria, or complex pathways connected to endocrine disruption. To the best of our knowledge, this is the first time a PAH-caused reduction of hepatic β-oxidation of fatty acids in avian embryos has been observed. The implication of this finding on risk assessment of PAH exposure in avian wildlife remains to be determined.

Association of polycyclic aromatic hydrocarbons (PAHs) and lead co-exposure with child physical growth and development in an e-waste recycling town

“…Although the precise mechanisms by which PAHs affect child development are not confirmed, some mechanisms including endocrine disruption (Westman et al, 2013), binding to human growth factor receptors and aryl hydrocarbon (Ah) receptor to induce P450 enzymes are suggested (Shimada et al, 2013). There are evidences that PAHs may act through disrupting estrogen-mediated pathways (Sievers et al, 2013).…”

Differential cellular metabolite alterations in HaCaT cells caused by exposure to the aryl hydrocarbon receptor-binding polycyclic aromatic hydrocarbons chrysene, benzo[ a ]pyrene and dibenzo[ a,l ]pyrene

“…Then, through catalysis of carnitine acyltransferase II, acyl-CoA is being recovered within the mitochondrial matrix and directed towards β-oxidation [51] . Recently, Westmann et al showed that fatty acid β-oxidation in chicken embryo liver was significantly reduced in response to the treatment with a mixture of 16 different PAHs [52] . In transgenic mice activation of AHR inhibited hepatic fatty acid β-oxidation along with acyl-CoA oxidase 1, the rate limiting enzyme in peroxisomal β-oxidation [53] .…”

Cardio-respiratory development in bird embryos: new insights from a venerable animal model

“…They enter tissues through inhalation, ingestion, and dermal contact, and their rate of absorption increases when they are present in mixtures. The liver is generally the most important site where toxicants undergo biotransformation (e.g., Westman et al (2013)), but generally most if not all organs are affected to some extent by PAH, with their toxicity dependent upon dose, concentration, time, route of exposure, further distribution, sensitivity, and ability of the organ to metabolize these compounds (Canga et al, 1993).…”