Metabolomic profiling identifies the mitochondria as a target of pentachlorophenol toxicity in the blood clam (Tegillarca granosa).

The pervasive presence of pentachlorophenol (PCP) in aquatic-benthic ecosystems poses a threat to organisms. However, the toxicological mechanisms of PCP in benthic organisms are limited. In this study, Tegillarca granosa, a representative bivalve species, was treated with environmentally relevant concentrations of PCP (1, 10, and 100 μg/kg) and positive control for 28 days via sediment exposure to investigate bioaccumulation potential, metabolomic profiles, and histopathology. The biota-sediment bioaccumulation factor for PCP was 9.1. Given the capability of PCP to act as an uncoupler of oxidative phosphorylation, studies were performed to determine key events in the adverse outcome pathway associated with this molecular initiating event. Metabolic profiles indicated a disruption in lipid metabolism, as well as imbalances in the quantity of calcium, which was associated with the synthesis of reactive oxygen species (ROS). A reduction in adenosine-5'-triphosphate (ATP) levels were seen in clams treated with PCP and in animals treated with carbonyl cyanide-4-(trifluoromethoxy)phenylhydrazone (FCCP), which served as a positive control. When clams were co-exposed to 100 μg/kg PCP and 500 μg/kg ATP, PCP toxicity was diminished and levels of mitochondrial calcium, as well as ROS, were reduced. These results suggest that mitochondrial impairment is a key event in the toxic mechanism of PCP to T. granosa.