Developmental and mitochondrial toxicity assessment of perfluoroheptanoic acid (PFHpA) in zebrafish (Danio rerio).

The potential toxicity of several perfluoroalkyl and polyfluoroalkyl substances (PFASs) to aquatic species are not well understood. Here, we assessed the sub-lethal toxicity potential of perfluoroheptanoic acid (PFHpA) to developing zebrafish. PFHpA was not acutely toxic to fish up to 50 µM and there was > 96% survival in all treatments. Exposure to 200 µM PFHpA decreased ATP-linked respiration of embryos. There was no evidence for ROS induction in 7-day-old larvae fish exposed to 0.1 µM or 1 µM PFHpA. Twenty-four transcripts related to mitochondrial complexes I through V were measured and atp06, cox4i1, and cyc1 levels were decreased in larval zebrafish in a concentration-dependent manner by PFHpA exposure. Locomotor activity was reduced in fish exposed to 0.1 µM PFHpA based on a visual motor response test. Anxiolytic-type behaviors were not affected by PFHpA. This study contributes to environmental risk assessments for perfluorinated chemicals.

Perfluorotetradecanoic Acid (PFTeDA) Induces Mitochondrial Damage and Oxidative Stress in Zebrafish (Danio rerio) Embryos/Larvae.

Industrial and consumer products, such as pesticides, lubricants, and cosmetics, can contain perfluorinated compounds (PFCs). Although many short-chain PFCs have been linked to physiological and behavioral changes in fish, there are limited data on longer-chain PFCs. The objective of this study was to determine the potential impact of perfluorotetradecanoic acid (PFTeDA) exposure on zebrafish (Danio rerio) during early developmental stages. We measured several endpoints including gene expression, mitochondrial bioenergetics, and locomotor activity in zebrafish. Survival, timing of hatching, and deformity frequency were unaffected by PFTeDA at the concentrations tested (0.01, 0.1, 1, and 10 µM) over a 7-day exposure period. The expression levels of mitochondrial-related genes (cox1 and mt-nd3) and oxidative stress-related genes (cat, hsp70, and hsp90a) were increased in larval fish with exposure to 10 µM PFTeDA; however, there was no change in oxidative respiration of embryos (i.e., basal respiration and oligomycin-induced ATP-linked respiration). Reactive oxygen species were reduced in larvae treated with 10 µM PFTeDA, coinciding with the increased transcription of antioxidant defense genes. Both the visual motor response test and light-dark preference test were conducted on 7 dpf larvae and yielded no significant findings. This study improves current knowledge regarding toxicity mechanisms for longer-chain PFCs such as PFTeDA.