The organochlorine pesticide toxaphene reduces non-mitochondrial respiration and induces heat shock protein 70 expression in early-staged zebrafish (Danio rerio).

Toxaphene is a restricted-use pesticide produced by reacting chlorine gas with camphene. It was heavily used as a pesticide for agricultural purposes in the 1960-1970s, but despite being banned >30 years ago, it can remain elevated in the soil due to its resistance to metabolic degradation; this has led to longstanding concerns about elevated levels of toxaphene and other organochlorine pesticides (OCPs) in the environment. The objectives of this study were to determine the effects of waterborne exposure to toxaphene on early life stages of zebrafish. Based on the LC₅₀, zebrafish embryos were exposed to control (embryo rearing media or DMSO) or to one dose of toxaphene ranging between 0.011 and 111.1 μg/mL from 6 h post fertilization (hpf) up to 120 hpf. Significant mortality and hatch time delays were observed in embryos exposed to toxaphene (ranging 0.11 and 1.11 μg/mL, depending on the assay). Higher prevalence of deformities was noted at higher doses (≥0.011 μg/mL), and these included pericardial edema and skeletal deformities. As energy production is important for normal development, mitochondrial bioenergetics were assessed in embryos following toxaphene exposure. Embryos exposed to 11.1 or 111 μg/mL toxaphene for 24 h showed lower non-mitochondrial respiration (~30%) compared to both solvent and no treatment controls. Expression of transcripts related to oxidative damage responses and apoptosis were measured and heat shock protein 70 was significantly increased with 111 μg/mL toxaphene (14.5 fold), while the expression levels of caspase 3, caspase 9, and superoxide dismutase 1 were not changed. These data demonstrate that developmental deformities induced by toxaphene include pericardial edema and skeletal deformity, and that toxaphene can affect oxidative phosphorylation in early staged zebrafish.