Polycyclic aromatic hydrocarbon and hypoxia exposures result in mitochondrial dysfunction in zebrafish.

Organisms are routinely subjected to a variety of environmental and chemical perturbations simultaneously. Often, multi-stressor exposures result in unpredictable toxicity that occurs through unidentified mechanisms. Here, we focus on polycyclic aromatic hydrocarbons (PAHs) and hypoxia, two environmental and physiological stressors that are known to co-occur in the environment. The aim of this study was to assess whether interactive mitochondrial dysfunction resulted from co-exposures of PAHs and hypoxia. Zebrafish embryos were co-exposed to non-teratogenic concentrations of an environmental PAH mixture and hypoxia beginning at 6 hpf for an acute period of 24 h and afterwards were given either no recovery period, 45 min, 5 -hs, or 18 -hs of recovery time in clean conditions. Mitochondrial function and integrity were assessed through the use of both in ovo and in vitro assays. Hypoxia exposures resulted in drastic reductions in parameters relating to mitochondrial respiration, ATP turnover, and mitochondrial DNA integrity. PAH exposures affected ATP production and content, as well as mitochondrial membrane dynamics and lactate content. While PAH and hypoxia exposures caused a broad range of effects, there appeared to be very little interaction between the two stressors in the co-exposure group. However, because hypoxia significantly altered mitochondrial function, the possibility remains that these effects may limit an individual's ability to respond to PAH toxicity and therefore could cause downstream interactive effects.

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