Effects of dietary bromadiolone exposure on rainbow trout (Oncorhynchus mykiss) and corresponding hepatic concentrations

Fish are exposed to residues of anticoagulant rodenticides in the environment, likely due to secondary poisoning or direct consumption of fragments of bait. The mode of action in which they affect fish is similar to mammals: inhibition of vitamin K epoxide reductase leads to a vitamin K deficiency, and consequently, to a coagulation disorder. However, distinct species- and compound-specific differences in the sensitivity and toxicity occur and data for the comparison of the effects on fish are still lacking. We exposed ca. 1-year old (body weight ∼180 g) rainbow trout (Oncorhynchus mykiss) in a preliminary 15 day-experiment and ca. 1.5-year old rainbow trout (body weight ∼360 g) in a 30 d-experiment to a single dose of bromadiolone-spiked feed. The onset of overt signs in individual trout took 12-14 d. Prolonged prothrombin time and hemorrhages were observed in some fish exposed to ≥ 10 mg/kg body weight bromadiolone. While at the end of the experiment no effect on vitamin K and undercarboxylated osteocalcin levels occurred, concentration of vitamin K epoxide reductase subunit 1-like 1 was reduced in rainbow trout exposed to ≥ 0.4 mg/kg body weight bromadiolone in the 30 d-experiment (p < 0.001). The experiment showed that high oral doses of bromadiolone can cause coagulopathy in fish, but the acute poisoning scenario tested in our study indicated no severe risk for fish at hepatic bromadiolone concentrations that have been detected to date in wild freshwater fish. However, to assess the risk of bromadiolone, further research is needed to investigate possible effects caused by multiple exposure to bromadiolone and its mixture toxicity in combination with other anticoagulant rodenticides, both of which are more realistic exposure scenarios for fish in the environment.