Transcriptional response in rainbow trout (Oncorhynchus mykiss) B cells and thrombocytes following in vivo exposure to benzo[a]pyrene

- Exposure to BaP caused elevated cyp1a1, 1a2, and 1a3 transcription in B cells.
- Exposure to BaP caused elevated cyp1a1, 1a2, and 1a3 transcription in thrombocytes.
- B cells and thrombocytes showed significantly different CYP transcript profiles.
- Ah receptor was upregulated by BaP only in liver tissue and spleen thrombocytes.
- BaP exposure did not affect p53 expression in any cell type or tissue.

Immune toxicity of polycyclic aromatic hydrocarbons (PAHs) in fishes has been frequently reported but the reasons for differential cell toxicity remains unclear. Rainbow trout were exposed in vivo with a single intraperitoneal injection of corn oil or 100 mg/kg of the immunotoxic PAH benzo[a]pyrene (B[a]P) in corn oil. Leukocytes were harvested from head kidney, spleen and blood after 14 days, the optimal time for B cell depletion found in a previous study. The mRNA expression of five cytochrome P450 (CYP) enzymes, the aryl hydrocarbon receptor (AhR), and an intrinsic pathway apoptosis checkpoint (p53) in B cells and thrombocytes were examined. Transcript levels were measured in immunomagnetically-isolated B cells and thrombocytes from those tissues as well as in liver as B cells had been previously shown to be responsive the BaP whereas thrombocytes were not. There was induction of CYP1A1 in liver, blood B cells, and blood and spleen thrombocytes; CYP1B1 in blood B cells, blood and spleen thrombocytes; CYP1A3 in liver, blood and spleen B cells, and blood thrombocytes; CYP1C1 in liver; and AhR in liver and spleen thrombocytes. There was no change in CYP1C2, or p53 mRNA levels across tissues or cell type. Induction in mRNA was observed 14 d after exposure, indicating a prolonged physiological effect of a single B[a]P injection. CYP1A1 and CYP1A3 were the most abundantly expressed CYP genes and CYP1B1 was generally least abundant. B[a]P-induced thrombocytes had a significantly different pattern of CYP expression than either liver or B cells. Given the importance of metabolites in the toxicity of PAHs, differences in CYP expression between tissues may explain differences in toxicity previously observed between B cells and thrombocytes.