Bile benzo[a]pyrene concentration and hepatic CYP1A induction in hypoxic adult tilapia (Oreochromis niloticus).

Aquatic hypoxia is a seasonal condition in some coastal and continental wetlands where co-exposure with polycyclic aromatic hydrocarbons (PAHs) pollution may be detrimental to the biota. In the present study, adult tilapia, an euryoxic fish of high economic importance, were intraperitoneally injected with benzo[a]pyrene (BaP) (20 mg kg(-1)) and then exposed to graded hypoxia to assess combined effects on some detoxification and fitness parameters. Seventy-two hours after a stepped decrease in dissolved oxygen (<2 mg L(-1)), BaP treatment resulted in a significant diminution on the biliary BaP concentration (70% of normoxic group) and an increase in blood glucose levels (2.17-fold compared with normoxic group). These effects returned to control values in the following 48 h of hypoxia exposure. BaP-induced CYP1A mRNA levels were unaffected by hypoxia, suggesting that reduced bile BaP concentration may be related with effects on protein amount or enzyme activities. LDH mRNA levels, blood lactate and hematocrit remained without change, suggesting no extreme detrimental effects for tilapia in the short-term of the BaP-hypoxia challenge. Our results indicate that BaP treatment and hypoxia targeted glucose metabolism and biliary BaP elimination, probably by favoring the storage of BaP in tilapia tissues.

Benzo(a)pyrene induces hepatic AKR1A1 mRNA expression in tilapia fish (Oreochromis niloticus).

AKR1A1 or aldehyde reductase is a member of the aldo-keto reductases superfamily that is evolutionarily conserved among species. AKR1A1 is one of the five AKRs (AKR1A1 and 1C1-1C4) implicated in the metabolic benzo(a)pyrene (BaP) activation to reactive BaP 7,8-dione. BaP is a polycyclic aromatic hydrocarbon (PAH) widely distributed in aquatic ecosystems and its metabolic activation is necessary to produce its toxic effects. Although the presence of AKR1A1 in fish has been reported, its tissue distribution in tilapia (Oreochromis niloticus) and AKR1A1 inducibility by BaP are not known yet. Moreover, cytochrome P4501A (CYP1A) mRNA expression in fish has been used as a PAH biomarker of effect. Therefore, BaP effects on AKR1A1 and CYP1A gene expressions in tilapia, a species of commercial interest, were investigated by real-time RT-PCR. A partial AKR1A1 cDNA was identified, sequenced and compared with AKR1A1 reported sequences in the GenBank DNA database. Constitutive AKR1A1 mRNA expression was detected mainly in liver, similarly to that of CYP1A. BaP exposure resulted in statistically significant AKR1A1 and CYP1A mRNA induction in liver (20- and 120-fold, respectively) at 24 h. On the other hand, ethoxyquin (EQ) was used as control inducer for AKR1A1 mRNA. Interestingly, EQ also induced CYP1A mRNA levels in tilapia liver. Our results suggest that teleost AKR1A1, in addition to CYP1A, are inducible by BaP. The mechanism of AKR1A1 induction by BaP and its role in fish susceptibility to BaP toxic effects remains to be elucidated.