DNA damage and health effects in juvenile haddock (Melanogrammus aeglefinus) exposed to PAHs associated with oil-polluted sediment or produced water

Abstract

The research objective was to study the presence of DNA damages in haddock exposed to petrogenic or pyrogenic polyaromatic hydrocarbons (PAHs) from different sources: 1) extracts of oil produced water (PW), dominated by 2-ring PAHs; 2) distillation fractions of crude oil (representing oil-based drilling mud), dominated by 3-ring PAHs; 3) heavy pyrogenic PAHs, mixture of 4/5/6-ring PAHs. The biological effect of the different PAH sources was studied by feeding juvenile haddock with low doses of PAHs (0.3-0.7 mg PAH/kg fish/ day) for two months, followed by a two-months recovery. In addition to the oral exposure, a group of fish was exposed to 12 single compounds of PAHs (4/5/6-ring) via intraperitoneal injection. The main endpoint was the analysis of hepatic and intestinal DNA adducts. In addition, PAH burden in liver, bile metabolites, gene and protein expression of CYP1A, GST activity, lipid peroxidation, skeletal deformities and histopathology of livers were evaluated. Juvenile haddock responded quickly to both intraperitoneal injection and oral exposure of 4/ 5/6-ring PAHs. High levels of DNA adducts were detected in livers three days after the dose of the single compound exposure. Fish had also high levels of DNA adducts in liver after being fed with extracts dominated by 2-ring PAHs (a PW exposure scenario) and 3-ring PAHs (simulating an oil exposure scenario). Elevated levels of DNA adducts were observed in the liver of all exposed groups after the 2 months of recovery. High levels of DNA adduct were found also in the intestines of individuals exposed to oil or heavy PAHs, but not in the PW or control groups. This suggests that the intestinal barrier is very important for detoxification of orally exposures of PAHs.

Substituted Two- to Five-Ring Polycyclic Aromatic Compounds Are Potent Agonists of Atlantic Cod (Gadus morhua) Aryl Hydrocarbon Receptors Ahr1a and Ahr2a

“…Hence, three modes of action have previously been described in teleost species, including Ahr-independent, Ahr-dependent, and Cyp1a metabolism-dependent. ,,, While adverse effects on Atlantic cod have been demonstrated after crude oil and produced water exposure, − limited information exists for this species regarding the toxicity mediated by the individual chemical constituents, such as unsubstituted and substituted PACs. However, it was shown in juvenile Atlantic haddock (Melanogrammus aeglefinus), which is another Gadiform species, that among 12 injected unsubstituted heavy PAHs, including BAP, benz­[ a ]­anthracene, dibenz­[ a , h ,]­anthracene, and CHR, produced high levels of DNA adducts in the liver . Furthermore, it has also been shown that intramuscular injections of NAP, CHR, and their corresponding dihydrodiol metabolites R , R -1,2-DHN and (1 R ,2 R )-1,2-dihydrochrysene-1,2-diol result in the formation of PAH-protein adducts in the Atlantic cod plasma proteome and possibly a triggered immune response .…”

Ontogeny-Specific Skeletal Deformities in Atlantic Haddock Caused by Larval Oil Exposure

“…The authors suggested that vertebral bone mineralization could be used as an early stress indicator of PAH pollution in sea bass. Vertebral malformation was also observed in juvenile haddock after a 2-month dietary exposure to produced water, oil, and heavy PAHs (Meier et al, 2020).…”

Benzo[a]pyrene-Induced Genotoxicity in Rats Is Affected by Co-Exposure to Sudan I by Altering the Expression of Biotransformation Enzymes

“…Furthermore, this adduct was also identified as a major DNA adduct in mouse [ 52 , 53 ] or in human liver cells [ 54 ]. The potential of BaP to generate DNA adducts was also observed in fish [ 55 ]. However, the level of DNA adducts likely differ between species as BaP metabolism differs significantly between species [ 56 ].…”