title: Exposure and time dependent DNA strand breakage in hepatopancreas of green-lipped mussels (Perna viridis) exposed to Aroclor 1254, and mixtures of B[a]P and Aroclor 1254.
abstract: Green-lipped mussels (Perna viridis) were exposed to Aroclor 1254 (0.5, 5 and 50 microgl(-1)) and a mixture of benzo[a]pyrene (B[a]P) and Aroclor 1254 (0.3+0.5 and 3+5 microgl(-1)) for 12 days. On day 0, 1, 3, 6 and 12, the levels of DNA strand breaks in the mussel hepatopancreas were monitored using an alkaline unwinding assay. The results were compared to the findings of a previous study in which the levels of DNA strand breakage in the same species were measured following exposure to various concentrations of B[a]P (0.3, 3 and 30 microgl(-1)). The results indicated that Aroclor 1254 at a concentration </=50 microgl(-1) did not cause any increase in DNA strand breaks while B[a]P at concentrations ranging from 0.3 to 3 microgl(-1) caused an increase in strand breaks after one day of exposure, followed by an apparent rapid recovery. In contrast, exposure to 30 microgl(-1) B[a]P caused no increase in DNA strand breaks over the exposure period. This was postulated to be due to an early elicitation of the DNA repair system by the relatively high exposure level of B[a]P. This hypothesis was tested in the present study, and the results suggest that exposure to the high B[a]P concentration might have elicited the defense mechanism within the mussels, resulting in no observed increase in DNA strand breaks. An increase in strand breaks was, however, evident when the mussels were exposed to lower B[a]P levels. The levels of DNA strand breaks were correlated with the body burden of B[a]P and Aroclor 1254 but no significant relationship was observed, possibly owing to the rapid metabolism of the toxicant and/or an effective DNA repair mechanism. As a result, DNA strand breakage in the hepatopancreas of green-lipped mussels may not be a suitable biomarker of exposure to the above toxicants in the marine environment. Our findings also suggest that it would be instructive to investigate (1) the role of DNA repair enzymes in the exposed mussels; and (2) the correlation between the activity of these enzymes and the body burden of specific toxicants.
authors.affiliation: Centre for Coastal Pollution and Conservation, Department of Biology and Chemistry, City University of Hong Kong, 83 Tat Chee Avenue, Kowloon, Hong Kong.
authors.forename: W H L
authors.initials: WH
authors.lastname: Siu
authors.forename: C L H
authors.initials: CL
authors.lastname: Hung
authors.forename: H L
authors.initials: HL
authors.lastname: Wong
authors.forename: B J
authors.initials: BJ
authors.lastname: Richardson
authors.forename: P K S
authors.initials: PK
authors.lastname: Lam
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001564:Benzo(a)pyrene / Q000633:toxicity*; D049872:Bivalvia / Q000187:drug effects / Q000235:genetics*; D020111:Chlorodiphenyl (54% Chlorine) / Q000633:toxicity*; D002849:Chromatography, Gas; D004249:DNA Damage; D004260:DNA Repair / Q000187:drug effects*; D043143:Hepatopancreas / Q000737:chemistry / Q000187:drug effects*; D013050:Spectrometry, Fluorescence; D013997:Time Factors
chemical_list: D020111:Chlorodiphenyl (54% Chlorine); D001564:Benzo(a)pyrene