title: A multilevel approach to predict toxicity in copepod populations: assessment of growth, genetics, and population structure.
abstract: One of the goals of environmental risk assessment (ERA) is to understand effects of toxicant exposure on individual organisms and populations. We hypothesized that toxicant exposure can reduce genetic diversity and alter genotype composition, which may ultimately lead to a reduction in the average fitness of the exposed population. To test this hypothesis, we exposed a copepod, Nitocra psammophila, to a toxic reference compound and assayed resulting alterations in genetic structure, i.e. expected heterozygosity and percent polymorphic loci, as well as other population- and fitness-related measures, i.e. population abundance, demographic structure and juvenile growth. The copepods were exposed to 0.11-1.1 microg of the pentabromo-substituted diphenyl ether (BDE-47) mg(-1) freeze-dried algae for 24 days (i.e. >1 generation). There was no significant decline in total population abundance. However, there were significant alterations in population structure, manifested as diminished proportion of nauplii and increased proportion of copepodites. In addition, individual RNA content in copepodites decreased significantly in exposed individuals, indicating declined growth. Finally, in the exposed populations, heterozygosity was lower and genotype composition was altered compared to the controls. These results therefore confirm the hypothesized reduction in overall genetic variability resulting from toxicant exposure. Multilevel approaches, such as the one used in the present study, may help unravel subtle effects on the population level, thus increasing the predictive capacity of future ERA.
authors.affiliation: Department of Systems Ecology, Stockholm University, SE-10691 Stockholm, Sweden. johanna@ecology.su.se
authors.forename: Johanna
authors.initials: J
authors.lastname: Gardeström
authors.forename: Elena
authors.initials: E
authors.lastname: Gorokhova
authors.forename: Michael
authors.initials: M
authors.lastname: Gilek
authors.forename: Mats
authors.initials: M
authors.lastname: Grahn
authors.forename: Bengt-Erik
authors.initials: BE
authors.lastname: Bengtsson
authors.forename: Magnus
authors.initials: M
authors.lastname: Breitholtz
mesh_terms: D000818:Animals; D033342:Copepoda / Q000187:drug effects* / Q000235:genetics; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D003710:Demography; D004781:Environmental Exposure; D005411:Flame Retardants / Q000633:toxicity*; D015870:Gene Expression / Q000187:drug effects; D014644:Genetic Variation / Q000187:drug effects*; D006128:Growth / Q000187:drug effects; D055768:Halogenated Diphenyl Ethers; D008018:Life Cycle Stages / Q000187:drug effects; D008297:Male; D010647:Phenyl Ethers / Q000633:toxicity*; D011075:Polybrominated Biphenyls / Q000633:toxicity*; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic / Q000187:drug effects; D012313:RNA / Q000032:analysis; D018570:Risk Assessment
chemical_list: D017931:DNA Primers; D005411:Flame Retardants; D055768:Halogenated Diphenyl Ethers; D010647:Phenyl Ethers; D011075:Polybrominated Biphenyls; D012313:RNA; C086401:pentabromodiphenyl ether; D004247:DNA