Fitness Parameters and DNA Effects Are Sensitive Indicators of Copper-Induced Toxicity in Daphnia magna
Author(s) -
Franck Atienzar
Publication year - 2001
Publication title -
toxicological sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.352
H-Index - 183
eISSN - 1096-6080
pISSN - 1096-0929
DOI - 10.1093/toxsci/59.2.241
Subject(s) - daphnia magna , fecundity , biology , rapd , population , daphnia , toxicity , zoology , reproduction , toxicology , branchiopoda , cladocera , ecology , chemistry , crustacean , genetic diversity , demography , organic chemistry , sociology
This study compared the effects occurring at molecular and population levels in Daphnia magna exposed to copper concentrations in the range of 15-120 microg/l. The qualitative and quantitative modifications arising in random amplified polymorphic DNA (RAPD) profiles as a measure of DNA effects were compared with a number of key ecological fitness parameters, namely, the age-specific survival, age-specific fecundity, net reproductive rate, and intrinsic rate of population increase. Results suggested that growth, reproduction, and most of the fitness parameters as well as genomic template stability (a qualitative measure reflecting changes in RAPD profiles) were significantly affected at copper concentrations of 90 and 120 microg/l. Among the fitness parameters, the age-specific fecundity and net reproductive rate were the most sensitive parameters of toxicity. Changes in RAPD patterns generally occurred at copper concentrations of 90 and 120 microg/l, but with one primer, changes significantly arose at all copper concentrations. Overall, molecular and population parameters compared well and represented a sensitive means to measure toxicity induced by copper in Daphnia magna. In conclusion, the measurement of parameters at both molecular and population levels is valuable for investigating the specific effects of agents interacting with DNA. Ultimately, this methodology may allow the ecotoxicological examination of the link between molecular alterations and measurable adverse effects at higher levels of biological organization.
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