The cellular energy allocation (CEA) methodology was used to assess the adverse effects of toxic stress on the energy budget of test organisms. This biochemical assay is quantified by determining changes in the available energy reserves, Ea (total carbohydrate, protein, and lipid content) and the energy consumption, Ec (electron transport activity). The CEA methodology was fully explored by using neonates of Daphnia magna exposed for 96 h to six model toxicants (CdCl2, K2Cr2O7, tributyltin chloride, linear alkylbenzene sulfonic acid, sodium pentachlorophenolate, and 2,4-dichlorophenoxyacetic acid). To evaluate the ecological relevance of the CEA parameter, we compared the suborganismal responses with population-level parameters (obtained from 21-d life-table experiments) such as the intrinsic rate of natural increase (rm) and the mean total offspring per female. The observed reductions in CEA values were both the result of a decrease in Ea and an increase in Ec. From all individual CEA components analyzed, the lipid reserve criterion was the most sensitive endpoint studied. Both the CEA-based lowest-observed-adverse-effect concentration (LOAEC) values and the effective concentration of 10% (EC10) values were significantly (p < 0.05) and linearly correlated with the chronic (21-d) LOAEC and EC10 values based on growth, survival, and reproduction. This relationship demonstrates the usefulness of the methodology to predict long-term effects. Furthermore, significant (p < 0.0001) sigmoid relationships between the 96-h CEA value (expressed as percentage relative to the control) and population-level effects were observed.

Typical approaches for analyzing mixture ecotoxicity data only provide a description of the data; they cannot explain observed interactions, nor explain why mixture effects can change in time and differ between endpoints. To improve our understanding of mixture toxicity we need to explore biology-based models. In this paper, we present an integrated approach to deal with the toxic effects of mixtures on growth, reproduction and survival, over the life cycle. Toxicokinetics is addressed with a one-compartment model, accounting for effects of growth. Each component of the mixture has its own toxicokinetics model, but all compounds share the effect of body size on uptake kinetics. The toxicodynamic component of the method is formed by an implementation of dynamic energy budget theory; a set of simple rules for metabolic organization that ensures conservation of mass and energy. Toxicant effects are treated as a disruption of regular metabolic processes such as an increase in maintenance costs. The various metabolic processes interact, which means that mixtures of compounds with certain mechanisms of action have to produce a response surface that deviates from standard models (such as ‘concentration addition’). Only by separating these physiological interactions from the chemical interactions between mixture components can we hope to achieve generality and a better understanding of mixture effects. For example, a biology-based approach allows for educated extrapolations to other mixtures, other species, and other exposure situations. We illustrate our method with the interpretation of partial life-cycle data for two polycyclic aromatic hydrocarbons in Daphnia magna.Electronic supplementary materialThe online version of this article (doi:10.1007/s10646-009-0417-z) contains supplementary material, which is available to authorized users.

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