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Using energy budgets to combine ecology and toxicology in a mammalian sentinel species

View Article: PubMed Central - PubMed

ABSTRACT

Process-driven modelling approaches can resolve many of the shortcomings of traditional descriptive and non-mechanistic toxicology. We developed a simple dynamic energy budget (DEB) model for the mink (Mustela vison), a sentinel species in mammalian toxicology, which coupled animal physiology, ecology and toxicology, in order to mechanistically investigate the accumulation and adverse effects of lifelong dietary exposure to persistent environmental toxicants, most notably polychlorinated biphenyls (PCBs). Our novel mammalian DEB model accurately predicted, based on energy allocations to the interconnected metabolic processes of growth, development, maintenance and reproduction, lifelong patterns in mink growth, reproductive performance and dietary accumulation of PCBs as reported in the literature. Our model results were consistent with empirical data from captive and free-ranging studies in mink and other wildlife and suggest that PCB exposure can have significant population-level impacts resulting from targeted effects on fetal toxicity, kit mortality and growth and development. Our approach provides a simple and cross-species framework to explore the mechanistic interactions of physiological processes and ecotoxicology, thus allowing for a deeper understanding and interpretation of stressor-induced adverse effects at all levels of biological organization.

No MeSH data available.


Related in: MedlinePlus

Fit of various physiological modes of action applied to the mink DEB model for growth in captive mink fed increasing doses of a PCB contaminated diet.Lines represent model fits for the different exposure groups: control (black), 0.25 μg PCB/g ww feed (red), 0.50 μg PCB/g ww feed (blue), 1.0 μg PCB/g ww feed (green). Growth was monitored only to day 4227.
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f3: Fit of various physiological modes of action applied to the mink DEB model for growth in captive mink fed increasing doses of a PCB contaminated diet.Lines represent model fits for the different exposure groups: control (black), 0.25 μg PCB/g ww feed (red), 0.50 μg PCB/g ww feed (blue), 1.0 μg PCB/g ww feed (green). Growth was monitored only to day 4227.

Mentions: The effects of the four exposure doses on the body size and reproduction rate of mink as modelled by stress on different pMoA are displayed in Figs 3 and 4, respectively. The model was fitted to the observed data by estimating the tolerance parameter (CT, CTh) and the no-effect concentration (NEC) (Table 2). While decreased feeding/assimilation as well as increased somatic maintenance costs captured PCB-induced growth retardation for the first 42 days of the mink lifetime, these pMoA resulted in long lasting and severe/fatal effects on growth and adult body weight that were not observed in the data. Though effects on early growth are documented in many studies232627, little evidence exists to suggest these continue so drastically into adulthood as predicted in the models for these pMoA. Furthermore, due to the interactions inherent in the model, the severe reductions in body size caused drastic reductions in reproduction rates that were not seen in the observed data (Fig. 4). These patterns therefore suggest two possible scenarios. First, assimilation and somatic maintenance are likely not the target pMoA for PCBs in mink. The alternate explanation is increased sensitivity in kits and/or developed tolerance in adults such that PCB effects are transient and occur only in young animals for these pMoA. Indeed, parental and developmental tolerance to toxicant effects is a confirmed phenomenon3031. Under this hypothesis, the suppressive effect on body size would cease in juveniles and adults would ultimately recover and reach ‘normal’ body size prior to first reproduction. Deciphering between scenarios would require more weight measurements for exposed mink throughout their lifetime.


Using energy budgets to combine ecology and toxicology in a mammalian sentinel species
Fit of various physiological modes of action applied to the mink DEB model for growth in captive mink fed increasing doses of a PCB contaminated diet.Lines represent model fits for the different exposure groups: control (black), 0.25 μg PCB/g ww feed (red), 0.50 μg PCB/g ww feed (blue), 1.0 μg PCB/g ww feed (green). Growth was monitored only to day 4227.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5384198&req=5

f3: Fit of various physiological modes of action applied to the mink DEB model for growth in captive mink fed increasing doses of a PCB contaminated diet.Lines represent model fits for the different exposure groups: control (black), 0.25 μg PCB/g ww feed (red), 0.50 μg PCB/g ww feed (blue), 1.0 μg PCB/g ww feed (green). Growth was monitored only to day 4227.
Mentions: The effects of the four exposure doses on the body size and reproduction rate of mink as modelled by stress on different pMoA are displayed in Figs 3 and 4, respectively. The model was fitted to the observed data by estimating the tolerance parameter (CT, CTh) and the no-effect concentration (NEC) (Table 2). While decreased feeding/assimilation as well as increased somatic maintenance costs captured PCB-induced growth retardation for the first 42 days of the mink lifetime, these pMoA resulted in long lasting and severe/fatal effects on growth and adult body weight that were not observed in the data. Though effects on early growth are documented in many studies232627, little evidence exists to suggest these continue so drastically into adulthood as predicted in the models for these pMoA. Furthermore, due to the interactions inherent in the model, the severe reductions in body size caused drastic reductions in reproduction rates that were not seen in the observed data (Fig. 4). These patterns therefore suggest two possible scenarios. First, assimilation and somatic maintenance are likely not the target pMoA for PCBs in mink. The alternate explanation is increased sensitivity in kits and/or developed tolerance in adults such that PCB effects are transient and occur only in young animals for these pMoA. Indeed, parental and developmental tolerance to toxicant effects is a confirmed phenomenon3031. Under this hypothesis, the suppressive effect on body size would cease in juveniles and adults would ultimately recover and reach ‘normal’ body size prior to first reproduction. Deciphering between scenarios would require more weight measurements for exposed mink throughout their lifetime.

View Article: PubMed Central - PubMed

ABSTRACT

Process-driven modelling approaches can resolve many of the shortcomings of traditional descriptive and non-mechanistic toxicology. We developed a simple dynamic energy budget (DEB) model for the mink (Mustela vison), a sentinel species in mammalian toxicology, which coupled animal physiology, ecology and toxicology, in order to mechanistically investigate the accumulation and adverse effects of lifelong dietary exposure to persistent environmental toxicants, most notably polychlorinated biphenyls (PCBs). Our novel mammalian DEB model accurately predicted, based on energy allocations to the interconnected metabolic processes of growth, development, maintenance and reproduction, lifelong patterns in mink growth, reproductive performance and dietary accumulation of PCBs as reported in the literature. Our model results were consistent with empirical data from captive and free-ranging studies in mink and other wildlife and suggest that PCB exposure can have significant population-level impacts resulting from targeted effects on fetal toxicity, kit mortality and growth and development. Our approach provides a simple and cross-species framework to explore the mechanistic interactions of physiological processes and ecotoxicology, thus allowing for a deeper understanding and interpretation of stressor-induced adverse effects at all levels of biological organization.

No MeSH data available.


Related in: MedlinePlus