Origin of Energy Metabolism Impairments - Ecological Biomarkers: Indicators of Ecotoxicological Effects - page 285

We also discuss in Chapter 10 that certain contaminants provoke hyperactivity of organ-
isms. This may be another cause of the impairment of energy metabolism as clearly shown
in larvae of the red drum ( Sciaenops ocellatus ) exposed to environmentally realistic doses
of atrazine (Alvarez and Fuiman 2005). Despite high food rations, a decrease in growth
rate paralleled behavioral changes, suggesting impairment of prey capture, ingestion, or
protein metabolism. It appears possible that increased metabolic rates cannot be counter-
balanced by a greater probability of encountering prey, expected from increased activity.
In juvenile brook trout ( Salvelinus fontinalis ), exposed for 30 days to 5 μg Cd L -1 , activity was
enhanced, clearly inducing a risk of cost to energy metabolism. Even a concentration 10
times lower (0.5 μg L -1 ) was sufficient to provoke a decrease in prey capture rate and a sub-
sequent decrease in energy uptake provided by food uptake. This may be compared to the
threshold (0.2 μg Cd L -1 ) considered relevant for the protection of aquatic life by Canadian
authorities. Conversely, the foraging activity of longnose dace ( Rhinichthys cataractae ) was
not affected by Cd, possibly as a result of species-specific relative Cd insensitivity (Riddell
et al. 2005).
Weis et al. (2011) have examined the causes and consequences of behavioral disturbances
in estuarine organisms, chronically exposed to contamination in the field (Table 10.2). As a
consequence of feeding impairments, the diet of contaminated fish species and blue crabs
Callinectes sapidus was impoverished compared to their noncontaminated conspecifics.
This poor diet can account in part for the reduced size observed in contaminated fish.
11.4 Responses of Digestive Enzyme Activities to Chemical Stressors
Absorption of chemical contaminants by aquatic animals may follow two main routes—a
direct aqueous route (by cutaneous and/or gill absorption) and an indirect dietary route
(by ingestion followed by digestive absorption), the relative importance of these two
routes depending on the biology of the organisms and the bioavailability of the contam-
inants to either route (Björk 1995; Wang and Fisher 1999; Rainbow 2002). According to
exposure route and the subsequent fate of pollutants within the organism (absorption,
distribution, metabolization/detoxification, accumulation, or elimination—all of which
are species- and pollutant-specific), a toxic effect is more or less likely to occur on digestive
enzyme activities. However, to date, there are very few studies that deal with the effects
of chemical stressors on the digestive capacity of aquatic organisms and, in the specific
case of invertebrates, they are almost exclusively concerned with exposure to trace metals
(Table 11.1).
The activities of digestive enzymes depend on different parameters (intrinsic hydrolytic
properties, rates of synthesis, rates of secretion for enzymes for extracellular activity) (Yan
et al. 1996) on which a pollutant is likely to have an effect by interacting directly or indi-
rectly with the protein. Metal ions are able to interact with enzymes by replacing (other)
essential metals present in the active site (e.g., Ca 2+ ) or by combining with hydroxyl or sulf-
hydryl groups carried by the proteins (Li et al. 2008). This may result in modification of the
three-dimensional conformation of the enzyme, eventually leading to an improvement in
its lytic properties (induced activity) or, more generally, to an impairment in its properties
(repressed activity).
This type of direct interaction between enzymes and trace metals has been high-
lighted in invertebrate species during in vitro exposures carried out on extracts of isolated