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detoxification capacity of MTs could be responsible for behavioral impairments in the
presence of excess Cd (Wallace and Estephan 2004 and literature quoted therein). In two
clones of Daphnia magna exposed to cadmium over several generations, MT concentra-
tion had a critical role in coping with chemical stress, leading to significant differences in
survival (Guan and Wang 2006). In the oligochaete worm Tubifex tubifex and the dipteran
Chironomus riparius exposed to Cd, above a MT concentration threshold (14 and 20 nmol
g −1 , respectively), compensatory mechanisms were no longer efficient, and impairments
of reproduction ( T. tubifex ) or growth ( C. riparius ) were observed (Gillis et al. 2002). From a
practical point of view, the saturation of MTs as a defense mechanism poses a problem for
the use of MT as a biomarker since very different levels of exposure can induce identical
responses (Amiard-Triquet and Roméo in Amiard-Triquet et al. 2011).
In algae, phytochelatins (also termed class III MTs) and other intracellular ligands are
produced in response to metal exposure (Perales-Vela et al. 2006). Phytochelatin induction
is highly variable depending on species. Species that produce few phytochelatins could
cope with metal toxicity by relying on biomineralization of metals in polyphosphate bod-
ies (Ballan-Dufrançais et al. 1991; Le Faucheur et al. 2006).
Mechanisms involving increased metal excretion have been reviewed by Mason and
Jenkins (1995). More recently, the role of multixenobiotic resistance (MXR) (see Section
3.3.5) has attracted increasing attention.
3.3.2 Antioxidative Defenses
The pros and cons of using responses to oxidative stress as biomarkers have been recently
reviewed (Regoli et al. in Amiard-Triquet et al. 2011; Abele et al. 2012). Toxic effects of
pollutants such as PAHs, PCBs, metals, or pesticides often depend on their capacity
to increase the cellular levels of reactive oxygen species (ROS). When ROS production
exceeds antioxidant defenses, oxidative stress leading to transient or permanent cellular
effects at the protein, lipid, or DNA levels can occur. The increase or the reduction in
ROS levels induced by pollutants depends on the balance between pro- and antioxidant
systems. Indeed, aerobic organisms have developed antioxidant defense systems that
enable them to cope with endogenous as well as exogenous ROS production. Among
the most widely studied parameters are, on the one hand, activities of enzymes such
as superoxide dismutases (SOD), catalase, glutathione peroxidases (GPx) or glutathione
reductase (GRd), and, on the other hand, LMW antioxidants such as reduced glutathione
(GSH) and vitamins E (α-tocopherol), B (β-carotene), or C (ascorbate). The procedures for
carrying out evaluation of antioxidant defenses have been recently reviewed (Abele et
al. 2012).
In aquatic environments, numerous studies have shown that antioxidant defense sys-
tems represent biomarkers that are able to reveal the early effects of xenobiotics that exert
their toxicity via oxidative stress (Viarengo et al. 2007; Regoli et al. in Amiard-Triquet et al.
2011; Abele et al. 2012). Utilization of molecular biomarkers is widely accepted to be the
most appropriate approach for early diagnostic of chemical pollution. Depending on the
duration and the intensity of the pro-oxidative toxic exposure, antioxidant defense systems
can be induced only during the first phase of the response of organisms to xenobiotics. No
variation at all or a transient response suggests adaptive or compensatory mechanisms in
organisms chronically exposed to pollutants (Regoli and Principato 1995; Fernández et al.
2010).
The dose-dependent increase in GPx activity in gastropod mollusks ( Austocochlea porcata )
exposed to different crude oil concentrations in the laboratory highlighted that these
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