Biology Reference
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to assess the exposure of organisms to contaminants present in their environment (Chapter
2). In addition to inducing MT synthesis or activating cytochrome P450 enzymes, metals,
PCBs, and PAHs can increase oxidative stress by increasing the concentrations of reac-
tive oxygen species naturally present in organisms. Cytotoxicity can occur, including lipid
peroxidation and DNA damage, but the degree of such damage depends on the efficiency
of enzymatic (superoxide dismutase, catalase, glutathione peroxidase, etc.) and nonenzy-
matic defenses. If DNA damage induced by metabolites resulting from contaminant bio-
transformation is not adequately repaired by specialized nuclear enzymes, this can lead
to an erroneous expression of the genome, including the activation of oncogenes, which
constitutes the first step of the transformation of a normal cell in a tumoral cell (Newman
and Clements 2008).
As an indicator of neurotoxicity effects, acetylcholinesterase (AChE) activity has been
initially considered a specific biomarker of exposure to organophosphate and carbamate
pesticides. More recently, however, other groups of chemicals present in the marine envi-
ronment including metals, detergents, hydrocarbons, and also cyanobacterium toxins
have been shown to affect AChE activity (Table 4.1).
This lack of biomarker specificity poses a problem for environmental management.
Although biomarkers are able to reveal the presence of contaminants, and subsequent
changes in the biology of organisms, any lack of specificity in their response reduces the
likelihood of precise targeting of a particular contaminant, thereby affecting management
decisions to reduce contamination and its impacts. To date, only a few biomarkers seem
really specific: δ-amino levulinic acid dehydratase inhibition in blood able to reveal lead
contamination, bile fluorescent compounds for petroleum hydrocarbons (Anderson and
Lee 2006), and imposex in gastropod mollusks in response to TBT contamination (Chapter
9). However, less specific biomarkers are also interesting environmental management tools
as general responses to the degradation of environmental conditions, and they are still
important in assessing the health status of a given medium exposed to chronic or acute
(e.g., oil spill) pollution pressure. Among these biomarkers, stress proteins, which contrib-
ute to cellular protection and are highly conserved throughout evolution from bacteria to
humans, can provide information on a large spectrum of environmental stress (Newman
and Clements 2008). Histological alterations generally result from the integration of bio-
chemical and physiological changes that may be caused by various chemical contaminants
(Newman and Clements 2008). Until now, no immune response specific for a given con-
taminant has been described, but this category of biomarkers is useful in detecting effects
linked to simultaneous exposure to multiple contaminants (Fournier et al. 2005). Lastly,
a variety of nonspecific biomarkers are important because they are involved in growth
and development and contribute to the success of reproduction with possible ecological
consequences on population sustainability and ecosystem functioning when key species
are impacted. To aggregate the benefit of specific, less specific, and general biomarkers, it
is generally recommended to date to use biomarkers in a battery for ecological risk assess-
ment, as recommended, for instance, by Anderson and Lee (2006) and Thain et al. (2008) in
oil spill risk assessment (Chapter 2).
Classically, biomarkers have been classified as biomarkers of exposure, effect, and sus-
ceptibility (Manahan 2003). However, the definitions of these classes vary depending on
different authors (Chapter 2). So, certain ecotoxicologists prefer the terminology proposed
by De Lafontaine et al. (2000), contrasting biomarkers of defense (Chapter 3) and biomark-
ers of damage (Chapters 4-6).
Biomarkers of defense include MTs, phase I, II, and III enzymes evoked above, as well
as antioxidant defenses (Regoli et al. in Amiard-Triquet et al. 2011) and stress proteins
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