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require resources, thus generating a cost of tolerance that can have repercussions on other
functions, including life-history and signal traits (Hõrak and Cohen 2010). Germline cells
may be especially vulnerable to oxidative stress with a risk of transgenerational effects on
offspring viability (Metcalfe and Alonso-Alvarez 2010). However, Costantini et al. (2010)
recommend that ecologists should be careful to avoid the oversimplification of pronounc-
ing all ROS as “bad,” since they are also essential components of cell signaling and regu-
lation (i.e., redox messengers). In addition, the exposure of an organism to a low dose of
a chemical agent or environmental stressor that is damaging at higher doses induces an
adaptive beneficial effect on the organism itself, a process termed hormesis (Mattson and
Calabrese 2010 quoted by Costantini et al. 2010), whereas enhancing photoautotrophs' own
protective systems may also improve the nutritional quality of foods for heterotrophic
organisms (Snoeijs et al. 2012). The quality of aquatic primary producers as food for other
organisms can both increase or decrease as a result of increased oxidative stress through
accumulation of antioxidants or through lower growth rates caused by oxidative damage,
respectively (Snoeijs et al. 2012).
Links between genomic changes, either deleterious or adaptive, and population effects
have been documented in Chapters 13 and 14. Measuring genotoxicity in early life stages and
juveniles may be envisaged to link more closely genotoxicity in individuals and population
dynamics. Gametes and larvae emitted by invertebrates into the water column are particularly
at risk from genotoxicity effects of contaminants entering the aquatic environment. The deter-
mining of genotoxic effects on these life stages at realistic environmental doses is crucial from
an ecological perspective. No doubt the development of the “omics” technologies will be use-
ful to investigate mechanisms underlying pollutant toxicity and to provide new tools for the
detection of genomic disturbance and pollution fingerprints. [See special issue of Environmental
Toxicology and Chemistry (Vol. 30, n°2) devoted to Omics and Environmental Science ].
Currently, several assays reviewed in Chapter 13 are efficient tools to detect genotoxic
impacts in species exposed in the field. The micronucleus and Comet assays are recommended
methods for assessing DNA damage in aquatic organisms under the auspices of OSPAR (2011).
Moore et al. demonstrate in Chapter 5 that the lysosomal-vacuolar system is very
strongly linked in a mechanistic manner to higher level physiological processes of pro-
tection, protein and cellular turnover, SfG, and is directly correlated with larval viability.
Developing an expert system for the integration of biomarker responses in mussels into
an animal health index, Dagnino et al. (2007) considered lysosomal membrane stability
to be the most representative biomarker of the development of stress syndrome. The link
with SfG in mussels and other bivalves is of particular interest since provisional values of
health status thresholds have been proposed (OSPAR 2007):
• Animals may be considered healthy if the SFG is greater than +5 J g -1 h -1 .
• Animals may be considered stressed but compensating if the SFG is between +5
and -2 J g −1 h −1 .
• Animals may be considered severely stressed if the SFG is less than -2 J g −1 h −1 .
Similarly, Crowe et al. (2004) were able to link SfG values of mussels from sites on the
west coast of the United Kingdom differentially affected by hydrocarbon contamination
with the diversity of associated macrofaunal communities. Diversity was reduced at sites
with mussels showing low SfG (<10 J g −1 h −1 ), compared with sites where mussels had an
SfG greater than 15 J g −1 h -1 . The possibility of lysosomal biomarker reactions having an
interpretative capacity in terms of ecosystem level effects is still tentative, but recent results
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