3.2 Monitoring of Oxidative Stress in Fish Models
3.2.1 Introduction
In aerobic organisms, the use of molecular oxygen for the metabolism of organic
carbon leads to the generation of reactive oxygen species (ROSs) that refer to oxygen
free radicals and nonradical reactive species. The deleterious effects of ROSs are
prevented by enzymatic or non-enzymatic antioxidant defence mechanisms. However, an excessive generation of ROS can overwhelm the organism’s antioxidant
capacity, thus inducing oxidative stress, protein and DNA damage, lipid peroxidation and cellular ageing. The exposure to environmental pollutants also induces
oxidative stress, through the formation of ROS during xenobiotic metabolism and
especially during the hydroxylation phase catalysed by the cytochrome P-450
monooxygenase system [44, 45]. In addition, antioxidant efficiency can also be
reduced by micropollutants.
3.2.2 Field Applications
A common approach is based on the comparison of oxidative stress levels between
fish populations at clean and polluted sites. Here, our aim was to explore the
influence of pollutant load on the ROS levels and antioxidant capacity of chubs at
an individual level in the Seine River basin. Feral chubs are expected to be exposed
to numerous aquatic pollutants, and it was shown that the muscle pollutant load of
chubs from the Seine River followed this pattern: phthalate diesters > pyrethroid
pesticides > polychlorinated biphenyls (PCBs) > PAHs > organochlorine pesticides > PBDEs [46]. Plasmatic levels of antioxidant efficiency significantly
decreased with increasing levels of phthalate metabolites in chub liver [47]. This
result corroborates a previous study in Carassius auratus that highlighted an inhibitory effect of phthalates on antioxidant enzyme activity and expression [48]. Similarly, a study in humans has pointed out that phthalate monoester metabolites in
urine samples are positively correlated with increased plasmatic markers of oxidative
stress [49]. Hence, the biotransformation of these widespread plasticisers may
reduce the antioxidant efficiency in wild chub from the Seine River. Thiobarbituric
acid reactive substances (TBARS) are good proxies of oxidative damage that are
formed as a byproduct of lipid peroxidation [45]. Our results pointed out a significant
increase of TBARS with increasing PCB burden in chub muscle [47], as experimentally shown in goodeid fish (Girardinichthys viviparous) exposed to sublethal
concentrations of PCBs [50]. Despite bans since 1975 (use in open systems) and
1987 (use in closed systems), PCBs are still of environmental concern, because these
historically persistent organic pollutants bioaccumulate over time in fish [23] and are
biomagnified across aquatic food webs [24].
252
M. Bonnard et al.
3.2.1 Introduction
In aerobic organisms, the use of molecular oxygen for the metabolism of organic
carbon leads to the generation of reactive oxygen species (ROSs) that refer to oxygen
free radicals and nonradical reactive species. The deleterious effects of ROSs are
prevented by enzymatic or non-enzymatic antioxidant defence mechanisms. However, an excessive generation of ROS can overwhelm the organism’s antioxidant
capacity, thus inducing oxidative stress, protein and DNA damage, lipid peroxidation and cellular ageing. The exposure to environmental pollutants also induces
oxidative stress, through the formation of ROS during xenobiotic metabolism and
especially during the hydroxylation phase catalysed by the cytochrome P-450
monooxygenase system [44, 45]. In addition, antioxidant efficiency can also be
reduced by micropollutants.
3.2.2 Field Applications
A common approach is based on the comparison of oxidative stress levels between
fish populations at clean and polluted sites. Here, our aim was to explore the
influence of pollutant load on the ROS levels and antioxidant capacity of chubs at
an individual level in the Seine River basin. Feral chubs are expected to be exposed
to numerous aquatic pollutants, and it was shown that the muscle pollutant load of
chubs from the Seine River followed this pattern: phthalate diesters > pyrethroid
pesticides > polychlorinated biphenyls (PCBs) > PAHs > organochlorine pesticides > PBDEs [46]. Plasmatic levels of antioxidant efficiency significantly
decreased with increasing levels of phthalate metabolites in chub liver [47]. This
result corroborates a previous study in Carassius auratus that highlighted an inhibitory effect of phthalates on antioxidant enzyme activity and expression [48]. Similarly, a study in humans has pointed out that phthalate monoester metabolites in
urine samples are positively correlated with increased plasmatic markers of oxidative
stress [49]. Hence, the biotransformation of these widespread plasticisers may
reduce the antioxidant efficiency in wild chub from the Seine River. Thiobarbituric
acid reactive substances (TBARS) are good proxies of oxidative damage that are
formed as a byproduct of lipid peroxidation [45]. Our results pointed out a significant
increase of TBARS with increasing PCB burden in chub muscle [47], as experimentally shown in goodeid fish (Girardinichthys viviparous) exposed to sublethal
concentrations of PCBs [50]. Despite bans since 1975 (use in open systems) and
1987 (use in closed systems), PCBs are still of environmental concern, because these
historically persistent organic pollutants bioaccumulate over time in fish [23] and are
biomagnified across aquatic food webs [24].
252
M. Bonnard et al.