Molecular and Histocytological Biomarkers - Ecological Biomarkers: Indicators of Ecotoxicological Effects - page 76

The main biomarkers of damage are molecular biomarkers (cortisol, markers of oxi-
dative stress and lipid peroxidation, neurotransmitters, particularly acetylcholinester-
ase (AChE), vitamins such as retinol), biomarkers of genotoxicity (notably DNA adducts,
micronucleus, and comet assays), subcellular and cellular biomarkers (lysosomal stabil-
ity, immunotoxicological responses), cytological alterations, notably carcinogenesis, and
physiological responses (metabolism impairments, imposex, survival of aquatic animals
in air, etc.).
In this chapter, we will not review all of these biomarkers of damage because some of
them are the subject of a particular chapter in this topic, but will concentrate speciically
on certain molecular and histocytological biomarkers of damage.
4.2 Molecular Biomarkers
4.2.1 Cortisol
The question of endocrine disruption is well developed in Chapters 8 and 9. In this chap-
ter, we consider only investigations devoted to cortisol, a biomarker of damage frequently
used in ecotoxicological monitoring.
Cortisol is a corticosteroid hormone synthesized in fish by interrenal tissue in response
to a stimulation by ACTH (adrenocorticotropic hormone). In fish, the induction of plasma
cortisol has been observed in response to general stress (handling, capture) or after expo-
sure to acute chemical stress (Hontela 2000 and literature cited therein). In immature
female rainbow trout ( Oncorhynchus mykiss ) intraperitoneally injected with vegetable oil
containing polycyclic aromatic hydrocarbons (PAHs) (β-NF or BaP at 10 mg kg -1 ), Tintos et
al. (2008) observed increased levels of plasma cortisol, and this response was accompanied
by metabolic changes (increased glucose and lactate levels in plasma, increased glycoge-
nolysis and gluconeogenesis in liver with both PAHs, stimulated amino acid catabolism in
liver of β-NF-treated individuals).
On the other hand, several studies provide contradictory conclusions. In juvenile
Atlantic salmon Salmo salar exposed just before the parr-smolt transformation to 1 or 10 μg
PCBs L −1 (PCB mixture Aroclor 1254), plasma cortisol was reduced by 58% in response to
exposure to either concentration. In addition, plasma triiodothyronine was reduced by
35-50%, and fish treated with the higher dose of A1254 also exhibited a 50% decrease in
gill Na + ,K + -ATPase activity and a 10% decrease in plasma chloride levels in freshwater.
Exposure to A1254 in the freshwater environment can inhibit preparatory adaptations that
occur during smolting, thereby reducing marine survival and sustainability of salmon
populations (Lerner et al. 2007). In another fish, the brown bullhead Ameiurus nebulosus ,
exposed to the polychlorobiphenyl (PCB) mixture, Aroclor 1248 (via intraperitoneal injec-
tion), cortisol was significantly lower in concentration as was the thyroid hormone, T3
(Iwanowicz et al. 2009). In rainbow trout exposed to dietary Aroclor 1254 (10 mg kg −1 body
mass/day) for 3 days, PCB exposure did not modify the acute stressor-induced plasma
cortisol, glucose, and lactate responses (Wiseman and Vijayan 2011). A field study in Ria
de Aveiro (Portugal) has shown that the fish Liza aurata at PAH-contaminated (Vagos) and
mercury-contaminated (Laranjo) sites displayed low cortisol and high glucose as well as
high lactate levels, but no clear relation was found between stress and thyroidal responses
(Oliveira et al. 2011).