Biology Reference
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During the growth phase of the eel, water and proteins are progressively
replaced by fat (lipids and lipoproteins; Degani et al., 1986). An European
silver eel of more than 500 g contains on average 30% of fat (Boëtius and
Boëtius, 1980, 1985). In silver eels, up to 80% of available energy is stored
as triglycerides in muscles (Boëtius and Boëtius, 1985; Sheridan, 1988).
Lipids stored during the growth stage are catabolized to provide the
energy necessary for migration, production of gametes and spawning.
Some compounds such as organophosphorus pesticides, that are widely
used in agriculture, can affect lipidogenesis in the eel. Thus, experimental
exposures to diazinon (Ceron et al., 1996), fenitrothion (Sancho et al., 1997)
and thiobencarb (Fernandez-Vega et al., 1999), as well as molinate (Sancho
et al., 2000) inhibit acetylcholinerase activity in different tissues (brain,
muscle, whole eye and plasma) of exposed eels. Eels exposed to endosulfan,
diazinon or fenitrothion have signifi cantly lower liver and muscle glycogen
content, as well as fat contents than before exposure (Gimeno et al., 1995;
Sancho et al., 1997, 1998). By studying the activity and expression level of
several enzymes involved in liver lipolysis and lipogenesis, Pierron et al.
(2007) demonstrated impairment of lipid storage by cadmium in yellow
eels.
Corsi et al. (2005) reported, in the European eels from the Ortebello
lagoon (Italy), presence of polychlorinated biphenyls (PCBs), lindane
and DDTs in muscle tissue and organophosphate insecticides (OP) and
carbamates (CBs) toxicity were also evidenced by reduced cholinesterase
(ChE) activity.
Robinet and Feunteun (2002) hypothesized that cortisol production
resulting from the repeated exposure to chemicals (demonstrated in other
fi sh: Hontela, 1997), likely lead to lipolysis, which adversely affect energy
accumulation in eels. This exaggerated lipolysis would be expected to
delay silvering and related emigration until enough fat is stored by eels.
However, several studies demonstrated that cortisol could stimulate both
silvering and sexual maturation (see Section 2.1.3). Epstein et al. (1971) and
Fontaine (1994) showed that high concentrations of plasma cortisol, lasting
at least 7 days, triggers silvering and an early physiological adaptation to
salinity. In addition, cortisol was shown to trigger gametogenesis (Olivereau,
1966), as well as synthesis and release of LH in vivo and in vitro (Huang et
al., 1999).
As we and other studies demonstrated that androgens are the
major factors controlling eel silvering, future experiments should aim at
investigating the potential impact of antiandrogens on the process of eel
silvering. In mammals, especially human, environmental anti-androgens
have already been shown to affect the reproductive development (Kelce
and Wilson, 1997) and timing of puberty (Den Hond and Schoeters, 2006;
Toppari and Juul, 2010).
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