Physiological and Genetic Responses to Environmental Stress
183
handling or capture in nets and trawls results in increased corticosterone in hatchling
(Morris, 1982), juvenile (Morris, 1982; Wibbels et al., 1987), and adult sea turtles
(Schwantes, 1986). Notably, forced submergence results in decreased corticosterone
in freshwater turtles (Keiver et al., 1992).
In addition, corticosterone release is sensitive to temperature. Jessop et al. (2000)
found that heat stress caused a 16-fold increase in circulating corticosterone in green
sea turtles. In soft-shelled turtles adrenomedullary activity is stimulated by high
temperatures and inhibited by low temperatures (Ray and Maita, 2001; Mahapatra
et al., 1989).
Stress also results in increased blood levels of the catecholamine hormones
epinephrine (EP), norepinephrine (NE), and dopamine, which, on an emergency
basis, facilitate the fight or fight response by enhancing oxygen uptake and transfer,
and the mobilization of energy substrates (Bonga, 1997). For example, forced submergence and acidosis greatly increases NE and EP levels in freshwater turtles
(Wasser and Jackson, 1991). Hyperosmotic conditions deplete NE in soft-shells,
whereas dehydration stress depletes EP but increases NE levels (Mahapatra et al.,
1991). On the other hand, aldosterone and corticosterone levels were not affected
by 4 days of freshwater exposure in Kemp’s ridley turtles (Ortiz et al., 2000).
Although excessive or extended elevation of the stress hormones is immediately
useful, it can have harmful effects by, for example, reallocating energy away from
growth and reproduction, and suppressing immune functions (see Section 6.4.2)
(Bonga, 1997). The experimental evidence for these effects is from species other
than sea turtles, but it is undoubtedly a vertebrate-wide phenomenon. In the male
common carp, prolonged elevation of cortisol levels inhibits testicular development
and impairs the synthesis of the 11 oxygenated androgens (Consten et al., 2001);
disease can also result in higher cortisol levels in fish (Mustafa et al., 2000; Sures
et al., 2001).
There is some indirect evidence of such effects in sea turtles. Valverde et al.
(1994) reported that olive ridley females restrained in the shade after nesting did
not show the expected next-day progesterone peak indicative of ovulation, whereas
unrestrained females captured in the water had ovulated (Valverde et al., 1992).
Other work however, indicates that this response may be species-specific; postnesting
loggerhead (Wibbels et al., 1992) and green turtles (Licht et al., 1980) subjected to
severe handling stresses ovulated normally.
Increased levels of stress hormones have a variety of other harmful effects on
turtles, including disturbed blood glucose levels (Keiver et al., 1992), impaired salt
gland function (Reina and Cooper, 2000), and a compromised immune function
(George, 1997).
Reina and Cooper (2000) found that both adrenaline and the cholinergic agonist
methacholine inhibited salt gland activity in hatchling green sea turtles. Because the
majority of salt excretion in sea turtles occurs through salt gland activity (Lutz,
1997), suppression of such activity could have significant effects on osmotic homeostasis in sea turtles, especially for hatchlings, which have an apparent requirement
for seawater intake and concomitant high secretion rates (Bennett et al., 1986;
Marshall and Cooper, 1988). Other potentially lethal ion imbalances may occur, for
example, when salt gland function is inhibited during cold stunning.
1123 book.book Page 183 Monday, November 11, 2002 11:11 AM
183
handling or capture in nets and trawls results in increased corticosterone in hatchling
(Morris, 1982), juvenile (Morris, 1982; Wibbels et al., 1987), and adult sea turtles
(Schwantes, 1986). Notably, forced submergence results in decreased corticosterone
in freshwater turtles (Keiver et al., 1992).
In addition, corticosterone release is sensitive to temperature. Jessop et al. (2000)
found that heat stress caused a 16-fold increase in circulating corticosterone in green
sea turtles. In soft-shelled turtles adrenomedullary activity is stimulated by high
temperatures and inhibited by low temperatures (Ray and Maita, 2001; Mahapatra
et al., 1989).
Stress also results in increased blood levels of the catecholamine hormones
epinephrine (EP), norepinephrine (NE), and dopamine, which, on an emergency
basis, facilitate the fight or fight response by enhancing oxygen uptake and transfer,
and the mobilization of energy substrates (Bonga, 1997). For example, forced submergence and acidosis greatly increases NE and EP levels in freshwater turtles
(Wasser and Jackson, 1991). Hyperosmotic conditions deplete NE in soft-shells,
whereas dehydration stress depletes EP but increases NE levels (Mahapatra et al.,
1991). On the other hand, aldosterone and corticosterone levels were not affected
by 4 days of freshwater exposure in Kemp’s ridley turtles (Ortiz et al., 2000).
Although excessive or extended elevation of the stress hormones is immediately
useful, it can have harmful effects by, for example, reallocating energy away from
growth and reproduction, and suppressing immune functions (see Section 6.4.2)
(Bonga, 1997). The experimental evidence for these effects is from species other
than sea turtles, but it is undoubtedly a vertebrate-wide phenomenon. In the male
common carp, prolonged elevation of cortisol levels inhibits testicular development
and impairs the synthesis of the 11 oxygenated androgens (Consten et al., 2001);
disease can also result in higher cortisol levels in fish (Mustafa et al., 2000; Sures
et al., 2001).
There is some indirect evidence of such effects in sea turtles. Valverde et al.
(1994) reported that olive ridley females restrained in the shade after nesting did
not show the expected next-day progesterone peak indicative of ovulation, whereas
unrestrained females captured in the water had ovulated (Valverde et al., 1992).
Other work however, indicates that this response may be species-specific; postnesting
loggerhead (Wibbels et al., 1992) and green turtles (Licht et al., 1980) subjected to
severe handling stresses ovulated normally.
Increased levels of stress hormones have a variety of other harmful effects on
turtles, including disturbed blood glucose levels (Keiver et al., 1992), impaired salt
gland function (Reina and Cooper, 2000), and a compromised immune function
(George, 1997).
Reina and Cooper (2000) found that both adrenaline and the cholinergic agonist
methacholine inhibited salt gland activity in hatchling green sea turtles. Because the
majority of salt excretion in sea turtles occurs through salt gland activity (Lutz,
1997), suppression of such activity could have significant effects on osmotic homeostasis in sea turtles, especially for hatchlings, which have an apparent requirement
for seawater intake and concomitant high secretion rates (Bennett et al., 1986;
Marshall and Cooper, 1988). Other potentially lethal ion imbalances may occur, for
example, when salt gland function is inhibited during cold stunning.
1123 book.book Page 183 Monday, November 11, 2002 11:11 AM