Physiological and Genetic Responses to Environmental Stress
185
increased antibody responses to a variety of antigens (Nelson and Demas, 1996). It
has been suggested that seasonal changes in immune responsiveness reflect seasonal
changes in the neuroendocrine system, with a regular relationship between neuroendocrine and lymphoid systems (Zapata et al., 1992).
Two studies have also found seasonal patterns of immune responsiveness in sea
turtles. McKinney and Bentley (1985) reported that lymphocyte blastogenic
responses in Chelonia mydas to the mitogens phytohemagglutinin (PHA) and concanavalin A (ConA) varied between individuals but did not correlate with size–age,
season, or temperature; however, responses to the mitogens pokeweed and
lipopolysaccharide (LPS) were measurable only in spring. More recently, Keller
et al. (2002) reported increases in both mitogen-induced lymphocyte proliferation
and overall white blood cell counts during the summer months in loggerhead turtles.
Differences in the seasonal patterns of immunological activity between other turtles
and sea turtles may be due to differences in peak hormone levels, because some
turtles breed immediately upon emerging from winter hibernation (Lee et al., 2002).
Although seasonal changes of the immune system have not been well described
in sea turtles, seasonal cycles in testosterone levels have been well documented
(Owens, 1997). The pattern is similar to other poikilotherms, with testosterone levels
highest in the winter and early spring and decreasing as the mating season progresses
(Wibbels et al., 1990). Because most species have seasonal fluctuations in reproductive activity, seasonal changes in immune function may be mediated by photoperiod
effects on reproductive function and steroidal activity. Reptiles differ from other
groups (mammals) in which laboratory studies show that decreasing photoperiods
enhance immune function, whereas field studies report an increase in lymphatic
tissue size and immune in winter (for a review, see Nelson and Demas, 1996). One
example is the saltwater crocodile hatchling (Crocodylus porosus), in which suboptimal temperatures induced stress and immunosuppression with significant decreases
in total white cell and lymphocyte counts (Turton et al., 1997).
The stress of coping with energetically demanding conditions can also indirectly
cause illness and death by compromising immune function (Nelson and Demas,
1996). Although it has been assumed that low environmental temperatures and other
stressors decrease immunoglobulin production and immune response in sea turtles,
as they do in other reptiles (Zapata et al., 1992), these assumptions have not been
examined. There has been no systematic examination of the relationships between
acute and long-term stress on the immune function in sea turtles.
6.4.3 GENE RESPONSE, MOLECULAR BIOMARKERS, AND THE
MEASUREMENT OF STRESS: POTENTIAL TOOLS FOR THE FUTURE
In addition to short-term stress markers such as corticosterone levels, all organisms
respond to environmental and physiological stress by altering gene expression (at
the transcriptional and/or translational level) for a variety of compounds, including
increasing synthesis of an evolutionarily conserved family of proteins known as the
heat shock or stress proteins (HSPs). The HSP family is elicited by stressors as
diverse as xenobiotics, heavy metals, heat, hypoxia, and osmotic stress.
1123 book.book Page 185 Monday, November 11, 2002 11:11 AM
185
increased antibody responses to a variety of antigens (Nelson and Demas, 1996). It
has been suggested that seasonal changes in immune responsiveness reflect seasonal
changes in the neuroendocrine system, with a regular relationship between neuroendocrine and lymphoid systems (Zapata et al., 1992).
Two studies have also found seasonal patterns of immune responsiveness in sea
turtles. McKinney and Bentley (1985) reported that lymphocyte blastogenic
responses in Chelonia mydas to the mitogens phytohemagglutinin (PHA) and concanavalin A (ConA) varied between individuals but did not correlate with size–age,
season, or temperature; however, responses to the mitogens pokeweed and
lipopolysaccharide (LPS) were measurable only in spring. More recently, Keller
et al. (2002) reported increases in both mitogen-induced lymphocyte proliferation
and overall white blood cell counts during the summer months in loggerhead turtles.
Differences in the seasonal patterns of immunological activity between other turtles
and sea turtles may be due to differences in peak hormone levels, because some
turtles breed immediately upon emerging from winter hibernation (Lee et al., 2002).
Although seasonal changes of the immune system have not been well described
in sea turtles, seasonal cycles in testosterone levels have been well documented
(Owens, 1997). The pattern is similar to other poikilotherms, with testosterone levels
highest in the winter and early spring and decreasing as the mating season progresses
(Wibbels et al., 1990). Because most species have seasonal fluctuations in reproductive activity, seasonal changes in immune function may be mediated by photoperiod
effects on reproductive function and steroidal activity. Reptiles differ from other
groups (mammals) in which laboratory studies show that decreasing photoperiods
enhance immune function, whereas field studies report an increase in lymphatic
tissue size and immune in winter (for a review, see Nelson and Demas, 1996). One
example is the saltwater crocodile hatchling (Crocodylus porosus), in which suboptimal temperatures induced stress and immunosuppression with significant decreases
in total white cell and lymphocyte counts (Turton et al., 1997).
The stress of coping with energetically demanding conditions can also indirectly
cause illness and death by compromising immune function (Nelson and Demas,
1996). Although it has been assumed that low environmental temperatures and other
stressors decrease immunoglobulin production and immune response in sea turtles,
as they do in other reptiles (Zapata et al., 1992), these assumptions have not been
examined. There has been no systematic examination of the relationships between
acute and long-term stress on the immune function in sea turtles.
6.4.3 GENE RESPONSE, MOLECULAR BIOMARKERS, AND THE
MEASUREMENT OF STRESS: POTENTIAL TOOLS FOR THE FUTURE
In addition to short-term stress markers such as corticosterone levels, all organisms
respond to environmental and physiological stress by altering gene expression (at
the transcriptional and/or translational level) for a variety of compounds, including
increasing synthesis of an evolutionarily conserved family of proteins known as the
heat shock or stress proteins (HSPs). The HSP family is elicited by stressors as
diverse as xenobiotics, heavy metals, heat, hypoxia, and osmotic stress.
1123 book.book Page 185 Monday, November 11, 2002 11:11 AM