Transcript Slide 1

Chapter 1
An Overview of Chemical
Bioregulation in Vertebrates
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Figure 1-1 Chemical bioregulation. The endocrine system, nervous system, and immune system each
secretes its own bioregulators: hormones, neurocrines, and cytocrines, respectively. However, all of these
systems influence each other, and from a homeostatic viewpoint we can assume they function as one great
bioregulatory system.
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Figure 1-2 Origins of chemical communication. (A) Early cells living in the primordial seas developed
“receptors” (here shown only on the cell membrane) for recognition of water-soluble toxins (blue circles) and
nutrients (red squares) as well as internal “receptors” (not shown) for lipids that could readily pass through the
membrane. Some of these “receptors” transferred these molecules into the cell for metabolism or detoxification.
(B) In addition to accumulating molecules intracellularly, early cells also released special molecules into the
environment that were detected via receptors on other cells and served as a mechanism for cell-to-cell
communication. Various features of these ancient mechanisms for accumulation, detoxification, metabolism, and
chemical communication have persisted in one form or another in all living cells to this day.
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Figure 1-3 Bioregulator organization. Chemical communication involves neurocrines, including
neurotransmitters or neuromodulators (1) and neurohormones (2), as well as hormones (3) and
autocrine/paracrine regulators (4). The liver and kidney serve as major sites for the metabolism and excretion of
bioregulators.
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Figure 1-4 Functional conceptualization of the endocrine system. Input from other endogenous or
exogenous factors can affect every level of regulation. The endocrine (only) glands typically respond to levels of
chemicals in the blood, and, although innervated, their secretion is not directly controlled by the nervous system.
Nonapeptide targets include the kidney and mammary gland as well as reproductive and vascular smooth
muscle. Endocrine glands controlled by tropic hormones from the pituitary include the gonads, thyroid, adrenal
cortex, and liver. Endocrine-only glands include the parathyroids, kidneys, heart, adipose tissue, and others.
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Figure 1-5 Life history of a hormone. A hormone is “born” in an endocrine cell and spends its short life “free” in
the blood or bound to binding proteins. It may be metabolized and/or excreted (“die”) before or after it binds to a
target cell where it causes changes that result in its characteristic effect. In some cases, the hormone is secreted
in an inactive form and must be metabolized to an active form before it can bind to its receptor and produce an
effect.
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Figure 1-6 Cytology of hormone-secreting cells. (A) Microscopic appearance of a steroid-secreting cell.
These adrenocortical cells, from juvenile salmon, secrete the steroid cortisol exhibit mitochondria with tubular
cristae and an abundance of smooth endoplasmic reticulum. (B) A growth-hormonesecreting cell from the coho
salmon (Oncorhynchus kisutch) showing dense secretory granules, well-developed Golgi apparatus, and
mitochondria with plate-like cristae. (Courtesy of Howard A. Bern and Richard Nishioka, University of California,
Berkeley.)
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Figure 1-7 Hormone-secreting cells appear in many formations. (A) Cords of cells secreting growth
hormone (orange) and gonadotropins (blue) in a pituitary gland. (B) Islet of insulinsecreting cells (arrow)
embedded within the darker stained exocrine pancreas. (C) A collection of follicles (consisting of an epithelium
surrounding a fluid-filled lumen) from a thyroid gland showing a thin epithelium and pink colloid (a protein
suspension) filling the lumen of the follicle. (D) Isolated clusters of testosteronesecreting interstitial cells (arrow)
located between seminiferous tubules in a testis.
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Figure 1-8 A homeostatic model. This simple homeostatic mechanism could represent a single cell as well as
an endocrine or neurocrine unit. The mechanism involves the detection of information (I) by a receptor (R) that
converts the information into biologically relevant cues or input (I´) and transmits this to the controller (C). The
controller compares the input to a programmed set point and makes physiological adjustments as needed by
producing output. This output travels by intracellular pathways (intracrines), neural axons (neurocrines), blood
(hormones), or even extracellular fluid (autocrines/paracrines) to effectors (E) that in turn cause a change in the
system that also feeds back via the same or different receptors to alert the controller that a change has occurred.
Because this type of feedback drives the system toward the set point, it is called negative feedback.
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Figure 1-9 A complex neuroendocrine homeostatic system. This mechanism involves the interaction of
neurohormones from the brain (controller), tropic hormones from the pituitary (E 2), and hormones from a variety
of endocrine glands to control more complicated events. Note that multiple receptors, multiple effectors (targets),
and multiple feedback loops may occur.
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Figure 1-10 Intersex gonad from white sucker (Catostomus commersoni). The left panel illustrates the
normal ovary from fish at a reference site above a wastewater treatment plant (WWTP). The middle panel shows
ovarian tissue to the left and spermatogenetic tissue to the right in an intersex gonad of a fish collected
downstream of the discharge from a WWTP. To the right is a section through a normal testis from the reference
site. Intersex fish also produce the female estrogendependent protein vitellogenin. (Courtesy of Alan Vajda,
University of Colorado, Denver.)
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Figure 1-11 Additive effect. The additive effect of a mixture of estrogenic chemicals working through the
estrogen receptor but with very different affinities for the receptor. Each chemical by itself at the dose indicated
has some stimulatory ability but not enough to reach the threshold dose necessary to get an overt effect.
However, when all three are present in a mixture, their effects are additive and an estrogenic effect occurs.
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Figure 1-12 Epigenetic programming. In this example, a general period of DNA demethylation takes place in
the testes when sperm are made followed by remethylation. After fertilization, demethylation allows for
functioning of genes necessary for very early development following fertilization. A later period of methylation and
histone modification is shown. (Adapted with permission from Morgan, H.D. et al., Human and Molecular
Genetics, 14, R47–R58, 2005.)
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