A Crab Is Not a Fish: Unique Aspects of the Crustacean Endocrine System and Considerations for Endocrine Toxicology

Abstract

Crustaceans-and arthropods in general-exhibit many unique aspects to their physiology. These include the requirement to moult (ecdysis) in order to grow and reproduce, the ability to change color, and multiple strategies for sexual differentiation. Accordingly, the endocrine regulation of these processes involves hormones, receptors, and enzymes that differ from those utilized by vertebrates and other non-arthropod invertebrates. As a result, environmental chemicals known to disrupt endocrine processes in vertebrates are often not endocrine disruptors in crustaceans; while, chemicals that disrupt endocrine processes in crustaceans are often not endocrine disruptors in vertebrates. In this review, we present an overview of the evolution of the endocrine system of crustaceans, highlight endocrine endpoints known to be a target of disruption by chemicals, and identify other components of endocrine signaling that may prove to be targets of disruption. This review highlights that crustaceans need to be evaluated for endocrine disruption with consideration of their unique endocrine system and not with consideration of the endocrine system of vertebrates.

Keywords: color change; ecdysteroid signaling; endocrine disruption; neuroendocrine disruption; sexual differentiation.

Figure 1

Endocrine control of moulting in decapod crustaceans (Malacostraca). (A) Organs directly involved in the control of moulting (release of CCAP and bursicon by the central nervous system and/or the pericardial organ as well as release of CHH by paraneurons of the fore- and hindgut not shown): MIH and CHH from the X-organ/sinus gland-complex negatively inhibit the synthesis of ecdysone by the moulting gland (Y-organ); MOIH (and in some species CHH) negatively inhibit the synthesis of MF, the stimulatory activity for ecdysteroid synthesis has been reported in several studies; ecdysteroids of the major forms 20E and PoA stimulate the epidermis via its corresponding EcR to decalcify and to lyse the membrane layer and the old cuticle by proteases, chitinase and chitobiase, and to synthesize material for the new cuticle. (B) Dynamic hemolymph titres of (neuro-)hormones involved in the control and/or physiological processes during moulting and ecdysis over an entire moult cycle. (C) Moult stages and main modifications of exoskeleton and growth (non-proportional presentation with respect to duration of each period). Abbreviations: CCAP, crustacean cardioactive peptide; CHH, crustacean hyperglycemic hormone; EcR, ecdysteroid receptor; MF, methyl farnesoate; MIH, moult-inhibiting hormone; MOIH, mandibular organ-inhibiting hormone; 20E, 20-hydroxyecdysone; PoA, ponasterone (A) ¹ (70); ² (71); ³ (72); ⁴ (73); ⁵ (74); ⁶ (75); ⁷ (76); ⁸ (77); ⁹ (78); ¹⁰ (79).