Endocrine Disruption in Crustaceans
Definition and Modes of Action of EDCs
An endocrine disruptor compound (EDC) is defined as an exogenous substance or mixture that alters function(s) of the endocrine system and consequently causes adverse effects in an intact organism, its progeny, or (sub)populations (Damstra et al., 2002).
Major modes of action include:
Alteration of hormone synthesis during transcription, translation, post-translational modifications, or secretion.
Disruption of hormone distribution, transport in blood or hemolymph, or degradation rate.
Interference with signal transduction in target cells through agonist or antagonist action at hormone receptors.
Modification of cellular proliferation in endocrine or target tissues.
Main Classes of EDCs in Aquatic Environments
Phenol-Derived Compounds: Alkylphenols and bisphenol A (BPA).
Pesticides and PCBs: Endosulfan, DDT and its metabolites, and triazine herbicides such as atrazine.
Flame Retardants: Brominated compounds known to depress thyroid hormone levels.
Pharmaceuticals and Personal Care Products: Non-steroidal anti-inflammatory drugs (NSAIDs such as naproxen and diclofenac), synthetic hormones (17a-ethinylestradiol), and UV-filters.
Organometallic Compounds: Tributyltin (TBT).
Insect Growth Regulators: Juvenoid mimics including pyriproxyfen, fenoxycarb, and methoprene.
Disruptive Effects on Crustacean Physiology
Reproduction and Vitellogenesis:
Pesticides (e.g., chlordecone, glyphosate) and nanoplastics alter gonadal growth, mature oocyte reabsorption, and sperm count/viability.
The use of vitellogenin (Vg) as a direct biomarker for xenoestrogenic activity remains controversial in crustaceans due to the lack of verified functional estrogen receptors.
Methyl Farnesoate Signaling:
Juvenoid mimic insecticides function as agonists of methyl farnesoate (the crustacean juvenile hormone), driving male offspring production in cladocerans like Daphnia magna and causing reproductive delays or failure.
Molting and Somatic Growth:
EDCs disrupt the ecdysteroid signaling pathway by acting on the ecdysteroid receptor (EcR) and retinoid X receptor (RxR) complex, or by inhibiting enzymes like chitobiase.
Compounds such as TBT, heptachlor, endosulfan, bisphenol A, and carbamazepine delay ecdysis, suppress ecdysone peaks, or decrease molting frequency.
Neuroendocrine Control and Metabolism:
Heavy metals (, ) and pharmaceuticals (fluoxetine) alter neurohormonal output from the eyestalk X-organ-sinus gland complex and thoracic ganglion, disrupting crustacean hyperglycemic hormone (CHH) and gonad-inhibiting hormone (GIH) pathways.
