Effects of exposure to diethyl phthalate, 4-(tert)-octylphenol, and 2,4,5-trichlorobiphenyl on activity of chitobiase in the epidermis and hepatopancreas of the fiddler crab, Uca pugilator.

Seven-day exposure of fiddler crabs, Uca pugilator, to diethyl phthalate at 50.0 mg l-1 significantly inhibited the activity of chitobiase (also known as N-acetyl-beta-glucosaminidase) in the epidermis and hepatopancreas. Epidermal chitobiase activity of crabs exposed to 10.0 mg l-1 4-(tert)-octylphenol for 7 days significantly decreased. PCB29 at 0.5 and 2.0 mg l-1 significantly inhibited chitobiase activity in the epidermis and hepatopancreas of crabs exposed for 3 days. The inhibitory effects rendered by diethyl phthalate and PCB29 can at least partly account for the delayed molting they cause because chitobiase is needed to break down the old exoskeleton of crustaceans prior to ecdysis. Since chitinolytic enzymes are apparently the products of ecdysteroid regulated genes in arthropods, the decline in chitobiase activity after exposure to diethyl phthalate, 4-(tert)-octylphenol, and PCB29 along with the delayed molting they cause strongly suggests that these xenobiotics disturb the Y-organ-ecdysteroid receptor axis. Such disturbance may involve an interaction between ecdysteroid receptors and steroid mimics where the steroid mimics act as antagonists of endogenous steroid molting hormones, and/or arise from the interference with synthesis and excretion of ecdysteroids by these compounds.