Scoliosis in fish is caused by several diverse agents that possibly act on the central nervous system, neuromuscular junctions, or ionic metabolism. The organochlorine pesticide Kepone induces scoliosis in the sheepshead minnow. Some effects associated with Kepone-induced scoliosis in these fish are disruption of myotomal patterns, inter- and intramuscular hemorrhage, fractured centra of vertebrae, and death. The histological syndrome of Kepone poisoning in fish and the clinical syndrome in humans suggest that the nervous system is a primary target for Kepone and that scoliosis is a secondary effect of Kepone poisoning in fish.
American oysters Crassostrea virginica exposed to high concentrations (600 mg I-') of nnitrosodiethylamine (DENA) during winter (February to May) showed significant enhancement of an epizootic apicomplexan parasite, Perkinsus rnarinus. The parasite reproduced and caused atypical lesions in exposed oysters in water temperatures at its lower range (20°C). The reasons for this enhancement are not clear but may reflect damage to the oysters' nonspecific, cellular defense mechanisms by the DENA without concomitant negative effects on the parasite.
Sheepshead minnows, Cyprinodon variegatus Laeepede, exposed to 5 5 to 31 /xg/1 of the herbicide trifluralin, throughout their first 28 days of life, developed a heretofore undescribed vertebral dysplasia. This dysplasia consisted of semisymmetrical hypertrophy of vertebrae (three to 20 times normal), characterized by foci of osteoblast and fibroblasts actively laying down bone and bone precursors. Effects of the abnormal vertebral development were dorsal vertebral growth into the neural canal, ventral compression of renal ducts, and longitudinal fusion of vertebrae. Fish, exposed for 51 days to 16-6 /ng/1 trifluralin and thereafter depurated for 41 days, showed no increase in vertebral dysplasia during depuration; however, residual spinal column damage was evident. Serum calcium concentrations were elevated in adult fish exposed for 4 days to 16-6 /xg/1 trifluralin. Fluorosis or mimicry of hypervitaminosis A are considered possible mechanisms for the osseous effect, but are not considered to be the only possible causes. The highly predictable nature of this disorder in experimental exposures strengthens the probability that young flsh may serve as experimental models for determining effects of chemicals on early vertebrate ontogeny, particularly in regard to skeletal development.
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