Embryonic dysplasia and adult retinal dystrophy in boron-deficient zebrafish

Boron (B) has been identified as a growth stimulator in embryonic trout and shown to be essential for embryogenesis in zebrafish. In the present study we describe adverse health endpoints of boron deficiency during two different stages of the lifecycle in zebrafish. The pathological manifestations of boron deficiency involved membrane alterations at both stages. Deficiency during the embryonic period was seen as dysplasia during the zygote and cleavage periods. In adults deficiency presented as retinal dystrophy. Boron deficient embryos were obtained from zebrafish maintained in water containing <0.2 μM B for six months. The initial stages of embryonic development, the zygote and cleavage periods, were marked by membrane blebbing and extrusion of cytoplasm in deficient, but not boron supplemented embryos (45 μM B). About 5 to 7% of the boron deficient embryos survived to produce offspring. The adult F1 boron deficient zebrafish were photophobic and histological evaluation of their eyes determined that the boron deficient adults had photoreceptor dystrophy. Compared to boron supplemented controls, the photoreceptor cells of the boron deficient adults were shortened due to a reduction in the myoid and outer segment regions. In boron deficient embryos and adults, the pathological changes were observed in cells that produce prodigious quantities of membrane. This outcome suggests that boron is required for the synthesis or processing of membrane or cytoskeletal proteins that function in the maintenance of membrane shape and integrity. J. Trace Elem. Exp. Med. 12:213–219, 1999.