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Abstract

UVR exposure is known to cause developmental defects in a variety of organisms including aquatic species but little is known about the underlying molecular mechanisms. In this work we used zebrafish (Danio rerio) embryos as a model system to characterize the UVR effects on fish species. Larval viability was measured for embryos exposed to several UVR spectral treatments by using a solar simulator lamp and an array of UV cutoff filters under controlled conditions in the laboratory. Survival rate and occurrence of development abnormalities, mainly caudal (posterior) notochord bending/torsion, were seriously affected in UV-exposed larvae reaching values of 53% and 72%, respectively, compared with non–UV-exposed larvae after 6 days postfertilization (dpf). In order to elucidate the molecular mechanisms involved, a matricellular glycoprotein named osteonectin and the expression of a DNA-repair related gene, p53, were studied in relation to UVR exposure. The results indicate that osteonectin and p53 expression were increased under UVR exposure due to wavelengths shorter than 335 nm (i.e. mainly UVB) and 350 nm (i.e. short UVA and UVB), respectively. Furthermore, parallel experiments with microinjections of osteonectin-capped RNA showed that malformations induced by osteonectin overexpression were similar to those observed after a UVR exposure. Consequently this study shows a potential role of osteonectin in morphological deformities induced by solar UV radiation in zebrafish embryos.