PubMed ID: 8291895
Author(s): Hauptman O, Albert DM, Plowman MC, Hopfer SM, Sunderman FW Jr. Ocular malformations of Xenopus laevis exposed to nickel during embryogenesis. Ann Clin Lab Sci. 1993 Nov-Dec;23(6):397-406. PMID 8291895
Journal: Annals Of Clinical And Laboratory Science, Volume 23, Issue 6, 1993
The pathogenesis of eye anomalies induced by exposure to Ni2+ (as nickel chloride) during embryogenesis was studied in the frog, Xenopus laevis. Eyes of control and Ni(2+)-exposed tadpoles were examined without staining using a dissecting microscope, by light microscopy of histological sections, and by electron microscopy. The ocular abnormalities of Ni(2+)-exposed tadpoles included (a) microphthalmia, (b) hypopigmentation, (c) hernias and cysts of the choroid and retina, and (d) iris coloboma; cataracts were uncommon. The pathogenesis of the ocular lesions appears to involve diffuse or focal dysplasia and loss of the retinal pigment epithelium, with dystrophy of photoreceptor outer segments and protrusion of neuroretina through gaps in the pigment epithelium. This study confirms that Ni2+ is a potent ocular teratogen for Xenopus embryos and points to the retinal pigment epithelium as a primary cellular target for Ni(2+)-induced embryotoxicity.