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Metabolic acidosis induces cataract in neonatal rats

Poster Details

First Author: PolinaBiletska UKRAINE

Co Author(s):    Yuriy Dyomin   Igor Gapunin           

Abstract Details



Purpose:

Cataract is the leading cause of legal blindness in the world. In childhood cataracts may occur as an isolated anomaly, as part of generalized ocular developmental defects (nonsyndromic) or as a component of a multisystem syndrome. Severe metabolic disorders associated with cataract formation. In this study we want to find out does metabolic acidosis induce cataract in experiment. Carboanhydrase inhibitors (Brinzolamide) induce a metabolic acidosis via an alternative biochemical mechanism (bicarbonate loss).Author have no financial interest.

Setting:

: Institute for Problems of Cryobiology and Cryomedicine of the National Academy of Sciences of Ukraine

Methods:

In our study we used newborn Wistar rats raised in four litters. Mothers and litters received standard laboratory diet and water ad libitum. Animals were kept under controlled lighting conditions (12:12-h light/dark). Newborn rats (n=34) were randomized to either intraperitoneal brinzolamide in dose 200 mg/kg (n=18) or saline (n=16), twice daily from days 2 to 7. After 5 days of recovery all rats were examined by biomicroscopy. We performed enucleation to euthanized animals. Each eye was kept immersed for at least 24 h at 4°C in a fixative solution containing 4% paraformaldehyde. Six paraffin-embedded sections (thickness, 5 µm) cut through the optic disc of each eye were prepared in a standard manner and stained with hematoxylin and eosin. Light microscope images were photographed using a digital camera.

Results:

All brinzolamide-injected animals had dense lenticular opacification. Saline-injected rats were negative for cataract formation. Histologically lenses from pups suffering from cataract showed the same extent of opacification. The opaque region was always restricted to the center of the lens. However, a variety of histological abnormalities in different degrees were observed in different portions of the cataractous lenses. The abnormalities observed were: swelling of the lens capsule, proliferation of epithelial cells, vacuolization of the hyaline layer, and disorder or collapse of the lens fibers. All these abnormalities were not always found in one lens.

Conclusions:

acidosis induced by high-dose brinzolamide injection is associated with cataract formation in neonatal rats. This result provides an alternative way of inducing cataract in animals. The animal model of metabolic cataract may be used for further investigations in etiology and prophylactic of this disease. FINANCIAL INTEREST: NONE

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