The effect of vitamins A, D, and E on apoptotic pathways in an experimental cataract model generated in chiİck embryos

The potent anti-inflammatory and immunosuppressive properties of glucocorticoids contribute to an increased risk of surprising side effects when used for a prolonged period or at high doses. Epidemiological studies and animal experimental models have demonstrated that posterior subcapsular cataract is one of the most significant ocular complications associated with glucocorticoids. Posterior subcapsular cataracts occur when undifferentiated fiber cells fail to differentiate properly and instead migrate and accumulate at the posterior pole of the lens alongside elongating normal fiber cells. The pathogenesis of posterior subcapsular cataract may involve multiple mechanisms, and recent studies focusing on the genomic effects of glucocorticoid receptors are associated with its pathogenesis. It is believed that apoptotic events occurring during the differentiation and migration of newly produced lens epithelial cells to lens fibers play a role in the pathogenesis of posterior subcapsular cataracts. The aim of this study is to create a steroid-induced cataract model in chick embryos and elucidate the apoptotic effects of hydrocortisone (HC) in cataract pathogenesis. Additionally, we aim to investigate the protective role of vitamins A, D, and E against cataractogenesis in humans by intervening with vitamins A, D, and E in steroid-treated embryos, in terms of their anti-apoptotic potential. In our study, we examined the levels of p53, NF-κB, Bcl-2 proteins, and p53, NF-κB, Bax and Bcl-2 mRNA expression levels in lenses obtained from hydrocortisone-induced chick embryos, which belong to the glucocorticoid class. We also investigated the effects of vitamins A, D, and E treatments on these markers. The application of HC significantly decreased the levels of p53, NF-κB, and Bcl-2 proteins, while all three doses of vitamin A increased the levels of p53, NF-κB, and Bcl-2 proteins, bringing them closer to normal levels. The moderate dose of vitamin D only increased the levels of Bcl-2 protein, while the high dose of vitamin D increased the levels of p53, NF-κB, and Bcl-2 proteins. Both moderate and high doses of vitamin E increased the levels of p53, NF-κB, and Bcl-2 proteins. Although there were no statistically significant changes in mRNA expressions, HC reduced the levels of p53, NF-κB, and Bax/Bcl-2 mRNA, while vitamin A restored the levels of p53, NF-κB, and Bax/Bcl-2 mRNA to normal levels. It was concluded that HC had a negative impact on p53, NF-κB, Bcl-2 levels in lenses and this negative effect could be reduced by vitamins A, D, and E. Keywords: Cataract, Apoptosis, Glucocorticoid, Lens, Vitamin A, Vitamin D, Vitamin E