The present study aimed to investigate the effect of serum derived from advanced platelet-rich fibrin on the healing of experimentally induced corneal ulceration in donkeys. Nine apparently healthy adult donkeys of both sexes were used after being proven normal after ophthalmological examination. A 6-mm-diameter centric corneal ulceration was induced chemically by using 1N sodium hydroxide solution.

The donkeys were then randomly allocated into two main groups: control group (A), in which the corneal ulcer was left for the period of the study without application of medicaments, and group (B), in which serum derived from advanced platelet-rich fibrin (s-PRF-drops) was applied to the eye three times/day for 35 days. Evaluation criteria included clinical and external ophthalmic examinations, fluorescein staining, ulcer healing by analysing serial digital photographs, and histopathology. Results revealed no significant changes in the evaluation criteria between treatment and control groups. Corneal ulcer healing was associated with corneal opacity, vascularisation, melanosis, and other complications that likely negate any potential benefit of administration of s-PRF as a treatment for corneal ulcer in donkeys. Histological results of the s-PRF-drops group were similar to the other group in the degree of re-epithelialisation and regularity of the collagen bundles, type, and maturity of the collagen. However, treatment by s-PRF drops

resulted in no epithelial keratinisation and slightly less sub-epithelial stromal inflammatory reaction.

Abstract

Unlike mild DNA damage exposure, DNA damage repair (DDR) is reported to be ineffective in full-grown mammalian oocytes exposed to moderate or severe DNA damage. The underlying mechanisms of this weakened DDR are unknown. Here, we show that moderate DNA damage in full-grown oocytes leads to aneuploidy. Our data reveal that DNA-damaged oocytes have an altered, closed, chromatin state, and suggest that the failure to repair damaged DNA could be due to the inability of DDR proteins to access damaged loci. Our data also demonstrate that, unlike somatic cells, mouse and porcine oocytes fail to activate autophagy in response to DNA double-strand break-inducing treatment, which we suggest may be the cause of the altered chromatin conformation and inefficient DDR. Importantly, autophagy activity is further reduced in maternally aged oocytes (which harbor severe DNA damage), and its induction is correlated with reduced DNA damage in maternally aged oocytes. Our findings provide evidence that reduced autophagy activation contributes to weakened DDR in oocytes, especially in those from aged females, offering new possibilities to improve assisted reproductive therapy in women with compromised oocyte quality.