Investigating Gamma-H2AX Localisation in DNA Double-Stand Breaks in the Cornea and Retina of a Rat Model in Alloxan-Induced Diabetes
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Keywords: Immunohistochemistry; Double Stranded Breaks; Malondiadehyde; Oxidative stress, Epithelial degeneration; vacuolationAbstract
Diabetes is associated with increased oxidative stress, which can lead to cellular damage in various tissues, including the eyes. This study investigates the impact of alloxan-induced diabetes on DNA double-strand breaks (DSBs) in the cornea and retina of albino rats. Fifteen rats were divided into three groups: a control group, a diabetic group, and a diabetic group treated with glibenclamide. Over a 14-day period, blood glucose levels were monitored, followed by euthanization and tissue analysis. Histopathological examinations revealed significant structural alterations in the corneal and retinal layers, including epithelial degeneration and vacuolation in the retina. Despite these changes and the elevated levels of malondialdehyde (MDA) observed, immunohistochemical staining for γH2AX, a marker of DNA DSBs, showed negative reactivity in the corneal and retinal tissues. These findings suggest that while oxidative stress contributes to histopathological changes in diabetic ocular tissues, DNA double-strand breaks may not be significantly induced in the early stages of diabetes. This study highlights the complexity of oxidative damage in diabetes, where DSBs may not be a primary mechanism in the initial phases of disease progression in the eye.