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Abstract
Retinitis pigmentosa (RP) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that primarily affect photoreceptors, resulting in the complete disorganization and remodeling of the retina. Progression of the disease is enhanced by increased oxidative stress in the retina, aqueous humor, plasma, and liver of RP animal models and patients. Melatonin has beneficial effects against age-related macular degeneration, glaucoma, and diabetic retinopathy, in which oxidative stress plays a key role. In the present study, we used the P23HxLE rat as an animal model of RP. Melatonin treatment (10 mg/kg b.w. daily in drinking water for 6 months) improved the parameters of visual function and decreased the rate of desynchronization of the circadian rhythm, both in P23HxLE and wild-type rats. Melatonin reduced oxidative stress and increased antioxidant defenses in P23HxLE animals. In wild-type animals, melatonin did not modify any of the oxidative stress markers analyzed and reduced the levels of total antioxidant defenses. Treatment with melatonin improved visual function, circadian synchronization, and hepatic oxidative stress in P23HxLE rats, an RP model, and had beneficial effects against age-related visual damage in wild-type rats.
Highlights
Retinitis pigmentosa (RP, MIM #268000) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that affects the photoreceptors and other retinal layers, resulting in the complete disorganization and remodeling of the retina [1]
P23HxLE rats wild-type rats, which is consistent with the loss of photoreceptors, a typical feature of wild-type rats, which is consistent with the loss of photoreceptors, a typical feature of RP
Melatonin treatment provided no benefit to P23HxLE rats or SDxLE
Summary
Retinitis pigmentosa (RP, MIM #268000) is a group of inherited neurodegenerative diseases characterized by a progressive loss of visual function that affects the photoreceptors and other retinal layers, resulting in the complete disorganization and remodeling of the retina [1]. Regardless of the primary cause, progression of the disease is enhanced by increased oxidative stress that occurs in the retina, inducing inflammation and apoptosis, and damaging macromolecules such as DNA, proteins, and lipids [2]. Antioxidants 2021, 10, 1853 models and patients [3]. The retina is affected; the hepatic oxidative status is affected by free radicals in the P23H rat model of RP [4]
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