Abstract

Aging of the retina is accompanied by a sharp increase in the content of lipofuscin granules and bisretinoid A2E in the cells of the retinal pigment epithelium (RPE) of the human eye. It is known that A2E can have a toxic effect on RPE cells. However, the specific mechanisms of the toxic effect of A2E are poorly understood. We investigated the effect of the products of photooxidative destruction of A2E on the modification of bovine serum albumin (BSA) and hemoglobin from bovine erythrocytes. A2E was irradiated with a blue light-emitting diode (LED) source (450 nm) or full visible light (400–700 nm) of a halogen lamp, and the resulting water-soluble products of photooxidative destruction were investigated for the content of carbonyl compounds by mass spectrometry and reaction with thiobarbituric acid. It has been shown that water-soluble products formed during A2E photooxidation and containing carbonyl compounds cause modification of serum albumin and hemoglobin, measured by an increase in fluorescence intensity at 440–455 nm. The antiglycation agent aminoguanidine inhibited the process of modification of proteins. It is assumed that water-soluble carbonyl products formed as a result of A2E photodestruction led to the formation of modified proteins, activation of the inflammation process, and, as a consequence, to the progression of various senile eye pathologies.

Highlights

  • Publisher’s Note: MDPI stays neutralThe retinal pigment epithelium (RPE) is a monolayer of pigment cells in close contact with the neural retina and separated by Bruch’s membrane from the choroid

  • Photooxidation of A2E leads to the formation of various oxygen-containing products, such as, for example, ketones and aldehydes [41,42,44]

  • The data obtained reveal that photooxidation of bisretinoid A2E results in the accumulation of water-soluble destruction products containing reactive aldehydes and ketones

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Summary

Introduction

The retinal pigment epithelium (RPE) is a monolayer of pigment cells in close contact with the neural retina and separated by Bruch’s membrane from the choroid. RPE cells are at high risk of photooxidative stress due to prolonged exposure to light, high oxygen content, and the presence of photosensitizing pigments, including the aged pigment lipofuscin [2,3,4]. Bisretinoid fluorophores are formed from all-trans-retinal as byproducts of the visual cycle. One of these fluorophores, A2E (N-retinylidene-N-retinyl ethanolamine) is most common in RPE lipofuscin [6,7], and its concentration in the cells can reach 20 μM with age [8]. It is important to note that fluorophore A2E accumulates in RPE cells during normal aging

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