Abstract

Purpose: Aluminium is known to have toxic effects on the central nervous system. We wanted to explore the effects of aluminium on cultured ARPE-19 cells, in particular, changes in the morphologic appearance, viability and in the phagocytic activity of these cells. Methods: After addition of different concentrations of aluminium to the cell cultures, cellular morphology was evaluated by photomicrographs; viability was determined by mitochondrial activity measurement and phagocytosis by uptake of europium-labeled FluoSpheres. Results: Pretreatment of the cells with aluminium led to the formation of clots in the cell culture and there was a relative weak dose-dependent decrease in viability. However, phagocytic activity was severely impaired at each concentration with a peak decrease of 92.45% (± 8.21) at 1000 μmol. Conclusions: Exposure to aluminium occurs mainly through contaminated food and beverages. Given that sufficient concentrations accumulate in the RPE, inhibition of the phagocytic activity of RPE cells might represent a novel important side effect of this metal. Although no conclusions can be drawn from in vitro results on the effect in vivo, it seems that caution is recommended with consumption of food with high concentrations of aluminium. The reduced viability of RPE cells, however, is clinically less relevant since the effect was relative weak in vitro.

Highlights

  • Diabetic retinopathy (DR) is a leading cause of visual loss in the working age population with with approximately 93 million people suffering from DR worldwide [1]

  • Anti-TNFα treatment prevents retinal leukostasis in DR In order to investigate whether anti-TNFα treatment prevents retinal leukostasis, the STZ-induced diabetic mice were IVT injected anti-TNFα antibody or PBS weekly

  • Consistence with our previous observations, diabetes caused an increase of adherent leukocyte in the retinal vasculatures

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Summary

Introduction

Diabetic retinopathy (DR) is a leading cause of visual loss in the working age population with with approximately 93 million people suffering from DR worldwide [1]. Diabetic macular edema (DME) and retinal neovascularization (NV), resulting from blood-retinal barrier (BRB) breakdown and hypoxia, are the two major causes of blindness in patients with DR. The common features of inflammation in DR include leukocyte adhesion and infiltration, microglia activation, and cytokines/chemokines expression. Targeting these inflammatory elements represents an attractive therapeutic strategy for the prevention and treatment of DME and proliferative DR (PDR). TNFα protein level is increased in diabetic rats relative to non-diabetic controls [6,7]. In PDR, TNFα protein is presented in the fibrovascular membranes of PDR [8] and increased in the vitreous fluid and plasma of patients with DR [9,10]. TNFα is associated with insulin resistance [14,15] and its polymorphism is associated with type 2 diabetic patients [12,16]

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