Brimonidine Can Prevent In Vitro Hydroquinone Damage on Retinal Pigment Epithelium Cells and Retinal Müller Cells

Abstract

HQ-induced toxicity is mediated through mitochondrial damaging, oxidative stress-related and necrosis-related pathways; Brimonidine significantly prevented the mitochondrial damaging and oxidative stress-related effects but had little effect on blocking the necrosis component of HQ-toxicity. Brimonidine protective effects differ between the different retinal cell types and high concentrations of Brimonidine (10×) have minimal damaging effects on human retinal cells.

Resveratrol Protects Against Hydroquinone-Induced Oxidative Threat in Retinal Pigment Epithelial Cells

“…Mitochondrial function is critical to cell survival, and HQ is known to target this organelle in RPE cells specifically through decreases in membrane potential. 26,27 Our work confirmed that HQ can virtually eliminate RPE mitochondrial respiration. To our knowledge, we are the first to demonstrate the specific effects of HQ on primary human RPE cells with the XFe24 Flux Analyzer.…”

Protective Effects of Memantine on Hydroquinone-Treated Human Retinal Pigment Epithelium Cells and Human Retinal Müller Cells

“…Previous studies have shown that HQ had toxic effects on cultured human RPE cells (ARPE-19) 49,56 , human Müller retinal cells (MIO-M1), 50,56 human microvascular endothelial cells and rat neurosensory retinal cells (R-28). 49 The present study demonstrates that MEM has dose-dependent protective properties in human ARPE-19 and MIO-M1 cells that were stressed with HQ.…”

“…55 Reversing the effects of HQ on cultured cells have been studied previously. 32,56 The zonulae occludentes junctions between RPE cells represent the outer blood retinal barrier. The RPE, which is adjacent to Bruch's membrane, is responsible for light absorption, phagocytosis of photoreceptor outer segments, and maintaining the subretinal space by transporting/secreting ions and mediators between the various retinal layers.…”

“…68There have been only a limited number of studies to identify potential drugs capable of reversing HQ toxicity. It was shown in ARPE-19 and MIO-M1 cells that Brimonidine exhibited protective properties against the HQ toxicity by increasing the cell viability and mitochondrial membrane potential, while decreasing the LDH and ROS levels 56. However, to date no other inhibitors have been reported that block the HQ cyto-toxic effects.A limitation to our study is the use of transformed cell lines (ARPE-19 and MIO-M1) to address retinal biology because these cultures can be very different from the non-transformed retinal cells.…”

Resvega Alleviates Hydroquinone-Induced Oxidative Stress in ARPE-19 Cells

“…In addition, it increases apoptosis, damages cellular macromolecules, activates cell signaling pathways, such as caspases, and it can be unfavorable for redox-sensitive molecules, such as nuclear factor kappa B (NF-κB) [5,6,[11][12][13][14][15]. Hydroquinone has been shown to increase oxidative stress, compromise cell viability, and decrease mitochondrial membrane potential in a concentration-dependent manner in human RPE cells [16,17]. In addition, hydroquinone induces the formation of membrane blebs, which promotes the development of drusen and induces actin protein rearrangement to globular aggregates in RPE cells [18][19][20].…”