Astaxanthin, a dietary carotenoid, protects retinal cells against oxidative stress in-vitro and in mice in-vivo

Abstract

We have investigated whether astaxanthin exerted neuroprotective effects in retinal ganglion cells in-vitro and in-vivo. In-vitro, retinal damage was induced by 24-h hydrogen peroxide (H2O2) exposure or serum deprivation, and cell viability was measured using a WST assay. In cultured retinal ganglion cells (RGC-5, a rat ganglion cell-line transformed using E1A virus), astaxanthin inhibited the neurotoxicity induced by H2O2 or serum deprivation, and reduced the intracellular oxidation induced by various reactive oxygen species (ROS). Furthermore, astaxanthin decreased the radical generation induced by serum deprivation in RGC-5. In mice in-vivo, astaxanthin (100 mg kg(-1), p.o., four times) reduced the retinal damage (a decrease in retinal ganglion cells and in thickness of inner plexiform layer) induced by intravitreal N-methyl-D-aspartate (NMDA) injection. Furthermore, astaxanthin reduced the expressions of 4-hydroxy-2-nonenal (4-HNE)-modified protein (indicator of lipid peroxidation) and 8-hydroxy-deoxyguanosine (8-OHdG; indicator of oxidative DNA damage). These findings indicated that astaxanthin had neuroprotective effects against retinal damage in-vitro and in-vivo, and that its protective effects may have been partly mediated via its antioxidant effects.

Lutein Protects RGC-5 Cells Against Hypoxia and Oxidative Stress

“…Effects of carotenoids on a specific cell population were investigated using an in vitro approach. Zeaxanthin and astaxanthin have been shown to protect RGC-5 cells from oxidative injuries [5,33]. In the present study, our results suggested that lutein treatment protected RGC-5 from CoCl 2 -induced chemical hypoxia and H 2 O 2 -induced oxidative stress.…”

“…Recently, intensive efforts have been made to explicate the neuroprotective effects of carotenoids in ocular diseases in vivo [12,31,32] and in vitro [5,33]. Lutein treatment in DR mice restored malondialdehyde and glutathione protein levels, glutathione peroxidase activity as well as electroretinogram response to control values [31].…”

“…During ischemia, depletion of ATP stores, ions imbalance, glutamate excitotoxicity, apoptosis and free radical production eventually lead to RGC death [1–3]. Reperfusion following ischemia results in oxidative stress, which also plays a role in RGC damage [4,5]. Investigations have been carried out to study the neuroprotection of RGCs using carotenoids [6].…”

The Novel Mechanisms Concerning the Inhibitions of Palmitate-Induced Proinflammatory Factor Releases and Endogenous Cellular Stress with Astaxanthin on MIN6 β-Cells

“…Because of this structure, extension of the conjugated system causes activation of astaxanthin as a radical sponge, and astaxanthin can exert both lipophilic and hydrophilic antioxidant activities. According to the studies examining the effects of the antioxidant activity of astaxanthin, it has a wide range of properties, including improvement of physical exercise capacity as evidenced by an anti-muscle fatigue effect and an endurance-enhancing effect [3,4], prophylactic and curative effects on arteriosclerosis [5,6], influences via activation of energy metabolism including that of lipids [7], and efficacy in the treatment of eye and skin disorders such as asthenopia [8,9] and inflammatory skin diseases [10]. …”

Role of Glutathione Peroxidase 4 in Glutamate-Induced Oxytosis in the Retina

“…Because excess extracellular glutamate induces oxidative stress and cell death, glutamate-induced neurotoxicity is commonly called “oxytosis [1]. ” Treatments with antioxidants ameliorated the progression of the mouse model of glaucoma [9,10] and diabetic retinopathy [11] and suppressed cytotoxicity in retinal ganglion cells (RGCs) induced by N-methyl-D-aspartate (NMDA), the selective agonist for the glutamate receptor (NMDA receptor) [12,13]. Furthermore, treatment with an antioxidant suppressed the elevation of glutamate levels in the retinas of diabetic rats [14].…”