astaxanthine and Cataract

Ferroptosis is a form of regulated cell death closely associated with oxidative stress and mitochondrial dysfunction and is characterised by the accumulation of reactive oxygen species (ROS) and lipid species and iron overload. Damage to human lens epithelial cells (LECs) is associated with age-related cataract progression. Astaxanthin (ATX), a carotenoid with natural antioxidant properties, counteracts ferroptosis in the treatment of various degenerative diseases. However, this mechanism has not been reported with respect to cataract treatment. In this study, the differential expression levels of glutathione peroxidase 4 (GPX4) in the lens of young and aged mice were analysed. Continuous ATX supplementation for 8 months upregulated GPX4 expression in the mouse LECs and delayed the progression of ferroptosis. Upon treatment with erastin, ROS and malondialdehyde accumulated and the mitochondrial membrane potential decreased. At the same time, the expressions of GPX4, SLC7A11, and ferritin were suppressed in human LECs. All of these phenomena were partially reversed by ATX and Fer-1, a ferroptosis inhibitor. This study confirmed that the ATX-mediated targeting of GPX4 might alleviate human LECs damage by inhibiting ferroptosis and ameliorating oxidative stress and that this could represent a promising therapeutic approach for age-related cataract.

Topics: Animals; Cataract; Epithelial Cells; Ferroptosis; Humans; Mice; Oxidative Stress; Reactive Oxygen Species

The purpose of this study was to investigate the effect of astaxanthin on metabolic cataract in rats with type 1 diabetes and its antioxidant capacity to lens.. Rats were randomly divided into four groups (n = 8): control group, diabetes mellitus (DM) group, low-dose astaxanthin (DM + AL) and low-dose astaxanthin (DM + AH) group. A rat model of type I diabetes mellitus was established by intraperitoneal injection of 60 mg/kg streptozotocin (STZ). After successful modeling, rats in the administration group were given different doses of astaxanthin (AST) for 12 weeks. The lens opacity of rats was observed by slit-lamp camera system. The double antibody sandwich method was used to detect the levels of advanced glycation end product (AGE), lipid peroxide/malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and glutathione (GSH) in the lens. Hematoxylin-eosin (HE) staining was used to examine the morphologic changes in the lens.. The severity of cataract in the lens was obviously increased after induced by STZ, whereas it was significantly decreased after treatment with AST (p < .05, respectively). In addition, in the AST groups, the levels of AGE and MDA in the lens tissue were notably decreased when compared with those in the DM group (p < .05, respectively). However, the levels of GSH, SOD, and CAT were increased in the AST group in comparison with those in the DM group (p < .05, respectively).. Astaxanthin may play an antioxidant role in the lens. Additionally, it exerts a protective function in the lens by delaying the development and progression of metabolic cataract and inhibiting the oxidative stress of lens in diabetic rats.

Topics: Animals; Anterior Eye Segment; Antioxidants; Blood Glucose; Body Weight; Cataract; Diabetes Mellitus, Type 1; Disease Progression; Lens, Crystalline; Male; Rats, Sprague-Dawley; Retina; Xanthophylls

To examine whether astaxanthin (AST) prevent the cataract formation induced by glucocorticoid in chick embryo.. Hydrocortisone hemisuccinate sodium (HC) (0.5 μmol/egg) was administered directly into the air chamber in the egg shell of chick embryo day 15. The eggs were then kept in an incubator at same conditions and administered 100 μL of 50 (HC + AST50 group), 80 (HC + AST80 group), 100 (HC + AST100 group) mg/mL of AST solutions dissolved in dimethyl sulfoxide (DMSO) 3 h after administration of HC. In addition, non-HC treated group (treated with physiological saline without HC and 100 μL of DMSO), HC-alone group (treated with 0.5 μmol of HC and 100 μL of DMSO), and AST100 group (treated with physiological saline without HC and 100 μL of DMSO) were also incorporated. After 48 h of treatment, lenses were removed from embryo and classified into five stages according to developed opacity. The amounts of reduced glutathione in the lenses and the blood glucose levels were measured.. The average scores of lens opacitiy were 2.63 ± 1.02 nmol/lens (HC-alone), 2.78 ± 0.97 nmol/lens (HC + AST50), 2.22 ± 1.20 nmol/lens (HC + AST80) and 1.84 ± 0.83 nmol/lens (HC + AST100; p < 0.05), respectively. Administration of AST decreased the lens opacity dose-dependently. The amounts of reduced glutathione in lenses were 11.6 ± 2.8 nmol/lens (HC-alone), 11.3 ± 2.7 nmol/lens (HC + AST50), 13.4 ± 2.4 nmol/lens (HC + AST80) and 13.7 ± 3.1 nmol/lens (HC + AST100; p < 0.05), respectively. Higher levels of AST prevented loss of reduced glutathione from the lens.. These findings support that AST protects glucocorticoid-induced cataract in chick embryo.

Topics: Animals; Cataract; Chick Embryo; Disease Models, Animal; Fibrinolytic Agents; Glucocorticoids; Lens, Crystalline; Oxidative Stress; Xanthophylls

Selenite, the most commonly encountered toxic form of selenium, in overdose, is used to induce cataracts in rats. This study demonstrated that selenite, but not selenate, would interact with the carotenoid astaxanthin (ASTX), as determined using isothermal titration calorimetry and NMR. The maximum absorption of ASTX decreased with increasing selenite concentration, indicating that the conjugated system of ASTX was changed by selenite. Such interactions between ASTX and selenite were also supported by the attenuation of selenite-induced turbidity by ASTX (0-12.5 microM) in vitro. In vivo experiments also showed that ASTX attenuated selenite-induced cataractogenesis in rats. In summary, this is the first report of a direct interaction of ASTX with selenite. This interaction is supported by an in vitro assay and may be partially responsible for the ASTX observed in vivo protection against selenite-induced cataractogenesis.

Topics: Animals; Cataract; Magnetic Resonance Spectroscopy; Rats; Rats, Wistar; Selenium; Sodium Selenite; Xanthophylls

The development of cataracts in Atlantic salmon, Salmo salar L., was studied in 16 groups of smolts fed diets differing in prooxidant (iron, copper, manganese) and antioxidant (vitamin E, vitamin C, astaxanthin) composition and lipid level for 23 weeks in sea water, using a 2(7-3) reduced factorial design. The seven dietary variables were systematically varied at low (requirement level and 150 g lipid kg(-1)) and high levels (below known toxic levels and 320 g lipid kg(-1)). A mean endpoint cataract incidence of approximately 36% was observed. High dietary levels of vitamin C and astaxanthin reduced cataract frequency, whereas high dietary lipid level, iron and manganese were associated with increased cataract frequencies. Considering the nutritional status of selected organs of the fish, only the status of ascorbic acid correlated negatively to cataract development (P < 0.05). The lens glutathione (GSH) status was not correlated to cataract frequency, nor statistically explained by the dietary variables. However, the study shows that balancing the diet with respect to pro- and antioxidant nutrients may significantly protect Atlantic salmon against development of cataracts. An incidence of reversible osmotic cataract observed at week 14 was positively correlated to plasma glucose concentration.

Topics: Animals; Antioxidants; Aqueous Humor; Ascorbic Acid; beta Carotene; Blood Glucose; Cataract; Copper; Diet; Dietary Fats; Eye; Fish Diseases; Glucose; Glutathione; Incidence; Iron; Lipids; Manganese; Nutritional Status; Reactive Oxygen Species; Salmo salar; Vitamin E; Xanthophylls; Zinc