The purpose of this study was to determine if different vitamin E components exhibit similar efficacy and mechanism of action in protecting Retinal pigment epithelium (RPE) cells from oxidative damage. We hypothesized that α-tocopherol (αT) is unique among vitamin E components in its cytoprotective mechanism of action against oxidative stress in RPE cells and that it requires protein synthesis for optimal antioxidant effect. We used cell viability assays, fluorescent chemical labeling of DNA and actin and immuno-labeling of the antioxidant proteins Nrf2 and Sod2 and of the tight junction protein, ZO-1, and confocal microscopy to determine the effects of αT and γT against oxidative stress in immortalized human RPE cells (hTERT-RPE). Using the four main vitamin E components, αT, γT, δ-tocopherol (δT) and α-tocotrienol (αTr), we ascertained that they exhibit similar, but not identical, antioxidant activity as αT when used at equimolar concentrations. In addition, we determined that the exposure time of RPE cells to α-tocopherol is critical for its ability to protect against oxidative damage. Lastly, we determined that αT, but not γT, partially requires the synthesis of new proteins within a 24-h period and prior to exposure to tBHP for optimal cytoprotection. We conclude that, unlike γT and δT, αT appears to be unique in its requirement for transport and/or signaling for it to be an effective antioxidant. As a result, more focus should be paid to which vitamin E components are used for antioxidant interventions.

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Purpose: To investigate the efficacy of topical application of 3% diquafosol sodium (DQS) and tocopherol (TCP) acetate mixtures in a mouse model of experimental dry eye (EDE).

Methods: After exposure to desiccating stress for 5 days, eye drops consisting of 3% DQS alone, 0.01% TCP alone, or 3% DQS and 0.005% or 0.01% TCP mixture were applied for the treatment of EDE. Tear volume, tear film break-up time (TBUT), corneal fluorescein staining scores (CFSS), and tear film lipid layer grades (TFLLG) were measured at 0, 5 and 10 days after treatment. The 2′,7′-dichlorodihydrofluorescein diacetate assay (DCFDA) for reactive oxygen species (ROS) production, enzyme-linked immunosorbent assay (ELISA) for malondialdehyde (MDA), and flow cytometry for CD4 + interferon (IFN)-γ+ T cells were evaluated on the ocular surface at 10 days after treatment. In addition, levels of tumour necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and chemokine CC motif ligand 4 (CCL4) in the conjunctiva were measured using a multiplex immunobead assay, and conjunctival goblet cells were counted by periodic acid-Schiff staining at 10 days after treatment.

Results: Both the TCP mixture groups indicated a significant improvement in TBUT, ROS production, and MDA concentrations compared to those in the DQS alone group. Furthermore, the 0.01% TCP mixture group also showed higher tear film lipid layer grades and conjunctival goblet cell density and lower corneal fluorescein staining scores, number of CD4 + IFN-γ+ T cells, and levels of TNF-α, IL-1β, and CCL4 than the DQS alone group (P < 0.05).

Conclusions: Application of eye drops containing the mixture of DQS and TCP could stabilize the tear film lipid layer, improve TBUT and corneal epithelial damages, decrease ROS production, inflammatory molecules, and T cells, and increase conjunctival goblet cell density on the ocular surface. Topical DQS and TCP mixtures may have a greater therapeutic effect on clinical signs, oxidative damage, and inflammation of dry eye than DQS eye drops.

A 41-year-old woman has come to our attention complaining of decreased visual acuity and monocular diplopia associated with upper and lower limb hypoesthesia. Malabsorption syndrome with vitamin A and E deficiency developed after a bariatric biliopancreatic diversion. The clinical ophthalmological signs and symptoms improved after oral vitamin supplementation therapy. The past medical history is essential in the case of a patient complaining of visual symptoms compatible with vitamin deficiency in order to detect the cause and to start a prompt therapy to avoid irreversible neurological and visual sequelae. The clinical features of our case closely resemble other cases described in the literature of patients affected by vitamin A and E deficiency secondary to malabsorption syndrome.

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We investigated the antioxidant effects of vitamin E on a glucocorticoid (GC) induced model of cataracts in chick embryos. We used 70 fertilized eggs divided into seven groups as follows: phosphate-buffered saline (PBS) group, olive oil treatment (OO) group, hydrocortisone treatment (HC) group, olive oil and hydrocortisone treatment (OO + HC) group, 50 mg/kg vitamin E and hydrocortisone treatment (HC + VE (50)) group, 25 mg/kg vitamin E and hydrocortisone treatment (HC + VE (25)) group and 15 mg/kg vitamin E and hydrocortisone treatment (HC + VE (15)) group. On day 17, chick embryos were removed from the eggs and lens and liver tissues were excised. Cataract formation was evaluated and total antioxidant status (TAS), total oxidant status (TOS), malondialdehyde (MDA) and glutathione peroxidase (GPx) were measured in lens and liver tissues; MDA was measured only in liver. The lenses in the HC + VE (50) group exhibited significantly higher levels of GPx and TAS, and lower levels of TOS than for HC and OO + HC groups. The livers of the HC + VE (50) group exhibited significantly higher levels of GPx and lower levels of MDA than for the HC and OO + HC groups. The HC + VE (50) group lenses were evaluated as grade 1, because the nuclei were completely free of cataracts, likely due to the antioxidative effect of high dose VE. VE is an effective antioxidant agent that exhibits a dose-response effect, for ameliorating the negative effects of GCs.

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