Vitamin D Attenuates Oxidative Damage and Inflammation in Retinal Pigment Epithelial Cells
Ali Mohammad Tohari 1,2, Reem Hasaballah Alhasani 2, Lincoln Biswas 2, Sarita Rani Patnaik 2, James Reilly 2, Zhihong Zeng 3,* and Xinhua Shu 2,4,
Vision category starts with the following
- 12% larger pupils in children who are Vitamin D deficient – Feb 2024 parasympathetic nervous system?
- Myopia, AMD, Dry Eye, and Diabetic Retinopathy are all associated with low Vitamin D - April 2023
- An ocular disease can be associated with low vitamin D and 1 of 5 poor vitamin D genes – June 2022
- Eye vitamin D may not be associated with blood VitD, but is associated with CYP27B1 and CYP24A1 – Nov 2019
- Vitamin D treats and prevents a variety of eye problems (need 70 ng) – June 2018
- Vitamin D and Myopia, AMD, Diabetic Retinopathy, Uveitis, Glaucoma, VDR etc. – May 2015
- Tears often have 25 % higher levels of vitamin D than does blood
Vision problems having many studies on VitaminDWiki
- Uveitis (inflamed eye) and Vitamin D - many studies
- Age-Related Macular Degeneration and Vitamin D - many studies
- Cataracts and Vitamin D - many studies
- Diabetic Retinopathy associated with low Vitamin D - many studies
- 7+ studies of Glaucoma and Vitamin D
- Dry Eyes treated by Omega-3 and Vitamin D – many studies
- 21+ studies of Myopia and Vitamin D
VitaminDWiki pages with ANTIOXIDANTS in title
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Age-related macular degeneration (AMD), the most common visual disorder in elderly people, is characterized by the formation of deposits beneath the retinal pigment epithelium (RPE) and by dysfunction of RPE and photoreceptor cells. The biologically active form of vitamin D, 1,25-(OH)2D3 (VITD), is categorized as a multifunctional steroid hormone that modulates many transcriptional processes of different genes and is involved in a broad range of cellular functions. Epidemiological and genetic association studies demonstrate that VITD may have a protective role in AMD, while single nucleotide polymorphisms in the vitamin D metabolism gene (CYP24A1) increase the risk of AMD. However, the functional mechanisms of VITD in AMD are not fully understood. In the current study, we investigated the impact of VITD on H2O2-induced oxidative stress and inflammation in human RPE cells. We demonstrate that exposure to H2O2 caused significantly reduced cell viability, increased production of reactive oxygen species (ROS), lowered expression of antioxidant enzymes and enhanced inflammation. VITD exposure notably counteracted the above H2O2-induced effects. Our data suggest that VITD protects the RPE from oxidative damage and elucidate molecular mechanisms of VITD deficiency in the development of AMD.
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