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光照及促氧化视网膜环境中的多不饱和脂质

Polyunsaturated Lipids in the Light-Exposed and Prooxidant Retinal Environment.

作者信息

Longoni Biancamaria, Demontis Gian Carlo

机构信息

Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, 56126 Pisa, Italy.

Department of Pharmacy, University of Pisa, 56126 Pisa, Italy.

出版信息

Antioxidants (Basel). 2023 Mar 2;12(3):617. doi: 10.3390/antiox12030617.

DOI:10.3390/antiox12030617
PMID:36978865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10044808/
Abstract

The retina is an oxidative stress-prone tissue due to high content of polyunsaturated lipids, exposure to visible light stimuli in the 400-480 nm range, and high oxygen availability provided by choroidal capillaries to support oxidative metabolism. Indeed, lipids' peroxidation and their conversion into reactive species promoting inflammation have been reported and connected to retinal degenerations. Here, we review recent evidence showing how retinal polyunsaturated lipids, in addition to oxidative stress and damage, may counteract the inflammatory response triggered by blue light-activated carotenoid derivatives, enabling long-term retina operation despite its prooxidant environment. These two aspects of retinal polyunsaturated lipids require tight control over their synthesis to avoid overcoming their protective actions by an increase in lipid peroxidation due to oxidative stress. We review emerging evidence on different transcriptional control mechanisms operating in retinal cells to modulate polyunsaturated lipid synthesis over the life span, from the immature to the ageing retina. Finally, we discuss the antioxidant role of food nutrients such as xanthophylls and carotenoids that have been shown to empower retinal cells' antioxidant responses and counteract the adverse impact of prooxidant stimuli on sight.

摘要

视网膜是一个易于产生氧化应激的组织,这是由于其多不饱和脂质含量高、暴露于400 - 480纳米范围内的可见光刺激以及脉络膜毛细血管为支持氧化代谢提供了高氧供应。事实上,脂质过氧化及其转化为促进炎症的活性物质已有报道,并与视网膜变性有关。在此,我们综述了近期的证据,这些证据表明视网膜多不饱和脂质除了氧化应激和损伤外,可能会对抗由蓝光激活的类胡萝卜素衍生物引发的炎症反应,从而使视网膜尽管处于促氧化环境仍能长期运作。视网膜多不饱和脂质的这两个方面需要对其合成进行严格控制,以避免因氧化应激导致脂质过氧化增加而超过其保护作用。我们综述了关于视网膜细胞中不同转录控制机制的新证据,这些机制在从未成熟到衰老的视网膜的整个生命周期中调节多不饱和脂质的合成。最后,我们讨论了叶黄素和类胡萝卜素等食物营养素的抗氧化作用,这些营养素已被证明能增强视网膜细胞的抗氧化反应,并抵消促氧化刺激对视力的不利影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/3d952a14c6e5/antioxidants-12-00617-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/186a753ce6c3/antioxidants-12-00617-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/640efb99d6d2/antioxidants-12-00617-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/d4eb155d3768/antioxidants-12-00617-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/222a6f8c1256/antioxidants-12-00617-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/3d952a14c6e5/antioxidants-12-00617-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/186a753ce6c3/antioxidants-12-00617-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/640efb99d6d2/antioxidants-12-00617-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/d4eb155d3768/antioxidants-12-00617-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/222a6f8c1256/antioxidants-12-00617-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef3b/10044808/3d952a14c6e5/antioxidants-12-00617-g005.jpg

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