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Retina, oxidative stress

L, Z, and MZ all contain a high number of double bonds and therefore a high number of free electrrMis [57]. This means that they form part of a defense mechanism against the production of ROS within the retina. Oxidative stress occurs... [Pg.3943]

ApoJ is another protein component of HDL which is highly expressed by the RPE and neural retina, especially under oxidative stress conditions (Wong et al., 2000, 2001). It can act as a complement regulatory protein, which by binding to and inactivating the membrane-attack complex can prevent cytolysis (Bartl et al., 2001). ApoJ accumulation was identified in drusen in AMD patients (Sakaguchi et al., 2002 Wong et al., 2000). [Pg.320]

As mentioned previously, the ability of carotenoids to inhibit oxidative stress was tested in vitro in many different cell types. In the retina only lutein and zeaxanthin accumulate in sufficient concentrations to exert direct antioxidant effects, therefore our further discussion of these antioxidant effects will be focused mainly on those two xanthophylls. [Pg.326]

Increased age and smoking are associated with an increased oxidative stress and depletion of low-molecular weight antioxidants in many tissues including the retina (Beatty et al., 2000). Epidemiological studies indicate that on average, smokers develop late stage AMD 10 years earlier than nonsmokers (Kelly et al., 2004 Klein et al., 1998 Mitchell et al., 2002 Thornton et al., 2005 Tomany et al., 2004). [Pg.329]

Several markers of oxidative stress have been identified in AMD retinas, including proteins modified by products of lipid peroxidation (Crabb et al., 2002 Gu et al., 2003 Hollyfield et al., 2003). Overall, there is growing body of evidence implicating oxidative stress in the development and progression of AMD (Anderson et al., 2002 Beatty et al., 2000 Seddon et al., 2004). [Pg.329]

Bazan, N. G. Neuroprotectin D1 (NPD1) a DHA-derived mediator that protects brain and retina against cell injury-induced oxidative stress. Brain Pathol. 15 159-166,2005. [Pg.615]

Ohira, A., Honda, O., Gauntt, C.D., Yamamoto, M., Hori, K., Masutani, H., Yodoi, J., and Honda, Y. 1994. Oxidative stress induces adult T cell leukemia derived factor/thioredoxin in the rat retina. Lab. Invest. 70 279-285. [Pg.153]

Neurons in general are particularly vulnerable to oxidative stress (Reiter, 1995 Halliwell, 2001). Factors predisposing retina to oxidative stress are as follows ... [Pg.59]

The ability of lycopene to act as an antioxidant and scavenger of free radicals is frequently cited as the most likely mechanism that could account for the hypothesized beneficial effects on human health.Supporting this theory, protection against oxidative stress has been shown in parallel with a preferential destraction of lycopene relative to P-carotene in a study of human skin irradiated with ultraviolet (UV) light. Further, the ability of carotenoids to act as antioxidants has been hypothesized as the mechanism underlying the protection of the human retina from photooxidation, a process that over time can result in the pathologies of age-related macular degeneration (AMD) and cataracts. ... [Pg.635]

Bazan NG (2005) Neuroprotectin Di (NPDi) a DHA-derived mediator that protects brain and retina against cell injury-induced oxidative stress. Brain Pathol 15 159-166 Bazan NG (2006) The onset of brain injury and neurodegeneration triggers the synthesis of docosanoid neuroprotective signahng. Cell Mol Neurobiol 26 901-913 Bazan NG (2007) Omega-3 fatty acids, pro-inflammatory signaling and neuroprotection. CurrOpin Clin Nutr Metab Care 10 136-141... [Pg.370]

Electron spin resonance spin trapping analysis of the signals obtained from the perfused rabbit retina showed that hydroxyl radical adducts were generated during the ischaemic period with no further increase at reperfusion (Muller et al. 1997). Electron spin resonance detection of the ascorbyl free radical/dimethyl sulfoxide complex in the retina confirmed that an oxidative stress occurred under ischaemia and was not increased under reperfusion. [Pg.550]

As already noted, apart from being induced by hypoxia, induction of HO-1 by agents that cause oxidative stress occurs in human skin fibroblasts (116), glial cells and astrocytes (117-119), the retina (120), and cultured retinoblastoma cells (121). The induction of HO-1 in response to oxidative stress is believed to have a protective role through the antioxidant properties of biliverdin and bilirubin. Of particular interest is the fact that in clinical conditions associated with chronic repeated episodes of hypoxia, such as obstructive sleep apnea syndrome (OSA), the episodic occurrence of hypoxia and reoxygenation provides for a potential scenario of not only hypoxia but also repetitive oxidative stress providing two stimuh for the induction of HO-1. [Pg.640]


See other pages where Retina, oxidative stress is mentioned: [Pg.134]    [Pg.136]    [Pg.136]    [Pg.326]    [Pg.329]    [Pg.338]    [Pg.578]    [Pg.606]    [Pg.332]    [Pg.169]    [Pg.319]    [Pg.97]    [Pg.410]    [Pg.636]    [Pg.131]    [Pg.2441]    [Pg.47]    [Pg.54]    [Pg.59]    [Pg.67]    [Pg.77]    [Pg.77]    [Pg.276]    [Pg.244]    [Pg.35]    [Pg.50]    [Pg.335]    [Pg.118]    [Pg.203]    [Pg.483]    [Pg.450]    [Pg.115]    [Pg.331]    [Pg.95]    [Pg.587]   


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