The significance of oxidative mechanisms in diseases of the retina

被引:11
作者
Augustin, AJ
Dick, HB
Offermann, I
Schmidt-Erfurth, U
机构
[1] Klinikum Karlsruhe, Augenklin, D-76133 Karlsruhe, Germany
[2] Johannes Gutenberg Univ Mainz, Augenklin, D-6500 Mainz, Germany
[3] Med Univ Lubeck, Augenklin, D-23538 Lubeck, Germany
关键词
oxidative metabolites; retina; diabetes; age-related macular degeneration (AMD);
D O I
10.1055/s-2002-35164
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
The eye is at high risk to be damaged by oxidative mechanisms. One major reason is the exposure to light throughout life. Anterior segment structures are mostly exposed to UV light. Visible blue light is believed to be a significant damaging mechanism for the retina. The biochemical composition of the posterior segment structures (unsaturated fatty acids) is an important factor making the eye more susceptible than other organs. Damaging mechanisms such as xanthin oxidase mechanisms are responsible for damage occurring in ischaemic diseases. These mechanisms are well known from diseases of other organs. Ischaemic processes are no longer believed to be the primary damaging mechanisms in diabetic retinopathy. Here, advanced glycation end products (AGE's) and related products may induce oxidative reactions and the expression of growth factors. In age-related macular degeneration photodynamic processes occurring. already in childhood are believed to be a major factor contributing to the pathogenesis of the disease process. In addition, the expression of growth factors and new vessel growth can be initiated via inflammatory reactions or oxidative metabolites. In this manuscript we give an overview on oxidative mechanisms involved in the pathogenesis of retinal diseases. Different therapeutical and preventive approaches such as the results of the ARED-Study and possible side effects are discussed.
引用
收藏
页码:631 / 643
页数:13
相关论文
共 130 条
[51]   The advanced glycation endproduct pentosidine induces the expression of PDGF-B in human retinal pigment epithelial cells [J].
Handa, JT ;
Reiser, KM ;
Matsunaga, H ;
Hjelmeland, LM .
EXPERIMENTAL EYE RESEARCH, 1998, 66 (04) :411-419
[52]  
HAYES KC, 1974, INVEST OPHTH VISUAL, V13, P499
[53]  
HEARSE DJ, 1986, ACTA PHYSIOL SCAND, V126, P65
[54]   INCREASED SUPEROXIDE PRODUCTION BY MONONUCLEAR-CELLS OF PATIENTS WITH HYPERTRIGLYCERIDEMIA AND DIABETES [J].
HIRAMATSU, K ;
ARIMORI, S .
DIABETES, 1988, 37 (06) :832-837
[55]   Advanced glycation end products induce expression of vascular endothelial growth factor by retinal Muller cells [J].
Hirata, C ;
Nakano, K ;
Nakamura, N ;
Kitagawa, Y ;
Shigeta, H ;
Hasegawa, G ;
Ogata, M ;
Ikeda, T ;
Sawa, H ;
Nakamura, K ;
Ienaga, K ;
Obayashi, H ;
Kondo, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1997, 236 (03) :712-715
[56]  
*IARC, 1998, IARC HDB CANC PREV, V2
[57]  
JAIN SK, 1989, J BIOL CHEM, V264, P21340
[58]   NEW APPROACHES TO THE PATHOGENESIS AND TREATMENT OF DIABETIC MICROANGIOPATHY [J].
JENNINGS, PE ;
BARNETT, AH .
DIABETIC MEDICINE, 1988, 5 (02) :111-117
[59]   Macular pigments lutein and zeaxanthin as blue light filters studied in liposomes [J].
Junghans, A ;
Sies, H ;
Stahl, W .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 2001, 391 (02) :160-164
[60]   PRODUCTION OF 12-HYDROXYEICOSATETRAENOIC ACID AND VITAMIN-E STATUS IN PLATELETS FROM TYPE-1 HUMAN DIABETIC SUBJECTS [J].
KARPEN, CW ;
CATALAND, S ;
ODORISIO, TM ;
PANGANAMALA, RV .
DIABETES, 1985, 34 (06) :526-531