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Br J Ophthalmol 2004;88:523-527 Background/aim: Endothelin 1 (ET-1) is considered the most potent vasoconstrictor in the body and the eye. This molecule may play a significant role in the pathobiology [...]

Background/aim: The authors investigated the concentrations of 8-isoprostaglandin [F.sub.2a], a marker of oxidative stress in vivo, and ascorbic acid, a protectant against oxidative damage, in the aqueous humour of patients [...]

Background/aim: The authors investigated the concentrations of 8-isoprostaglandin F[sub 2a'], a marker of oxidative stress in vivo, and ascorbic acid, a protectant against oxidative damage, in the aqueous humour of patients with exfoliation syndrome (XFS) and cataract and compared the results with those in age matched patients with cataract, but without XFS, to determine whether XFS is associated with increased oxidative stress. Methods: Aqueous humour was aspirated at the beginning of phacoemulsification cataract surgery from 27 eyes of 27 cataract patients with XFS and 27 eyes of 27 age matched cataract patients without XFS. 8-Isoprostaglandin F[sub 2a] concentration in the aqueous was determined with a commercial immunoassay; ascorbic acid concentration was measured with a microplate assay method. Results:. The mean concentration of 8-isoprostaglandin F[sub 2a] in the aqueous from patients with XFS (2429 (SD 2940) pg/ml; range 400-10500 pg/ml) was significantly higher than that measured in the aqueous of age matched control patients (529.1 (226.8) pg/ml; range 325-1000 pg/ml); (p = 0.0028). Furthermore, mean ascorbic acid concentration in XFS patients (0.75 (0.39) mM; range 0.28-1.70 mM) was significantly lower than that found in control patients (1.19 (0.47) mM; range 0.53-2.4 mM); (p = 0.0005). There was a reverse correlation between 8-isoprostaglandin F[sub 2a] and ascorbic acid concentration. Conclusion: 8-Isoprostaglandin F[sub 2a] was significantly increased in the aqueous of patients with XFS, and ascorbic acid was decreased, providing evidence of a role for free radical induced oxidative damage in the pathobiology of XFS. [ABSTRACT FROM AUTHOR]