May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Total Antioxidant Power in the Vitreous of Diabetic Retinopathy Patients
Author Affiliations & Notes
  • K. Matsuno
    Ophthalmology, Tokyo Med Univ Kasumigaura Hosp, Ibaraki, Japan
  • M. Osako
    Ophthalmology, Tokyo Med Univ Kasumigaura Hosp, Ibaraki, Japan
  • M. Usui
    Ophthalmology, Tokyo Med Univ, Tokyo, Japan
  • Footnotes
    Commercial Relationships  K. Matsuno, None; M. Osako, None; M. Usui, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 381. doi:
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      K. Matsuno, M. Osako, M. Usui; Total Antioxidant Power in the Vitreous of Diabetic Retinopathy Patients . Invest. Ophthalmol. Vis. Sci. 2005;46(13):381.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: Recent studies indicate that oxidative stress, especially from reactive oxygen species (ROS), is related to the progression of diabetic retinopathy (DR). We measured total antioxidant power (TAP) in the vitreous obtained from diabetic patients, and investigated the relation between TAP and DR stages. Since Fe2+ from vitreous hemorrhage may promote production of hydroxyl radical, one of the ROS (Fenton reaction), we also investigated the influence of vitreous hemorrhage on the TAP. Methods:Forty–eight eyes with DR and 16 control eyes with macula hole were studied. The DR eyes were divided into the three stages; non–proliferative (18 eyes), active (14 eyes), and quiescent (16 eyes). Vitreous hemorrhage was observed in 14 eyes. Vitreous fluid samples were obtained during the vitreous surgery, and stored immediately at –80°C until analysis. TAP was measured using the Oxford Biomedical Research assay. Results:TAP in the vitreous was significantly lower in the DR group (1.62±0.49) than in the macula hole group (4.08±0.92) (P<0.0001). The TAP were 1.82±0.61 in the non–proliferative stage, 1.58±0.34 in the active stage, and 1.42±0.38 in the quiescent stage. No significant differences were found among these three groups. No difference was detected between the proliferative (active and quiescent) and non–proliferative stage. The TAP were 1.58±0.34 in the vitreous hemorrhage group and 1.63±0.55 in non–vitreous hemorrhage group, with no significant difference. Conclusions:The antioxidant power in the vitreous was reduced in DR compared with non–DR patients. The decrease in antioxidant power may be related to the occurrence of DR rather than the progression of retinopathy because no difference was found in the three stages of DR. Our results also indicated that vitreous hemorrhage was not related to the reduction in TAP.

Keywords: diabetic retinopathy • antioxidants • vitreoretinal surgery 

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