May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Role of Reactive Oxygen Species in Retinal Leukostasis of Diabetic Rats
Author Affiliations & Notes
  • P. Chen
    Eye, Henry, Detroit, MI
  • V.R. Thandra
    Eye, Henry, Detroit, MI
  • G.M. Scicli
    Eye, Henry, Detroit, MI
  • P.A. Edwards
    Eye, Henry, Detroit, MI
  • A.G. Scicli
    Eye, Henry, Detroit, MI
  • Footnotes
    Commercial Relationships  P. Chen, None; V.R. Thandra, None; G.M. Scicli, None; P.A. Edwards, None; A.G. Scicli, None.
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 1711. doi:
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      P. Chen, V.R. Thandra, G.M. Scicli, P.A. Edwards, A.G. Scicli; Role of Reactive Oxygen Species in Retinal Leukostasis of Diabetic Rats . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1711.

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

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Introduction: : Early in diabetic retinopathy there is increased arrested leukocytes (leukostasis) and leukocyte–induced capillary plugging in the retina. We hypothesized that reactive oxygen species (ROS) mediate retinal leukostasis in diabetes.

Purpose: : To study whether retinal leukostasis in diabetic rats is altered by treatment with antioxidants.

Methods: : Rats with streptozotocin–induced diabetes (glycemia ≥250 mg/dl) were divided in three groups (6–8 rats/group): Group 1, untreated diabetic rats; Group 2, diabetic rats treated with a combination of tempol (∼ 70mg/kg/day), a superoxide dismutase mimetic, and N–Acetyl Cysteine. (NAC, ∼ 1g/kg/day), a gluthatione based antioxidant: Group 3, diabetic rats treated with the NAD(P)H oxidase inhibitor apocynin (∼ 45mg/kg/day). All treatments were given in the drinking water. After two weeks of treatment static retinal leukocytes were labeled with acridine orange, visualized with a Scanning Laser Ophthalmoscope and counted. Leukostasis was expressed as 10–5cells/pixels2.

Results: : Compared with controls, diabetic rats had increased retinal leukostasis: 0.1± 0.06 vs. 2.3 ± 0.17 (p<0.01). Retinal leukostasis in diabetic rats was decreased by treatment with tempol–NAC to 0.7±0.1 (p<0.001 vs. untreated diabetes) and by treatment with apocynin to 0.3±0.1 (n.s. vs. normal control; p< 0.001 vs. untreated diabetes. Thus inhibition of NAD(P)H oxidase abolished the augmented retinal leukostasis of early diabetes.

Conclusions: : Retinal leukostasis in early diabetes is mediated by ROS. The activity of NAD(P)H oxidase is required for leukostasis in the diabetic retina to occur.

Keywords: diabetic retinopathy • antioxidants • inflammation 

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