July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Light-induced damage in the retinal pigment epithelium of a mouse model
Author Affiliations & Notes
  • Toshio Narimatsu
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan
    Ophthalmology, Keio University School of Med, Shinjuku, Tokyo, Japan
  • Kazuo Tsubota
    Ophthalmology, Keio University School of Med, Shinjuku, Tokyo, Japan
  • Yoko Ozawa
    Laboratory of Retinal Cell Biology, Keio University School of Medicine, Shinjuku, Tokyo, Japan
    Ophthalmology, Keio University School of Med, Shinjuku, Tokyo, Japan
  • Footnotes
    Commercial Relationships   Toshio Narimatsu, None; Kazuo Tsubota, None; Yoko Ozawa, None
  • Footnotes
    Support  None
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 1687. doi:
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      Toshio Narimatsu, Kazuo Tsubota, Yoko Ozawa; Light-induced damage in the retinal pigment epithelium of a mouse model. Invest. Ophthalmol. Vis. Sci. 2019;60(9):1687.

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

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Abstract

Purpose : We previously reported that the light exposure induced disorder of cell-cell junction of the retinal pigment epithelium (RPE) which is included in the pathogenesis of age-related macular degeneration (AMD), and N-Acetyl-L-cysteine (NAC), an antioxidant, rescued the damage, suppressing inflammations (Narimatsu et al. 2013). We also previously reported that the RPE damage was rescued by lutein, another antioxidative factor which acts as a scavenger; additionally, we found that lutein induced endogenous antioxidative enzymes in the RPE-choroid complex, which may also contribute to reducing local reactive oxygen species (ROS) (Kamoshita, Narimatsu et al. 2016). In the current study, we further analyzed the effects of NAC in the model.

Methods : Six- to 7-week-old BALB/c mice were divided into 3 groups, and of them, 2 groups were exposed to fluorescent light at 2000 lux for 3 hours after 12 hours of dark adaptation. The two groups were intraperitoneally treated either by NAC (500 mg/kg) or control vehicle twice 12 hours before and just before light exposure. The other group was treated by vehicle followed by no light exposure. These protocols were the same as the previous study in which the RPE damage was analyzed (Narimatsu et al. 2013). Levels of ROS were analyzed by DCFH-DA 6 hours after light exposure, and the mRNA levels of antioxidative enzymes (SOD2 and catalase) were analyzed by quantitative real-time RT-PCR 24 hours after light exposure both in the RPE-choroid complex.

Results : The ROS levels were increased by light exposure and suppressed by NAC. The mRNAs of antioxidative enzymes were induced by light exposure when treated with vehicle. However, the enzymes were not induced when treated by NAC.

Conclusions : Endogenous antioxidative enzymes were induced by light exposure. However, NAC did not induce the enzymes. Nonetheless, NAC suppressed local ROS to the levels which prevented the light-induced RPE damage as we previously reported, suggesting that light-induced endogenous antioxidative enzymes did not have, however, NAC itself had a sufficient ability to reduce ROS in the RPE-choroid complex to prevent pathogenesis. NAC may have prevented the damage irrespective of endogenous antioxidative enzymes.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.

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