April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
S-Adenosylmethionine Is Neuroprotective Following Acute Ischemic Retinal Injury
Author Affiliations & Notes
  • N. L. Barnett
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • L. N. Moxon-Lester
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • P. B. Colditz
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • K. Takamoto
    Centre for Clinical Research, University of Queensland, Brisbane, Australia
  • Footnotes
    Commercial Relationships  N.L. Barnett, None; L.N. Moxon-Lester, None; P.B. Colditz, None; K. Takamoto, None.
  • Footnotes
    Support  NHMRC (Australia) Grant 401529
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 684. doi:
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      N. L. Barnett, L. N. Moxon-Lester, P. B. Colditz, K. Takamoto; S-Adenosylmethionine Is Neuroprotective Following Acute Ischemic Retinal Injury. Invest. Ophthalmol. Vis. Sci. 2009;50(13):684.

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

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Purpose: : Although a large number of photoreceptors survive ischemia-reperfusion, their function is often impaired. Phototransduction in the retina requires a number of S-adenosylmethionine (SAMe)-dependent methylation reactions e.g. creatine synthesis, phosphatidylcholine synthesis and transducin methylation. These methylation reactions may be down-regulated after ischemia. The purpose of this study was to determine whether administration of SAMe after ischemia could improve retinal function.

Methods: : Unilateral retinal ischemia was induced in anaesthetized (ketamine / xylazine / acepromazine i.p.) adult rats, 200-250g, by increasing the intraocular pressure to 110 mmHg for 60 minutes. The contralateral eye served as a non-ischemic control. Immediately after ischemia, 2 µl SAMe was injected into the vitreous (final concentration, 100 µM), followed by daily oral administration of SAMe (280 mg/kg/day) for a further 5 or 10 days. Retinal function was assessed by scotopic flash electroretinography (ERG). Retinal injury was assessed by morphometric analysis of retinal sections. The expression of the creatine transporter was determined by immunohistochemistry.

Results: : SAMe did not alter any parameter of the ERG in control, non-ischemic retinas. A significant reduction in the amplitudes of the ERG a-waves (RmP3), b-waves and oscillatory potentials was induced by the ischemic insult followed by 5 or 10 days of reperfusion. Following the post-ischemic administration of SAMe for 10 days, ischemic RmP3 values were significantly greater than those recorded from the ischemic retinas that had not had SAMe supplementation (control 424 ± 31 µV, n=13; ischemia 144 ± 44 µV, n=7; ischemia plus SAMe 325 ± 46 µV, n=6). Moreover, ischemic RmP3 values were no longer significantly different from those recorded from non-ischemic controls, demonstrating a significant protection of photoreceptor function by SAMe. Morphometric analysis showed that SAMe also ameliorated the ischemia-induced retinal damage. Furthermore, an apparent decrease in creatine transporter expression was observed following ischemia.

Conclusions: : These data suggest that creatine transport, and creatine synthesis as well as other methylation reactions, may be compromised by an ischemic insult, contributing to retinal dysfunction and injury. SAMe supplementation may provide an effective neuroprotective strategy.

Keywords: neuroprotection • ischemia • retina 

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