• Exposure to Bright Light and the Concurrent Use of Photosensitizing Drugs. J.E. Roberts, C.E. Reme , J. Dillon, and M. Terman. New England Journal of Medicine. 1992; 326(22): 1500-01

  "Furthermore, photosensitizing drugs can potentiate the damaging effects of ultraviolet and visible radiation on the eye."
  "We recommend the following precautions. a washout period for potentially dangerous drugs before extended exposure to bright lights."

• Presumed Sertraline Maculopathy. Sener EC, Kiratli H. Acta Ophthalmol Scand 2001; 79(4):428-30.

  "PURPOSE: To report a unique case of a woman who developed simultaneous bilateral maculopathy presumed to result from intake of sertraline hydrochloride, a serotonin reuptake inhibitor.
  ..during twenty months of follow-up her visual acuity and abnormalities in other psychophysical tests did not improve. 
  CONCLUSION: Patients started on sertraline should be informed of the potential risk of developing maculopathy, and they should be examined regularly to detect possible early alterations.

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• Potential Ocular Phototoxicity of Antidepressant Drugs with Light Therapy of Winter Depressives. R.H. Wang, C.E. Reme, R. Whitt, J. Dillon, and J.E. Roberts. Photodermatology Photoimmunology & Photomedicine 1991;8(1):49

  "we examined the potential photoxicity of six common antidepressant and neuroleptic drugs (Amitrityline (AM), Chlorpromazine (CPZ), Imipramine (IM), Iprindol (IP), Prozac (PR), and Thioridazine (TH). We found that the potential of phototoxicity of the six drugs tested was CP=IP > TH > IM > AM=PR"

• Phototoxicity to the Retina: Mechanisms of Damage. Glickman RD.Int J Toxicol 2002 Nov-Dec;21(6):473-90

  "In addition to tissue damage caused directly by light absorption, light toxicity can be produced by the presence of photosensitizing agents. Drugs excited to reactive states by ultraviolet (UV) or visible light produce damage by type I (free radical) and type II (oxygen dependent) mechanisms. Some commonly used drugs, such as certain antibiotics, nonsteroidal anti-inflammatory drugs (NSAIDs), and psychotherapeutic agents, as well as some popular herbal medicines, can produce ocular phototoxicity."

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• Regulation of Gene Expression by Melatonin: A Microarray Survey of the Rat Retina. Wiechmann AF. J Pineal Res 2002 Oct;33(3):178-85

  "Our previous work has demonstrated that melatonin treatment increases the sensitivity of the rat retina to light-induced photoreceptor cell death. This raises the possibility that inappropriate exposure of photoreceptors to melatonin may result in visual impairment, caused by a loss of retinal photoreceptors."

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• Drugs-Induced Phototoxicity as a Risk for Age-Related Macular Degeneration  
  E. de la marnierre, M. Quaranta, M. Mauget-Faysse. ARVO 2001: 4296

  "neovascular AMD was positively associated with thiazide diuretics (p<0.001)" "Conclusions: These findings suggest that severe neovascular AMD are associated with thiazide diuretics long-lasting treatment.

• Retinal Pigment Epithelium Melanin and Ocular Toxicity. Dayhaw-Barker P. Int J Toxicol 2002 Nov-Dec;21(6):451-4

  "Ocular morphology is specifically directed at facilitating the transmittance of visible light to the retina for the purposes of photoreceptor absorption and phototransduction, thereby initiating the process of vision. By absorbing excess radiation, melanin significantly enhances this process. It can also act as a photoprotector by quenching reactive oxygen species and other radicals produced as a result of the high oxygen dependency of the retina for its metabolism. However, melanin also binds numerous pharmaceuticals, a process that can result in ocular toxicity."  
  "Many of the drugs that have been identified as causing these effects are known photosensitizers in which radiation plays a significant role in eliciting the pathologies. The phototoxic effects range from minor histological/ chemical changes, which do not impact the quality of vision, to pigmentary retinopathies, which could potentially involve the loss of sight."

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• Phototoxic Effects of Vigabatrin (Sabril™) in the Acute Rat Retinal Preparation.  Y.Izumi, M.Ishikawa, A.M. Benz, M.Izumi, C.F. Zorumski,  ARVO 2003: 2850/B689

  "Vigabatrin (VGA, Sabril™), a structural analog of gamma-aminobutyric acid, is an irreversible inhibitor of gamma-aminobutyric acid transaminase. Because of its effects on GABA accumulation in the extracellular space, VGA is being developed as an antiepileptic agent for drug-resistant seizures. Oculotoxicity of VGA was first characterized as visual field defects. VGA may also induce optic nerve atrophy and it has recently been shown that VGA induces apoptosis in photoreceptors.
  These observations indicate that VGA’s oculotoxicity is acute when the retina is exposed to light."

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