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Phototoxicity to the retina: mechanisms of damage.

Abstract

Light damage to the retina occurs through three general mechanisms involving thermal, mechanical, or photochemical effects. The particular mechanism activated depends on the wavelength and exposure duration of the injuring light. The transitions between the various light damage mechanism may overlap to some extent. Energy confinement is a key concept in understanding or predicting the type of damage mechanism produced by a given light exposure. As light energy (either from a laser or an incoherent source) is deposited in the retina, its penetration through, and its absorption in, various tissue compartments is determined by its wavelength. Strongly absorbing tissue components will tend to "concentrate" the light energy. The effect of absorbed light energy largely depends on the rate of energy deposition, which is correlated with the exposure duration. If the rate of energy deposition is too low to produce an appreciable temperature increase in the tissue, then any resulting tissue damage necessarily occurs because of chemical (oxidative) reactions induced by absorption of energetic photons (photochemical damage). If the rate of energy deposition is faster than the rate of thermal diffusion (thermal confinement), then the temperature of the exposed tissue rises. If a critical temperature is reached (typically about 10 degrees C above basal), then thermal damage occurs. If the light energy is deposited faster than mechanical relaxation can occur (stress confinement), then a thermoelastic pressure wave is produced, and tissue is disrupted by shear forces or by cavitation-nonlinear effects. Very recent evidence suggests that ultrashort laser pulses can produce tissue damage through nonlinear and photochemical mechanisms; the latter because of two-photon excitation of cellular chromophores. 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. Specific cellular effects and damage end points characteristic of light damage mechanisms are described.

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  • Publisher Full Text
  • Authors+Show Affiliations

    Department of Ophthalmology, University of Texas Health Science Center, San Antonio, Texas 78229-3900, USA. glickman@uthscsa.edu

    Source

    MeSH

    Animals
    Endpoint Determination
    Hot Temperature
    Humans
    Lasers
    Photolysis
    Radiation Injuries
    Retina
    Retinal Diseases
    Sunlight
    Temperature

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Research Support, U.S. Gov't, Non-P.H.S.
    Review

    Language

    eng

    PubMed ID

    12537644

    Citation

    Glickman, Randolph D.. "Phototoxicity to the Retina: Mechanisms of Damage." International Journal of Toxicology, vol. 21, no. 6, 2002, pp. 473-90.
    Glickman RD. Phototoxicity to the retina: mechanisms of damage. Int J Toxicol. 2002;21(6):473-90.
    Glickman, R. D. (2002). Phototoxicity to the retina: mechanisms of damage. International Journal of Toxicology, 21(6), pp. 473-90.
    Glickman RD. Phototoxicity to the Retina: Mechanisms of Damage. Int J Toxicol. 2002;21(6):473-90. PubMed PMID: 12537644.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Phototoxicity to the retina: mechanisms of damage. A1 - Glickman,Randolph D, PY - 2003/1/23/pubmed PY - 2003/6/5/medline PY - 2003/1/23/entrez SP - 473 EP - 90 JF - International journal of toxicology JO - Int. J. Toxicol. VL - 21 IS - 6 N2 - Light damage to the retina occurs through three general mechanisms involving thermal, mechanical, or photochemical effects. The particular mechanism activated depends on the wavelength and exposure duration of the injuring light. The transitions between the various light damage mechanism may overlap to some extent. Energy confinement is a key concept in understanding or predicting the type of damage mechanism produced by a given light exposure. As light energy (either from a laser or an incoherent source) is deposited in the retina, its penetration through, and its absorption in, various tissue compartments is determined by its wavelength. Strongly absorbing tissue components will tend to "concentrate" the light energy. The effect of absorbed light energy largely depends on the rate of energy deposition, which is correlated with the exposure duration. If the rate of energy deposition is too low to produce an appreciable temperature increase in the tissue, then any resulting tissue damage necessarily occurs because of chemical (oxidative) reactions induced by absorption of energetic photons (photochemical damage). If the rate of energy deposition is faster than the rate of thermal diffusion (thermal confinement), then the temperature of the exposed tissue rises. If a critical temperature is reached (typically about 10 degrees C above basal), then thermal damage occurs. If the light energy is deposited faster than mechanical relaxation can occur (stress confinement), then a thermoelastic pressure wave is produced, and tissue is disrupted by shear forces or by cavitation-nonlinear effects. Very recent evidence suggests that ultrashort laser pulses can produce tissue damage through nonlinear and photochemical mechanisms; the latter because of two-photon excitation of cellular chromophores. 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. Specific cellular effects and damage end points characteristic of light damage mechanisms are described. SN - 1091-5818 UR - https://www.unboundmedicine.com/medline/citation/12537644/Phototoxicity_to_the_retina:_mechanisms_of_damage_ L2 - http://journals.sagepub.com/doi/full/10.1080/10915810290169909?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -