May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Contact Lens Intolerance: Role of Oxidative Stress and Mitochondrial Injury Induced by Mutlipurpose Solutions
Author Affiliations & Notes
  • M. Dutot
    Laboratoire de Toxicologie, Faculté de Pharmacie, Université René Descartes–Paris5, Paris, France
    Unité de Pharmaco–Toxicologie Cellulaire,
    Centre Hospitalier National d’Ophtalmologie (CHNO) des XV–XX, Paris, France
  • C. Baudouin
    Service 3,
    Centre Hospitalier National d’Ophtalmologie (CHNO) des XV–XX, Paris, France
    Institut des Cordeliers, INSERM–U598, Paris, France
  • J.–M.M. Warnet
    Laboratoire de Toxicologie, Faculté de Pharmacie, Université René Descartes–Paris5, Paris, France
    Unité de Pharmaco–Toxicologie Cellulaire,
    Centre Hospitalier National d’Ophtalmologie (CHNO) des XV–XX, Paris, France
  • P. Rat
    Laboratoire de Toxicologie, Faculté de Pharmacie, Université René Descartes–Paris5, Paris, France
    Unité de Pharmaco–Toxicologie Cellulaire,
    Centre Hospitalier National d’Ophtalmologie (CHNO) des XV–XX, Paris, France
  • Footnotes
    Commercial Relationships  M. Dutot, None; C. Baudouin, None; J.M. Warnet, None; P. Rat, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 923. doi:
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      M. Dutot, C. Baudouin, J.–M.M. Warnet, P. Rat; Contact Lens Intolerance: Role of Oxidative Stress and Mitochondrial Injury Induced by Mutlipurpose Solutions . Invest. Ophthalmol. Vis. Sci. 2005;46(13):923.

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

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Abstract

Abstract: : Purpose: Millions of people wear contact lens and they widely use multipurpose solutions (MPS) containing preservatives for contact lens disinfection and rinse. At the same time, contact lens intolerance is increasing maybe due to adsorption of MPS on contact lens leading to MPS releasing on ocular surface with chronic cytotoxic effects. Our purpose was to investigate apoptosis through oxidative stress and mitochondrial injury induced by MPS on conjunctiva. Methods: Four MPS were investigated (OptifreeTM, RenuTM, SolocareTM and CompleteTM) compared to 0.9% NaCl. Cytotoxicity was evaluated using a cytofluorometer (SafireTM, Tecan, France) adapted to microplates after a 15–minute and 3–hour incubation on a human WKD conjunctival cell line. Membrane integrity, reactive oxygen species and anion superoxide overproductions, intracellular metabolism, mitochondrial mass and mitochondrial activity were assessed using neutral red, DCFH–DA, dihydroethidium, alamar blue, nonyl acridine orange and JC–1 tests, respectively. Apoptosis was confirmed with the cell death receptor and caspase activations evaluated using immunochemistry and rhodamine 110–DEVD dye. Results:Different cytotoxicity pathways dependent on the preservative (quaternary ammonium or PHMB–biguanide) were observed. Some MPS induced oxidative stress with increased mitochondrial mass, others induced a decrease in reactive oxygen species production with mitochondrial alterations, but every MPS stimulated apoptosis with cell death receptor activation and caspase induction. We can modulate cell death receptor activation with unpreserved sea derivates. Conclusions: Preservatives as quaternary ammonium and PHMB, used in ophthalmic formulations are known to be cytotoxic and could explain the cytotoxic mechanism induced by MPS. MPS should not be considered as rinse products because they can induce damage to ocular surface and then contact lens intolerance. The implication of cell death receptor is interesting because unpreserved sea derivates could be used as contact lens rinse products.

Keywords: contact lens • cell death/apoptosis • conjunctiva 
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