PURPOSE: The tear film is essential for the integrity of the ocular surface. In ocular diseases such as dry eye syndrome (DES), tear film osmolarity is increased relative to normal physiological conditions. DES can be caused by deficiency in lachrymation, hyperevaporation, or surface alterations. Carnitines, shown to have osmoregulatory properties, are thought to regulate tear film osmolarity, thus protecting the corneal surface from damage. We investigated the presence of carnitine in tears, compared tear carnitine concentrations in healthy subjects and in DES patients and speculate on carnitine's potential role as a protective agent in the tear film. METHODS: Tears were collected from 10 healthy subjects and 10 DES patients. Carnitine levels were assessed by high performance liquid chromatography-mass spectrometry. RESULTS: Carnitine and its derivatives were detected in the tear samples. In DES patients, concentrations were substantially lower than in healthy subjects; the mean concentrations were L-carnitine, 3.27 +/- 0.80 and 8.94 +/- 0.50 microMol/L; L-acetylcarnitine, 1.66 +/- 0.50 and 3.05 +/- 0.65 microMol/L; and L-propionylcarnitine, 0.30 +/- 0.11 and 0.57 +/- 0.13 microMol/L, in DES patients and healthy subjects, respectively. CONCLUSIONS: Although increased tear film osmolarity has been previously observed in DES patients, our study showed lower carnitine levels in DES patients than in healthy subjects, rather than the increased levels expected, although a causal relationship between carnitine levels and hyperosmolarity has not been established. The damage to ocular surface cells because of exposure to hypertonic tear film observed in DES may be partially because of an imbalance in the concentration of carnitine molecules in the tear film relative to the ocular surface cells. We propose, therefore, that carnitine solutions may have a role in preventing the adverse effects of observed hyperosmolarity and suggest that further studies are now warranted to investigate the clinical application of carnitine in the treatment of DES.
PURPOSE: The tear film is essential for the integrity of the ocular surface. In ocular diseases such as dry eye syndrome (DES), tear film osmolarity is increased relative to normal physiological conditions. DES can be caused by deficiency in lachrymation, hyperevaporation, or surface alterations. Carnitines, shown to have osmoregulatory properties, are thought to regulate tear film osmolarity, thus protecting the corneal surface from damage. We investigated the presence of carnitine in tears, compared tear carnitine concentrations in healthy subjects and in DES patients and speculate on carnitine's potential role as a protective agent in the tear film. METHODS: Tears were collected from 10 healthy subjects and 10 DES patients. Carnitine levels were assessed by high performance liquid chromatography-mass spectrometry. RESULTS:Carnitine and its derivatives were detected in the tear samples. In DES patients, concentrations were substantially lower than in healthy subjects; the mean concentrations were L-carnitine, 3.27 +/- 0.80 and 8.94 +/- 0.50 microMol/L; L-acetylcarnitine, 1.66 +/- 0.50 and 3.05 +/- 0.65 microMol/L; and L-propionylcarnitine, 0.30 +/- 0.11 and 0.57 +/- 0.13 microMol/L, in DES patients and healthy subjects, respectively. CONCLUSIONS: Although increased tear film osmolarity has been previously observed in DES patients, our study showed lower carnitine levels in DES patients than in healthy subjects, rather than the increased levels expected, although a causal relationship between carnitine levels and hyperosmolarity has not been established. The damage to ocular surface cells because of exposure to hypertonic tear film observed in DES may be partially because of an imbalance in the concentration of carnitine molecules in the tear film relative to the ocular surface cells. We propose, therefore, that carnitine solutions may have a role in preventing the adverse effects of observed hyperosmolarity and suggest that further studies are now warranted to investigate the clinical application of carnitine in the treatment of DES.
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