Copper and zinc serum levels in Stargardt's disease and retinitis pigmentosa
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Psilas, K.
Kalfakakou, V.
Kalogeropoulos, C.
Kitsos, G.
Zoumpouli, E.
Aspiotis, M.
Galani, A.
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peer-reviewed
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Trace Elements and Electrolytes
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Copper (Cu) and zinc (Zn) are essential trace elements for the structure and function of the retina, particularly for the pigment epithelium and photoreceptors, where they participate as coenzymes in very important reactions. This study was to determine whether patients with Stargardt's disease and with typical retinitis pigmentosa show changes in serum levels for Cu and Zn, Serum analysis for Cu and Zn concentrations was performed by means of a Perkin Elmer 560 atomic absorption spectrophotometer, in 10 patients with retinitis pigmentosa (group RP), 10 patients with Stargardt's disease (group St) and 10 normal individuals (group N) of the same age range, all were inhabitants of the same region. Statistical analysis of the results was carried out using the Student's t test. The mean serum levels (+/- SD) of Zn (mu g/ml) in groups RP, St, aad N were 0.51 +/- 0.1, 0.79 +/- 0.1, and 0.98 +/- 0.15, respectively. The mean serum levels (+/- SD) of Cu (mu g/ml) in groups RP, St, and N were 1.04 +/- 0.2, 0.95 +/- 0.14, and 0.94 +/- 0.1, respectively, Zinc serum levels were found to be significantly lower (p < 0.001) in retinitis pigmentosa and Stargardt's disease (p = 0.003) compared to those of normal subjects. In addition, zinc serum levels were significantly lower (p < 0.001) in patients with retinitis pigmentosa compared to those with Stargardt's disease. Cu serum levels did not differ significantly between the groups. Our results suggest that these 2 retinal diseases are associated with disturbances mainly of zinc metabolism. Zn serum levels difference between Stargardt's disease and typical retinitis pigmentosa is probably related to the pathophysiology and type of lesions in these diseases.
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copper, retinitis pigmentosa, stargardt's disease, trace elements, zinc, macular degeneration, fundus-flavimaculatus, retinal dysfunction, rds gene, dystrophy, metabolism, deficiency, taurine
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<Go to ISI>://A1997WV69800007
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en
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Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής