CHLOROQUINE-INDUCED LIPIDOSIS IN THE RAT RETINA - FUNCTIONAL AND MORPHOLOGICAL-CHANGES AFTER WITHDRAWAL OF THE DRUG

Background: The antimalarial and antirheumatic drug chloroquine is one of the most infamous amphiphilic cationic drugs in clinical ophthalmo logy. It is known to cause lipidosis and photoreceptor degeneration in the human and the rat retina. Methods: We treated female albino Wista r rats (mean weight 200 g) orally weight chloroquine (95 mg/kg body we ight for 12 weeks, followed by a period of 4 months with normal feed. After initial electroretinography in all rats, measurements were made after 4 and 12 weeks of treatment and 16 weeks after withdrawal. The r ats were prepared for histological examination. Results: Treatment of rats with chloroquine caused severe lipidosis in the neuroretina: phot oreceptor cell degeneration was slight. After 12 weeks of treatment, t he b-wave amplitude was reduced to 30% of the initial value; the a-wav e amplitude was reduced, but remained within the range of normal value s. After withdrawal of chloroquine the lipidosis remitted, but the deg eneration of the photoreceptor cell layer continued to progress. Despi te remission of lipidosis, electroretinography demonstrated functional disturbances, marked by reduction of the a- and b-wave amplitudes to 25% and 16% of initial values. respectively. Conclusions: Seen from th e point of view of function, it is doubtful whether lipidosis is the p rimary cause of changes in the electroretinogram or of receptor cell d egeneration.