Mechanisms of retinal damage in chloroquine retinopathy

Ivanina, T.A.; Lebedeva, M. N.; Сакина, Н. Л.; Babizhaev, M. A.; Ermakova, V. N.

doi:10.1007/bf00842190

Cited by 2 publications

(2 citation statements)

References 6 publications

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“…RPE cells largely remain intact, but eventually the POS deteriorate (Ivanina et al, 1983). Although it has been speculated that oxidative stress is a primary mechanism of chloroquine-induced retinal toxicity (Ivanina et al, 1987; Toler, 2004), there is extensive evidence suggesting that chloroquine primarily inhibits lysosomal degradation (Ivanina et al, 1989; Schraermeyer, 1992; Mahon et al, 2004; Peters et al, 2005). The high affinity of chloroquine for melanin and its potential to accumulate within the eye are thought to be an important pathogenic mechanism, but its significance is still obscure.…”

Section: Toxic Effects On the Pigment Epitheliummentioning

confidence: 99%

An Overview on the Toxic Morphological Changes in the Retinal Pigment Epithelium after Systemic Compound Administration

Mecklenburg

Schraermeyer

2007

Toxicol Pathol

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Many medications that are administered systemically for nonocular conditions may evoke ocular toxicological complications. Therefore, the eye is routinely investigated histopathologically in preclinical in vivo toxicity studies. The retinal pigment epithelium is a likely target for systemically administered compounds, since the underlying choroid is highly vascularized. The specialized pigment epithelium has numerous functions that all maintain the integrity and function of photoreceptors. Consequently, toxic effects on the pigment epithelium will eventually affect the neural retina. The potential of pigment epithelial cells to respond to toxic injury is limited, but a standardized terminology to describe its morphological changes does not exist in the scientific literature. Detailed morphologic analysis, however, might allow early detection of retinotoxicity and may provide evidence on the underlying pathomechanism. We here review toxic effects on the pigment epithelium focusing in particular on the morphology of toxic cell injury. Morphological changes comprise hypertrophy, intracytoplasmic accumulation of cellular components, loss of cell polarity, degeneration, metaplasia, and formation of subretinal membranes. Some of these changes are reversible whereas others are permanent, leading to impaired function of the pigment epithelium and eventually to photoreceptor loss and retinal atrophy.

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Section: Toxic Effects On the Pigment Epitheliummentioning

confidence: 99%

An Overview on the Toxic Morphological Changes in the Retinal Pigment Epithelium after Systemic Compound Administration

Mecklenburg

Schraermeyer

2007

Toxicol Pathol

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“…Chloroquine retinopathy is characterized by ocular vascular spasm, macular edema, mottling, the appearance of membraneous cytoplasmic inclusions in the * Dedicated to Professor Dr. G. Zbinden on the occasion of his retirement Abbreviations: GFAP: glial fibrillary acidic protein, MAP: microtubule associated protein, NR: neutral red, MTT: thiazolyblue tetrazoliumbromide, NF: neurofilament, PNA-lectin: Arachis Hypogaea (peanut) lectin, RPE: retinal pigment epithelium, chloroquine: 7-chloro-4'4-diethylamino-1-methylbutylamino quinoline Offprint requests to: A. Bruinink ganglion cells and in the cells of the inner granular layer, in more advanced stages by visual field disturbances and other functional changes, and finally by a complete loss of the outer segments of rod photoreceptor cells (Wilson 1961;Henkind et al 1963;Meier-Ruge 1965;Kearns and Hollenhorst 1966;Carr 1968;Krill et al 1971;Ivanina et al 1983). At present, the mechanisms by which chloroquine induces occular damage are not clear (Ivanina et al 1988;Nagai et al 1987;Titus 1989). Several possible mechanisms have been proposed (Abraham and Hendy 1970;Mackenzie 1970;Stauber et al 1981;Ivanina et al 1983;Fredman et al 1987).…”

Section: Introductionmentioning

confidence: 97%

Neurotoxic effects of chloroquine in vitro

1991

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In order to investigate chloroquine retinopathy, the effect of chloroquine on the viability and differentiation of primary cell cultures of embryonic chick neuronal retina, retinal pigment epithelium (RPE), brain and meninges were investigated. The sensitivity of the cells, measured as reduction of viability, showed the following order: RPE greater than brain greater than meninges greater than neuronal retina. The human serum chloroquine concentration range which leads to ocular damage in vivo was identical to the concentration range in the culture medium which affected RPE viability. In addition, the differentiation of nerve cells in brain cell cultures was affected at much lower chloroquine concentrations than astroglia cells or nerve cells in neuronal retina cell cultures. Some possible mechanisms for chloroquine retinopathy were assessed.

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Mechanisms of retinal damage in chloroquine retinopathy

Cited by 2 publications

References 6 publications

An Overview on the Toxic Morphological Changes in the Retinal Pigment Epithelium after Systemic Compound Administration

An Overview on the Toxic Morphological Changes in the Retinal Pigment Epithelium after Systemic Compound Administration

Neurotoxic effects of chloroquine in vitro

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