Different vulnerability of rat retinal cells to methylmercury exposure

Goto, Yoshinobu; Shigematsu, Junya; Tobimatsu, Shozó; Sakamoto, Taiji; Kato, Motohiro

doi:10.1076/ceyr.23.3.171.5469

Cited by 9 publications

(6 citation statements)

References 9 publications

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“…Very few studies of methylmercury and retina or pineal gland have been reported. − Goto et al examined methylmercury chloride effects upon electro-retinograms in rats and observed dose- and time-dependent changes, suggesting that photoreceptors are sensitive to methylmercury . Weber et al showed long-term functional changes in the retinal bipolar cells of the adult zebrafish following developmental exposure to methylmercury chloride .…”

Section: Results and Discussionmentioning

confidence: 99%

Methylmercury Targets Photoreceptor Outer Segments

et al. 2013

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Human populations experience widespread low level exposure to organometallic methylmercury compounds through consumption of fish and other seafood. At higher levels, methylmercury compounds specifically target nervous systems, and among the many effects of their exposure are visual disturbances, including blindness, which previously were thought to be due to methylmercury-induced damage to the visual cortex. Here, we employ high-resolution X-ray fluorescence imaging using beam sizes of 500 × 500 and 250 × 250 nm(2) to investigate the localization of mercury at unprecedented resolution in sections of zebrafish larvae ( Danio rerio ), a model developing vertebrate. We demonstrate that methylmercury specifically targets the outer segments of photoreceptor cells in both the retina and pineal gland. Methylmercury distribution in both tissues was correlated with that of sulfur, which, together with methylmercury's affinity for thiolate donors, suggests involvement of protein cysteine residues in methylmercury binding. In contrast, in the lens, the mercury distribution was different from that of sulfur, with methylmercury specifically accumulating in the secondary fiber cells immediately underlying the lens epithelial cells rather than in the lens epithelial cells themselves. Since methylmercury targets two main eye tissues (lens and photoreceptors) that are directly involved in visual perception, it now seems likely that the visual disruption associated with methylmercury exposure in higher animals including humans may arise from direct damage to photoreceptors, in addition to injury of the visual cortex.

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Section: Results and Discussionmentioning

confidence: 99%

Methylmercury Targets Photoreceptor Outer Segments

et al. 2013

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“…Earlier studies performed at the cellular level showed that methylmercury affects rods but not cones (Fox & Sillman, 1979); more recently, an effect in cones has been shown (Goto et al, 2001). It was also demonstrated that rat retinal cells have different vulnerabilities to methylmercury, cones being more sensitive than rods, bipolar cells, and Müller cells (Goto et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…It was also demonstrated that rat retinal cells have different vulnerabilities to methylmercury, cones being more sensitive than rods, bipolar cells, and Müller cells (Goto et al, 2001). Intracellular recordings from rods showed that the effect of mercuric chloride was an early increase followed by depression of the rod response (Tessier-Lavigne et al, 1985).…”

Section: Discussionmentioning

confidence: 99%

Multifocal and full-field electroretinogram changes associated with color-vision loss in mercury vapor exposure

et al. 2004

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We evaluated the color vision of mercury-contaminated patients and investigated possible retinal origins of losses using electroretinography. Participants were retired workers from a fluorescent lamp industry diagnosed with mercury contamination (n = 43) and age-matched controls (n = 21). Color discrimination was assessed with the Cambridge Colour Test (CCT). Retinal function was evaluated by using the ISCEV protocol for full-field electroretinography (full-field ERG), as well as by means of multifocal electroretinography (mfERG). Color-vision losses assessed by the CCT consisted of higher color-discrimination thresholds along the protan, deutan, and tritan axes and significantly larger discrimination ellipses in mercury-exposed patients compared to controls. Full-field ERG amplitudes from patients were smaller than those of the controls for the scotopic response b-wave, maximum response, sum of oscillatory potentials (OPs), 30-Hz flicker response, and light-adapted cone response. OP amplitudes measured in patients were smaller than those of controls for O2 and O3. Multifocal ERGs recorded from ten randomly selected patients showed smaller N1-P1 amplitudes and longer latencies throughout the 25-deg central field. Full-field ERGs showed that scotopic, photopic, peripheral, and midperipheral retinal functions were affected, and the mfERGs indicated that central retinal function was also significantly depressed. To our knowledge, this is the first demonstration of retinal involvement in visual losses caused by mercury toxicity.

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“…Although the cerebellum and cortex are the best-characterized targets of MeHg toxicity in both humans and rodents, some studies have demonstrated that retinal cells are also vulnerable to MeHg damage (8). However, the mechanisms of neurotoxicity induced by MeHg in these cells are poorly understood.…”

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confidence: 99%

Methylmercury intoxication activates nitric oxide synthase in chick retinal cell culture

Herculano

Crespo-López

Lima

et al. 2006

Braz J Med Biol Res

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The visual system is a potential target for methylmercury (MeHg) intoxication. Nevertheless, there are few studies about the cellular mechanisms of toxicity induced by MeHg in retinal cells. Various reports have indicated a critical role for nitric oxide synthase (NOS) activation in modulating MeHg neurotoxicity in cerebellar and cortical regions. The aim of the present study is to describe the effects of MeHg on cell viability and NOS activation in chick retinal cell cultures. For this purpose, primary cultures were prepared from 7-dayold chick embryos: retinas were aseptically dissected and dissociated and cells were grown at 37ºC for 7-8 days. Cultures were exposed to MeHg (10 µM, 100 µM, and 1 mM) for 2, 4, and 6 h. Cell viability was measured by MTT method and NOS activity by monitoring the conversion of L- [H 3 ]-arginine to L-[H 3 ]-citrulline. The incubation of cultured retina cells with 10 and 100 µM MeHg promoted an increase of NOS activity compared to control (P < 0.05). Maximum values (P < 0.05) were reached after 4 h of MeHg incubation: increases of 81.6 ± 5.3 and 91.3 ± 3.7%, respectively (data are reported as mean ± SEM for 4 replicates). MeHg also promoted a concentration-and timedependent decrease in cell viability, with the highest toxicity (a reduction of about 80% in cell viability) being observed at the concentration of 1 mM and after 4-6 h of incubation. The present study demonstrates for the first time the modulation of MeHg neurotoxicity in retinal cells by the nitrergic system.

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Different vulnerability of rat retinal cells to methylmercury exposure

Cited by 9 publications

References 9 publications

Methylmercury Targets Photoreceptor Outer Segments

Methylmercury Targets Photoreceptor Outer Segments

Multifocal and full-field electroretinogram changes associated with color-vision loss in mercury vapor exposure

Methylmercury intoxication activates nitric oxide synthase in chick retinal cell culture

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