Effects of mercury intoxication on the response of horizontal cells of the retina of thraira fish (Hoplias malabaricus)

Methyl mercury (MeHg) is highly neurotoxic, affecting visual function in addition to other central nervous system functions. The effect of mercury intoxication on the amplitude of horizontal cell responses to light was studied in the retina of the fish Hoplias malabaricus. Intracellular responses were recorded from horizontal cells of fish previously intoxicated with MeHg by intraperitoneal injection (IP group) or by trophic exposure (T group). Only one retina per fish was used. The doses of MeHg chloride administered to the IP group were 0.01, 0.05, 0.1, 1.0, 2.0, and 6.0 mg/kg. The amplitudes of the horizontal cell responses were lower than control in individuals exposed to 0.01 (N = 4 retinas), 0.05 (N = 2 retinas) and 0.1 mg/kg (N = 1 retina), whereas no responses were recorded in the 1.0, 2.0, and 6.0 mg/kg groups. T group individuals were fed young specimens of Astyanax sp previously injected with MeHg corresponding to 0.75 (N = 1 retina), 0.075 (N = 8 retinas) or 0.0075 (N = 4 retinas) mg/kg fish body weight. After 14 doses, one every 5 days, the amplitude of the horizontal cell response was higher than control in individuals exposed to 0.075 and 0.0075 mg/kg, and lower in individuals exposed to 0.75 mg/kg. We conclude that intoxication with MeHg affects the electrophysiological response of the horizontal cells in the retina, either reducing or increasing its amplitude compared to control, and that these effects are related to the dose and/or to the mode of administration.

Effects of low-dose exposure of rat fetuses pancreas to methylmercury: morphometric and stereologic studies

El cloruro de metilmercurio (20 mg/kg de peso corporal), cuando fue administrado oralmente a ratas Wistar en el día 10 de la preñez, dio origen a fetos y placentas de menor peso. Hubo muerte y reabsorción fetal, a pesar de no existir malformaciones macroscópicas. Histológicamente, los acinos pancreáticos, aumentados de tamaño, mostraron forma irregular con grandes núcleos picnóticos en los animales tratados. Los núcleos variaron en tamaño y forma. El lumen de los acinos era menor. En el citoplasma, débilmente eosinófilo, se observaron escasos gránulos de secreción. Los ductos eran desorganizados y presentaron núcleos mayores. Los islotes pancreáticos eran inmaduros y menos organizados. Las alteraciones morfológicas fueron analizadas mediante técnicas morfométricas y estereológicas

Morphologic, morphometric and stereologic analysis of palatine mucosa of rat fetuses after methylmercury administration to the dams during pregnancy

El cloruro de metilmercurio, administrado oralmente a ratas wistar en el día 10 de la gestación (20 mg/kg), originó fetos y placentas menores y cordones umbilicales más cortos. Las incidencias de mortalidad y de reabsorciones se encontraron aumentadas. Histológicamente, el epitelio del paladar duro fue más fino, debido a la reducción significativa del espesor de capa espinosa, con células de menor tamaño y más numerosas. Por otro lado, el epitelio del paladar blando no mostró alteraciones del espesor, y las células presentaron las mismas características. Morfométriucamente, el vólumen celular estaba disminuido en los epitelios del paladar duro y blando. La densidad numérica celular fue mayor en los epitelios del paladar blando y duro. No se observaron alteraciones del espesor de la queratina en el epitelio de los dos regiones palatinas.

Effects of methylmercury exposure during the second stage of rapid postnatal brain growth on negative geotaxis and on delta-aminolevulinate dehydratase of suckling rats

In the present study, we examined the effects of exposure to methylmercury (0, 2.3, 4.6, 6.9 and 9.2 mg/kg, daily for 5 consecutive days, sc) during the second stage of rapid postnatal brain development (8 to 12 days of age) on the sulfhydryl-containing enzyme delta-aminolevulinate dehydratase (ALA-D, E.C. 4.2.1.24) from brain, liver and kidney and on motor performance (latency to complete a negative geotaxis response) of rats. ALA-D specific activity of 13-day old rats of both sexes (7-12 per group) was reduced significantly in rats treated with 6.9 mg/kg and 9.2 mg/kg in brain (about 40 per cent , P < 0.05) and in liver (about 25 per cent , P < 0.05). Renal ALA-D specific activity was not affected by methylmercury treatment. The in vitro IC50 for inhibition of brain, liver and renal ALA-D was 79.3, 81.8 and 39.1 microM, respectively. The latency to complete the negative geotaxis response of 12-day old rats was increased by 6.9 (7.9 +/- 0.7 s, mean +/- SEM) and 9.2 mg/kg methylmercury (7.8 +/- 0.5 s) when compared with control rats (5.8 +/- 0.3 s), suggesting an impairment in motor performance of exposed rats. These results demonstrate that exposure to relatively high doses of methylmercury during the second stage of brain development causes a significant reduction in brain and hepatic ALA-D. The absence of inhibition of ALA-D by lower doses may be related to the relatively low in vitro sensitivity of the enzyme to methylmercury. The possible involvement of ALA-D inhibition on the neurotoxicity of methylmercury deserves additional investigation

Distribution of mercury and evaluation of testicular steroidogenesis in mercuric chloride and methylmercury administered rats.

Intraperitoneal administration of methylmercury chloride (MMC) and mercuric chloride (MC) to male rats in doses of 5, 10 micrograms MMC/kg or 50, 100 micrograms MC/kg for 90 days induced cellular disintegration of Leydig cells which was conspicuous on day 30 and onwards in the exposed groups. Progressive degeneration of Leydig cells and decrease in their nuclear diameter and population were associated with gradual increase in deposition of mercury. Gradual diminution of 3 beta-hydroxy-delta 5-steroid dehydrogenase activity in Leydig cells after MMC or MC treatment was correlated with different structural deformations of the cells over 90 days. Moreover, a significant decrease in serum testosterone levels by day 90 confirmed steroidogenic impairment after MMC or MC treatment.