Chronic effects of methylmercury (MeHg) were examined pathologically in male Wistar rats fed on diet containing 0, 1 or 5 ppm Hg (as MeHg) for two years. Organs including the central nervous tissues were examined histopathologically using hematoxylin and eosin (H & E), Klüver-Barrera (KB), PAS or phenol-congo red stains. The peripheral nerve system tissues were also examined, using H & E and trichrome stains. Furthermore, immunoglobulins of renal specimens were demonstrated by direct immunofluorescence microscopy. Localization of mercury in the paraffin-embedded sections of the nervous tissue, kidney, liver, pancreas, spleen and testis was demonstrable by the photoemulsion histochemical method. In the 5 ppm group, mercury was readily detectable in tissues of the rats exposed for one year, one and half years, two years and two and half years. Mercury was detected in the cells of the brain such as neurons, neuroglial cells, and phagocytes, and also in most organs, particularly in the epithelium of renal tubules, liver cells, myocardium, in the macrophages of pancreas, spleen and testis. In the 1 ppm group, mercury was detectable in the epithelium of renal tubules and liver cells. Fibrosis of the glomeruli was found in the rat group given a high dose of methylmercury with all experimental methods. Granular IgG, IgM and C3 deposits were demonstrated in the glomeruli by direct immunofluorescence microscopy. The etiology of the pathological changes of glomeruli was suspected to be autoimmune glomerulopathy due to inorganic mercury filtration for a long time. It was difficult to determine the clinical signs and symptoms and pathological changes in the nervous system in spite of the deposition of mercury in the brain.

To examine chronic effects of methylmercury (MeHg), male Wistar rats were fed on MeHg-contaminated diet, 0, 1 and 5 ppm Hg, under a restricted feeding schedule of 16 g/rat/day for 6 days a week. Rats were killed at 6-month intervals for examination of Hg accumulation, tissue levels of glutathione, metallothionein and lipid peroxide, as well as anti-oxidative enzyme activities. The survival of the 5 ppm Hg group, 50% of which died by the end of 32nd month of the exposure, was somewhat shorter than control and 1 ppm Hg groups, 50% of which survived for 34 months. Although the rats showed no neurological signs or decreased body weight gain even in 5 ppm Hg-exposed group until the end of the 2nd year, crossing of hind limb was evident after 2.5 years in all three groups. Accordingly, the neurological sign observed here possibly due to aging rather than MeHg toxicity. Tissue Hg levels showed a dose-dependent accumulation except for the kidney, where the highest Hg accumulation was observed among tissues examined. Renal Hg levels in the 1 ppm group showed about 40% of those in the 5 ppm group. Significant effects by MeHg were evident only in the kidney, where glutathione and metallothionein levels increased in both MeHg-exposed groups. However, lipid peroxide levels elevated only in 1 ppm group. Among the antioxidative enzymes examined, the renal glutathione peroxidase was found to be the most labile enzyme against MeHg exposure. Renal dysfunction suggested by increased plasma creatinine levels was also significant in 5 ppm Hg rats at 2 years. Furthermore, anemia which would be caused by reduced erythropoietin production in the kidney was also evident in this group. The present study suggested that the kidney was the most susceptible organ against MeHg toxicity under the present exposure schedule and that the renal dysfunction might at least partly account for the shortened survival in 5 ppm Hg rats.

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ABSTRACTcontaining MeHg-L-cysteine complexes in aqueous solution, which had been reverse-extracted from the -

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