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Chronic effects of methylmercury in rats. I. Biochemical aspects
A Yasutake1, A Nakano, K Miyamoto
1National Institute for Minamata Disease, Japan.
Abstract:
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.
Insights
Chronic methylmercury (MeHg) exposure primarily impacts the kidney in rats, causing dysfunction and reduced survival. Neurological signs observed were likely due to aging, not MeHg toxicity.
Area of Science:
- Toxicology
- Environmental Health
- Biochemistry
Background:
- Methylmercury (MeHg) is a potent neurotoxin with known chronic health effects.
- Understanding MeHg's impact on organ systems beyond the nervous system is crucial for comprehensive risk assessment.
- Kidney function and oxidative stress markers are key indicators of heavy metal toxicity.
Purpose of the Study:
- To investigate the chronic effects of methylmercury (MeHg) exposure on Wistar rats.
- To determine the primary target organ and mechanisms of MeHg toxicity under prolonged, low-dose exposure.
- To evaluate the impact of MeHg on renal function, oxidative stress, and survival rates.
Main Methods:
- Male Wistar rats were fed diets containing 0, 1, or 5 ppm mercury (Hg) for up to 34 months.
- Tissue mercury accumulation, glutathione, metallothionein, and lipid peroxide levels were measured.
- Antioxidative enzyme activities, plasma creatinine, and survival rates were assessed at 6-month intervals.
Main Results:
- Kidneys showed the highest Hg accumulation in a dose-dependent manner, with significant increases in glutathione and metallothionein.
- Lipid peroxide levels increased in the 1 ppm group, and renal glutathione peroxidase activity decreased.
- Renal dysfunction (elevated creatinine) and anemia were observed in the 5 ppm group after 2 years, correlating with shortened survival.
Conclusions:
- The kidney is the most susceptible organ to chronic methylmercury (MeHg) toxicity under the tested exposure conditions.
- MeHg-induced renal dysfunction, potentially leading to anemia, contributes to reduced survival rates.
- Observed neurological signs in aged rats were likely unrelated to MeHg toxicity.