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Neurotoxic response of infant monkeys to methylmercury
Abstract:
Four infant monkeys were dosed orally with 500 microgram Hg/kg body wt./day /as methylmercury (MeHg) chloride dissolved sodium carbonate) beginning at 1 day of age. Neurological and behavioral signs of MeHg toxicity and blood Hg levels were monitored weekly. At first sign of MeHg intoxication, dosing with MeHg was terminated and the infants were monitored to assess reversal of the signs of MeHg toxicity. The first signs of MeHg toxicity, exhibited as a loss in dexterity and locomotor ability, were observed after 28--29 days of treatment; the blood Hg levels were 8.0--9.4 microgram Hg/g blood. Dosing was terminated at 28--29 days of treatment but the signs of MeHg toxicity continued to develop. The infants became ataxic, blind, comatose and were necropsied at 35--43 days after initiating treatment with MgHg. The mercury concentrations in tissues analyzed after necropsy were highest in liver (55.8 +/- 3.2 microgram Hg/g) followed by occipital cortex (35.6 +/- 4.8 microgram Hg/g) renal cortex (32.8 +/- 1.6 microgram Hg/g). The frontal and temporal cortices had 27.0 +/- 3.4 and 29.6 +/- 4.9 microgram Hg/g respectively while the cerebellar Hg concentration averaged 13.0 +/- 1.5 microgram Hg/g. The mean blood/brain ratio was 0.21 +/- 0.4. Histopathologic lesions were marked in the cerebrum with less severe lesions in the cerebellar nuclei. The Purkinje and granular cells of the cerebellar vermis appeared histologically normal. Lesions were not observed in the peripheral nervous system. The signs of MeHg intoxication, the tissue distribution of MeHg and histopathologic lesions observed in the infant monkeys were similar to those reported for adult monkeys.
Insights
Infant monkeys exposed to methylmercury (MeHg) chloride developed severe neurological and behavioral toxicity, similar to adults. Despite stopping exposure, symptoms progressed, leading to severe outcomes and significant mercury accumulation in tissues.
Area of Science:
- Toxicology
- Neuroscience
- Developmental Biology
Background:
- Methylmercury (MeHg) is a potent neurotoxin with known effects on adult nervous systems.
- Limited data exists on the specific neurotoxic effects and tissue distribution of MeHg in infant non-human primates.
- Understanding MeHg toxicity in early development is crucial for assessing risks to vulnerable populations.
Purpose of the Study:
- To investigate the neurological and behavioral effects of oral methylmercury (MeHg) chloride exposure in infant monkeys.
- To determine the blood and tissue mercury levels associated with MeHg intoxication in young primates.
- To compare the histopathological lesions and toxicological profile of MeHg in infant monkeys to that of adult monkeys.
Main Methods:
- Four infant monkeys were orally administered methylmercury (MeHg) chloride daily from one day of age.
- Neurological, behavioral, and blood mercury levels were monitored weekly throughout the study.
- Exposure was terminated upon the first signs of toxicity, with subsequent monitoring for reversal or progression of symptoms.
Main Results:
- Signs of MeHg toxicity, including loss of dexterity and locomotor ability, appeared after 28-29 days of exposure (blood Hg: 8.0–9.4 µg/g).
- Despite termination of dosing, toxicity signs progressed to ataxia, blindness, and coma, with necropsy occurring 35-43 days post-initiation.
- Highest mercury concentrations were found in the liver, occipital cortex, and renal cortex; histopathology revealed marked cerebral lesions.
Conclusions:
- Infant monkeys exhibit significant neurodevelopmental susceptibility to methylmercury (MeHg) chloride.
- The observed signs of toxicity, tissue distribution, and histopathological lesions in infants closely resemble those reported in adult monkeys.
- These findings highlight the severe neurotoxic potential of MeHg during early development, with limited recovery observed after exposure cessation.