Effects of Methyl Mercury in Postnatal Developing Rats

Sakamoto, Mineshi; Nakano, Atsuhiro; Kajiwara, Yuji; Naruse, Ichiro; Fujisaki, Tadashi

doi:10.1006/enrs.1993.1048

Cited by 63 publications

(25 citation statements)

References 12 publications

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“…In fact, the relationship between MeHg-induced motor deficits and MeHg-induced cerebellar damage is a well-described phenomenon [37]. In this regard, we have reported decreased locomotor activity in animals exposed to MeHg during adulthood [38,39] and the early postnatal period [6].…”

Section: Discussionmentioning

confidence: 96%

Postnatal Methylmercury Exposure Induces Hyperlocomotor Activity and Cerebellar Oxidative Stress in Mice: Dependence on the Neurodevelopmental Period

et al. 2006

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During the early postnatal period the central nervous system (CNS) is extremely sensitive to external agents. The present study aims at the investigation of critical phases where methylmercury (MeHg) induces cerebellar toxicity during the suckling period in mice. Animals were treated with daily subcutaneous injections of MeHg (7 mg/kg of body weight) during four different periods (5 days each) at the early postnatal period: postnatal day (PND) 1-5, PND 6-10, PND 11-15, or PND 16-20. A control group was treated with daily subcutaneous injections of a 150 mM NaCl solution (10 ml/kg of body weight). Subjects exposed to MeHg at different postnatal periods were littermate. At PND 35, behavioral tests were performed to evaluate spontaneous locomotor activity in the open field and motor performance in the rotarod task. Biochemical parameters related to oxidative stress (levels of glutathione and thiobarbituric acid reactive substances, as well as glutathione peroxidase and glutathione reductase activity) were evaluated in cerebellum. Hyperlocomotor activity and high levels of cerebellar thiobarbituric acid reactive substances were observed in animals exposed to MeHg during the PND 11-15 or PND 16-20 periods. Cerebellar glutathione reductase activity decreased in MeHg-exposed animals. Cerebellar glutathione peroxidase activity was also decreased after MeHg exposure and the lowest enzymatic activity was found in animals exposed to MeHg during the later days of the suckling period. In addition, low levels of cerebellar glutathione were found in animals exposed to MeHg during the PND 16-20 period. The present results show that the postnatal exposure to MeHg during the second half of the suckling period causes hyperlocomotor activity in mice and point to this phase as a critical developmental stage where mouse cerebellum is a vulnerable target for the neurotoxic and pro-oxidative effects of MeHg.

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Section: Discussionmentioning

confidence: 96%

Postnatal Methylmercury Exposure Induces Hyperlocomotor Activity and Cerebellar Oxidative Stress in Mice: Dependence on the Neurodevelopmental Period

et al. 2006

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“…This selective entry could explain the high susceptibility of cerebellum neurons to mercury toxicity. Indeed, mercury exposure induces motor deficits, targeting cerebellar cells (27,28). Neuromelanin in the substantia nigra also accumulates an extremely high amount of lead.…”

Section: Discussionmentioning

confidence: 99%

New melanic pigments in the human brain that accumulate in aging and block environmental toxic metals

Zecca

Bellei²,

Costi³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

211

355

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Neuronal pigments of melanic type were identified in the putamen, cortex, cerebellum, and other major regions of human brain. These pigments consist of granules 30 nm in size, contained in organelles together with lipid droplets, and they accumulate in aging, reaching concentrations as high as 1.5-2.6 g/mg tissue in major brain regions. These pigments, which we term neuromelanins, contain melanic, lipid, and peptide components. The melanic component is aromatic in structure, contains a stable free radical, and is synthesized from the precursor molecule cysteinyl-3,4-dihydroxyphenylalanine. This contrasts with neuromelanin of the substantia nigra, where the melanic precursor is cysteinyl-dopamine. These neuronal pigments have some structural similarities to the melanin found in skin. The precursors of lipid components of the neuromelanins are the polyunsaturated lipids present in the surrounding organelles. The synthesis of neuromelanins in the various regions of the human brain is an important protective process because the melanic component is generated through the removal of reactive/toxic quinones that would otherwise cause neurotoxicity. Furthermore, the resulting melanic component serves an additional protective role through its ability to chelate and accumulate metals, including environmentally toxic metals such as mercury and lead.lipids ͉ neuromelanin ͉ brain aging ͉ neurodegenerative

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“…Recent reviews on the neurotoxicology of mercury and its compounds provide more detailed information (4, 32, 36). (26).…”

Section: Introductionmentioning

confidence: 99%

Review Article: A Review of Experimental Methylmercury Toxicity in Rats: Neuropathology and Evidence for Apoptosis

Nagashima

1997

Toxicol Pathol

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Effects of Methyl Mercury in Postnatal Developing Rats

Cited by 63 publications

References 12 publications

Postnatal Methylmercury Exposure Induces Hyperlocomotor Activity and Cerebellar Oxidative Stress in Mice: Dependence on the Neurodevelopmental Period

Postnatal Methylmercury Exposure Induces Hyperlocomotor Activity and Cerebellar Oxidative Stress in Mice: Dependence on the Neurodevelopmental Period

New melanic pigments in the human brain that accumulate in aging and block environmental toxic metals

Review Article: A Review of Experimental Methylmercury Toxicity in Rats: Neuropathology and Evidence for Apoptosis

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