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ToxSci Advance Access published online on June 15, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfi224
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© The Author 2005. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received March 15, 2005
Accepted June 3, 2005

Neurotoxicology

The effects of methylmercury on mitochondrial function and reactive oxygen species formation in rat striatal synaptosomes are age-dependent

Anne Dreiem 1*, Caitlyn C. Gertz 1, and Richard F. Seegal 2

1 New York State Department of Health, Wadsworth Center, Albany, New York, 12201
2 New York State Department of Health, Wadsworth Center, Albany, New York, 12201; School of Public Health, University at Albany, Albany, New York, 12222

* To whom correspondence should be addressed.
Anne Dreiem, E-mail: adreiem{at}wadsworth.org


  Abstract

Methylmercury (MeHg) is especially toxic to the developing central nervous system. In order to understand the reasons for this age-dependent vulnerability, we compared the effects of MeHg on formation of reactive oxygen species (ROS) and mitochondrial function in striatal synaptosomes obtained from rats of various ages. Basal ROS levels were greater, and basal mitochondrial function was lower, in synaptosomes from younger animals, compared to adult animals. MeHg induced ROS formation in synaptosomes from rats of all ages, although the increases were greatest in synaptosomes from the younger animals. MeHg also reduced mitochondrial metabolic function, as assessed by MTT reduction, as well as mitochondrial membrane potential; again, the greatest changes were seen in synaptosomes from early postnatal animals. These age-dependent differences in susceptibility to MeHg are most likely due to a less efficient ROS detoxifying system and lower activity of mitochondrial enzymes in tissue from young animals.

Keywords: Methylmercury; synaptosomes; reactive oxygen species; mitochondria; development.
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