Leonardo Oliveira Bittencourt and Aline Dionizio contributed equally to this work. Methylmercury MeHg is an important toxicant that causes cognitive dysfunctions in humans. This study aimed to investigate the proteomic and biochemical alterations of the hippocampus associated with behavioural consequences of low doses of MeHg in a long-term exposure model, and to realistically mimic in vivo the result of human exposure to this toxicant.
Adult Wistar male rats were exposed to a dose of MeHg at 0. Total mercury Hg content was significantly increased in the hippocampal parenchyma. The increase in the Hg levels was capable of reducing neuron and astrocyte cell density in the CA1, CA3, hilus and dentate gyrus regions, increasing both malondialdehyde and nitrite levels and decreasing antioxidant capacity against peroxyl radicals. The proteomic analysis detected proteins with altered expression due to MeHg exposure, including proteins with no expression, proteins with de novo expression and proteins with up- or down-regulated expression.
This proteomic approach revealed alterations in pathways related to chemical synapses, metabolism, amino acid transport, cell energy, neurodegenerative processes and myelin maintenance.
Therefore, even at low doses of MeHg exposure, it is possible to cause hippocampal damage in adult rats at many organisational levels, triggering oxidative stress and proteome misbalance, featuring a neurodegenerative process and culminating in long- and short-term memory and learning deficits.
Investigation of biochemical and morphological parameters underlying the cognitive dysfunction after MeHg exposure. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account. Advanced Search. Search Menu. Article Navigation.
