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Oxidative Medicine and Cellular Longevity
Volume 2018 (2018), Article ID 7878050, 11 pages
Research Article

Hippocampal Dysfunction Provoked by Mercury Chloride Exposure: Evaluation of Cognitive Impairment, Oxidative Stress, Tissue Injury and Nature of Cell Death

1Laboratory of Functional and Structural Biology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil
2Laboratory of Pharmacology of Inflammation and Behavior, Institute of Health Sciences, Federal University of Pará, Belém, PA, Brazil
3Laboratory of Ecotoxicology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil
4Laboratory of Tissue Culture and Cytogenetics, Evandro Chagas Institute, Ananindeua, PA, Brazil
5Laboratory of Molecular Pharmacology, Institute of Biological Sciences, Federal University of Pará, Belém, PA, Brazil

Correspondence should be addressed to Rafael Rodrigues Lima; rb.apfu@amilafar

Received 22 November 2017; Revised 31 January 2018; Accepted 21 February 2018; Published 10 April 2018

Academic Editor: Julia Bornhorst

Copyright © 2018 Walessa Alana Bragança Aragão et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Mercury (Hg) is a highly toxic metal, which can be found in its inorganic form in the environment. This form presents lower liposolubility and lower absorption in the body. In order to elucidate the possible toxicity of inorganic Hg in the hippocampus, we investigated the potential of low doses of mercury chloride (HgCl2) to promote hippocampal dysfunction by employing a chronic exposure model. For this, 56 rats were exposed to HgCl2 (0.375 mg/kg/day) via the oral route for 45 days. After the exposure period, the animals were submitted to the cognitive test of fear memory. The hippocampus was collected for the measurement of total Hg levels, analysis of oxidative stress, and evaluation of cytotoxicity, apoptosis, and tissue injury. It was observed that chronic exposure to inorganic Hg promotes an increase in mercury levels in this region and damage to short- and long-term memory. Furthermore, we found that this exposure model provoked oxidative stress, which led to cytotoxicity and cell death by apoptosis, affecting astrocytes and neurons in the hippocampus. Our study demonstrated that inorganic Hg, even with its low liposolubility, is able to produce deleterious effects in the central nervous system, resulting in cognitive impairment and hippocampal damage when administered for a long time at low doses in rats.