Effects of mercuric chloride on spatial memory deficit induced by beta-amyloid and evaluation of mitochondrial function markers in the hippocampus of rats
Mercury is a highly poisonous heavy metal found in the environment abundantly in its inorganic form. Although some pieces of evidence have been provided about the possible role of inorganic mercury in the pathology of Alzheimer’s disease (AD), its effect on cognitive and mitochondrial functions have not yet been completely understood. Thus, the purpose of the present study was to examine the effects of chronic exposure to mercuric chloride (0.4, 0.8 and 1.6 mg/kg/day for 3 weeks) through drinking water (by gavage) on spatial learning and memory and hippocampal mitochondrial function in beta-amyloid treated rats (1µg/µL per side, intrahippocampally). Acquisition and retention of spatial memory were evaluated by the Morris water maze (MWM) test. Several parameters of hippocampal mitochondrial function were also measured. The results indicated that mercury impaired spatial learning, memory and aggravated Aβ-induced memory impairments are in a concentration-dependent manner. Further, mercury exposure resulted in a significant increase in ROS generation, MMP collapse, mitochondrial swelling, glutathione oxidation, lipid peroxidation, outer membrane damage, reduced cytochrome c oxidase (complex IV) activity and elevated ADP/ATP ratio in the rats' hippocampus. The findings of the current study revealed that chronic mercury exposure leads to mitochondrial dysfunction which results in spatial memory impairments. The results also showed that mercury can potentiate the toxic effects of Aβ on spatial memory and hippocampal mitochondrial function.