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 abundantly found in the environment in its inorganic form. Although 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 the chronic exposure to mercuric chloride (0.4, 0.8 and 1.6 mg kg-1 per day for 3 weeks) through drinking water (by gavage) on spatial learning and memory and hippocampal mitochondrial function in beta-amyloid treated rats (1 µg per µL per side, intrahippocampally). The 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 and memory as well as aggravated Aß-induced memory impairments in a concentration-dependent manner. Furthermore, mercury exposure resulted in a significant increase in ROS generation, MMP collapse, mitochondrial swelling, glutathione oxidation, lipid peroxidation, and outer membrane damage. In addition, a reduced cytochrome c oxidase (complex IV) activity and elevated ADP/ATP ratio in the rats' hippocampus was also observed. The findings of the current study revealed that chronic mercury exposure led to mitochondrial dysfunction, which resulted in spatial memory impairments. The results also showed that mercury can exacerbate the toxic effects of Aß on spatial memory and hippocampal mitochondrial function.

Molecular and biochemical evidence on the role of zearalenone in rat polycystic ovary.

Globally, food and animal feed contamination with mycotoxins is one of the most important challenges affecting human health. Zearalenone is a non-steroidal mycotoxin with estrogen-like activity that has been reported to induce reproductive dysfunctions including polycystic ovary in women. The aim of this study was to assess the possible impact of prolonged low dose zearalenone (0.1 mg/kg b.w.) exposure to increase the risk of developing polycystic ovary in rats. We found that zearalenone increases the plasma insulin, glucose, testosterone, progesterone and luteinizing hormone levels, while the plasma estradiol level was reduced. Zearalenone also incited tumor necrosis factor-α and the secreted frizzled-related protein-4 expressions. Histological examination showed atresia of follicles in the treated group. It is concluded that zearalenone intoxication intensely manipulates the plasma hormonal factors and the level of gene expressions related to the polycystic ovary in rats, thus increases the risk of its progression.