Chronic Exposure to Low Doses of Mercury Impairs Sperm Quality and Induces Oxidative Stress in Rats

2014 ◽  
Vol 77 (1-3) ◽  
pp. 143-154 ◽  
Author(s):  
Caroline S. Martinez ◽  
Alyne G. Escobar ◽  
João Guilherme D. Torres ◽  
Daniela S. Brum ◽  
Francielli W. Santos ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Walessa Alana Bragança Aragão ◽  
Francisco Bruno Teixeira ◽  
Nathalia Carolina Fernandes Fagundes ◽  
Rafael Monteiro Fernandes ◽  
Luanna Melo Pereira Fernandes ◽  
...  

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.


2013 ◽  
Vol 04 (11) ◽  
pp. 24-29 ◽  
Author(s):  
Selva Rivas-Arancibia ◽  
Luis Fernando Hernández-Zimbrón ◽  
Erika Rodríguez-Martínez ◽  
Gabino Borgonio-Pérez ◽  
Varsha Velumani ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e111202 ◽  
Author(s):  
Caroline S. Martinez ◽  
João Guilherme D. Torres ◽  
Franck M. Peçanha ◽  
Janete A. Anselmo-Franci ◽  
Dalton V. Vassallo ◽  
...  

2012 ◽  
Vol 3 (7) ◽  
pp. 1-7
Author(s):  
L. TAZROUT L. TAZROUT ◽  
◽  
K. TALEA K. TALEA ◽  
S. EL AMRANI S. EL AMRANI ◽  
I. M’TOUGUY I. M’TOUGUY ◽  
...  

2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.


2006 ◽  
Vol 98 (4) ◽  
pp. 1278-1289 ◽  
Author(s):  
Chor Hui Vivien Koh ◽  
Matthew Whiteman ◽  
Qiao-Xin Li ◽  
Barry Halliwell ◽  
Andrew M. Jenner ◽  
...  

2013 ◽  
Vol 12 (1) ◽  
Author(s):  
Nithya Elango ◽  
Vallikkannu Kasi ◽  
Bhuvaneswari Vembhu ◽  
Jeyanthi Govindasamy Poornima

2016 ◽  
Vol 65 ◽  
pp. 29-38 ◽  
Author(s):  
Marciana Sanabria ◽  
Maira Smaniotto Cucielo ◽  
Marina Trevizan Guerra ◽  
Cibele dos Santos Borges ◽  
Thais Petrochelli Banzato ◽  
...  

2021 ◽  
pp. 101327
Author(s):  
Melanie Wiesner-Reinhold ◽  
João Victor Dutra Gomes ◽  
Corinna Herz ◽  
Hoai Thi Thu Tran ◽  
Susanne Baldermann ◽  
...  

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