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Molecular mechanism of brain impairment caused by drinking-acquired fluorosis and selenium intervention
Xiangren Zheng1, Yan Sun1, Lulu Ke1
1College of Chemistry and Life Science at Zhejiang Normal University, Jinhua 321004, PR China.
Abstract:
This study investigated the molecular mechanism of brain impairment induced by drinking fluoridated water and selenium intervention. Results showed that the learning and memory of rats in NaF group significantly decreased. Moreover, the number of apoptotic cells, the expression levels of Cytc mRNA and protein, and the expression levels of Caspase-9 and Caspase-3 mRNA significantly increased; by contrast, Caspase-9 and Caspase-3 protein levels significantly decreased. Compared with the NaF group, the mRNA levels of Cytc and Caspase-9, as well as the protein levels of Cytc in NaF+Se group, significantly decreased. Conversely, the protein levels of Caspase-3 and Caspase-9, as well as the mRNA levels of Caspase-3, significantly increased. Thus, the mitochondrial CytC-Caspase-9-Caspase-3 apoptosis pathway in the hippocampus was one of the mechanisms leading to fluorosis-induced brain damage. Furthermore, the Cytc signaling molecules were possibly the key target molecules in fluorosis-induced apoptosis, and selenium could alleviate fluorosis-induced brain injury.
Insights
Fluoridated water (NaF) impaired rat learning and memory by activating the mitochondrial apoptosis pathway. Selenium intervention (NaF+Se) alleviated this brain injury, suggesting Cytc signaling as a key target.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Fluoridated water consumption is widespread, but its effects on brain health, particularly at the molecular level, require further elucidation.
- Brain impairment, characterized by cognitive deficits, is a growing concern, necessitating research into underlying mechanisms and potential interventions.
- Apoptosis, or programmed cell death, plays a critical role in neuronal function and survival, and its dysregulation can lead to neurological disorders.
Purpose of the Study:
- To investigate the molecular mechanisms of brain impairment induced by exposure to fluoridated water (NaF).
- To examine the role of the mitochondrial apoptosis pathway, specifically involving Cytochrome c (Cytc), Caspase-9, and Caspase-3, in fluorosis-induced brain damage.
- To evaluate the potential neuroprotective effects of selenium intervention against NaF-induced brain injury.
Main Methods:
- Rats were divided into groups, including a control group, a fluoridated water (NaF) group, and a selenium-supplemented fluoridated water (NaF+Se) group.
- Learning and memory functions were assessed using behavioral tests.
- Molecular analyses were performed to measure mRNA and protein expression levels of key apoptosis-related molecules (Cytc, Caspase-9, Caspase-3) in the hippocampus.
Main Results:
- Exposure to fluoridated water (NaF) significantly decreased learning and memory in rats.
- NaF exposure led to increased apoptotic cells and elevated mRNA and protein levels of Cytc, along with increased mRNA of Caspase-9 and Caspase-3, but decreased protein levels of Caspase-9 and Caspase-3.
- Selenium intervention (NaF+Se) partially reversed these effects, decreasing Cytc mRNA and protein levels while increasing Caspase-3 and Caspase-9 protein levels and Caspase-3 mRNA levels compared to the NaF group, indicating modulation of the apoptosis pathway.
Conclusions:
- The mitochondrial Cytc-Caspase-9-Caspase-3 apoptosis pathway in the hippocampus is implicated as a key mechanism in fluorosis-induced brain damage.
- Cytc signaling molecules appear to be critical targets in NaF-induced apoptosis.
- Selenium demonstrates neuroprotective potential by alleviating fluorosis-induced brain injury, possibly through modulation of the mitochondrial apoptosis pathway.
