AI Article Synopsis
- This study investigated the effects of paraoxon, a toxic metabolite of the pesticide parathion, on the prefrontal cortex of rats by examining changes in apoptosis-related gene expression and brain structure.
- Adult male Wistar rats were exposed to different doses of paraoxon, and after either 14 or 28 days, researchers measured key proteins associated with cell death, specifically Bax, Bcl-2, and caspase-3, alongside analyzing neuronal injury and astrocyte activation.
- Results indicated that higher doses of paraoxon significantly increased markers of apoptosis and reduced neuron counts, while simultaneously increasing astrocyte levels, suggesting that paraoxon causes substantial neuronal damage and highlights the importance of managing related conv
Article Abstract
Paraoxon is the bioactive metabolite of organophosphate (OP) pesticide, parathion. This study aimed to evaluate the expression of apoptosis-related genes and histopathological changes in rat prefrontal cortex following exposure to three different doses of paraoxon. Paraoxon (0.3, 0.7, or 1 mg/kg) or corn oil (vehicle) were intraperitoneally injected to adult male Wistar rats. After 14 or 28 days, mRNA and protein levels of Bax, Bcl-2, and caspase-3 were measured in prefrontal cortex using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blotting, respectively. In addition, neuronal injury and astrocyte activation were assessed using cresyl violet staining and glial fibrillary acidic protein (GFAP) immune-positive cells, respectively. Treatment with 0.7 and 1 mg/kg of paraoxon increased mRNA and protein levels of Bax and caspase-3 at 14 and 28 days post-exposure, while mRNA and protein levels of Bcl-2 decreased only in 1 mg/kg group after 14 days. Furthermore, a significant decrease in the number of neurons and a significant increase in the number of GFAP-positive cells were observed in rats receiving 0.7 and 1 mg/kg of paraoxon at both time points. Collectively, our results showed that apoptosis is a major mechanism for neuronal damage after exposure to paraoxon. Also, paraoxon-induced neuronal loss was correlated with activation of astrocytes. Since paraoxon-induced neuronal damage is closely related to convulsion, clinical management of convulsion could protect neuronal brain damage.
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| http://dx.doi.org/10.1007/s12640-019-00106-x | DOI Listing |
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