Manganese (Mn) is an essential trace element of human. However, excessive Mn can cause manganism. Mn selectively accumulated in Mn-exposed workers' hippocampus which is crucial for higher brain functions such as learning, memory, and motivation during our postnatal life. Studies suggested sodium para-aminosalicylic acid (PAS) appeared to be therapeutic for manganism. We aimed to explore whether PAS could block Mn-induced neuronal injury in hippocampus in vitro. Hippocampal neurons were exposed to 50 μM manganese chloride (MnCl(2)) for 24 h, following by 50, 500, or 5000 μM PAS treatment for 24 h. Cell viability, apoptosis rate, mean fluorescence intensity of mitochondrial and DNA damage were respectively performed. MnCl(2) significantly decreased neurons' viability and fluorescence intensity of comet head of DNA, while increasing the apoptosis rate, mean fluorescence intensity of mitochondrial, percentage of tail DNA, and Olive tail moment of DNA. PAS reduced the percentage of tail DNA and Olive tail moment of Mn-exposed neurons. These data suggested that Mn caused hippocampal neurons' injury, and 50-5000 μM PAS could inhibit Mn-induced DNA damage.
Keywords: Hippocampus; Manganese; Neuron; Sodium para-amino salicylic acid.
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