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https://www.selleckchem.com/products/d-1553.html 16-66.01 mg kg-1) than TEL (52.3 mg kg-1). Ba showed significant concentrations in 6 samples collected on the São Paulo River, a region close to the oil refining area. The enrichment factor (EF) showed that most elements did not show enrichment, except for Zn. Through Igeo there was a tendency towards serious pollution of Ba, Cu, and Zn; moderately polluted by Cr. Principal component analysis (PCA) and Spearman's classification showed a correlation greater than 70% between the variables. According to Nemerow Synthetic Pollution (PN), both areas are polluted by Al, Ba, Cr, Cu, Fe, Mn, Ni, Ti, V, and Zn.Autotaxin (ATX) and its product lysophosphatidic acid (LPA) have been implicated in lung fibrosis and cancer. We have studied their roles in DNA damage induced by carcinogenic crystalline silica particles (CSi). In an earlier study on bronchial epithelia, we concluded that ATX, via paracrine signaling, amplifies DNA damage. This effect was seen at 6-16 h. A succeeding study showed that CSi induced NLRP3 phosphorylation, mitochondrial depolarization, double strand breaks (DSBs), and NHEJ repair enzymes within minutes. In the current study we hypothesized a role for the ATX-LPA axis also in this rapid DNA damage. Using 16HBE human bronchial epithelial cells, we show ATX secretion at 3 min, and that ATX inhibitors (HA130 and PF8380) prevented both CSi-induced mitochondrial depolarization and DNA damage (detected by γH2AX and Comet assay analysis). Experiments with added LPA gave similar rapid effects as CSi. Furthermore, Rac1 was activated at 3 min, and a Rac1 inhibitor (NSC23766) prevented mitochondrial depolarization and genotoxicity. In mice the bronchial epithelia exhibited histological signs of ATX activation and signs of DSBs (53BP1 positive nuclei) minutes after a single inhalation of CSi. Our data indicate that CSi rapidly activate the ATX-LPA axis and within minutes this leads to DNA damage in bronchial epithelial

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