Abcb1 is involved in the efflux of trivalent inorganic arsenic from brain microvascular endothelial cells

Arsenic (As) can penetrate brain tissue through the blood-brain barrier (BBB), and the ATP-binding cassette subfamily B member 1 (Abcb1) has been shown to facilitate the transport of inorganic arsenic (iAs) in animal liver, small intestine, and yeast. However, the relationship between Abcb1 and BBB has not been reported, and the mechanism of brain microvascular endothelial cells Abcb1 on the transport of iAs needs to be further studied. Increased arsenic levels were observed in mice exposed to 25 mg/L or 50 mg/L of sodium arsenite (NaAsO2) in drinking water, and both arsenic uptake and efflux were detected in bEnd.3 cells treated with 16 μmol/L NaAsO2. Elevated levels of Abcb1 protein were found in the NaAsO2-exposed mouse brain microvascular endothelium and in NaAsO2-treated bEnd.3 cells. Inhibition of Abcb1’s efflux function significantly reduced the 2-hour arsenic efflux rate in bEnd.3 cells loaded arsenic. Conversely, overexpression of either Abcb1a or Abcb1b significantly increased the 2-hour arsenic efflux rate in these cells loaded arsenic. These findings suggest that Abcb1 may play a crucial role in mediating arsenic efflux from mouse brain microvascular endothelial cells. [Display omitted] •Brain microvascular endothelial cells bEnd.3 can uptake and efflux arsenic.•Arsenic exposure increased Abcb1 expression in mouse brain microvascular endothelial cells.•Overexpression of Abcb1a and Abcb1b significantly increased the 2-hour arsenic efflux rate of bEnd.3 cells.•Inhibition of Abcb1 efflux function significantly decreased the 2-hour arsenic efflux rate of bEnd.3 cells.