Abstract
Animal studies have shown that chemotherapeutic agent doxorubicin (DOX) causes fetal toxicity, including renal abnormalities. Although DOX‐associated nephropathy includes oxyradical stress and glomerular injury, its effect on fetal glomerular cells remains unclear. This study aimed to examine the effect of DOX on fetal glomerular mesangial cell (FE‐GMC) survival. Furthermore, we tested the hypothesis that NADPH oxidase (NOX)‐dependent reactive oxygen species generation contributes to DOX‐induced alterations in FE‐GMCs. Confocal microscopy and high‐performance liquid chromatography revealed that the level of 2‐hydroxyethidium was increased in DOX‐treated cells when compared to DMSO controls, which was reversed by selective NOX inhibitor, apocynin. Apocynin also attenuated DOX‐induced caspase 3/7 activation in FE‐GMCs. These data suggest that DOX induces apoptosis in porcine FE‐GMCs by promoting NOX‐dependent oxidative stress. Caspase‐mediated cell death may contribute to the toxic effects of DOX on the developing kidney.Support or Funding InformationR01DK101668; R01DK101668‐04S1This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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