Accelerated urinary excretion of methylmercury following administration of its antidote N-acetylcysteine requires Mrp2/Abcc2, the apical multidrug resistance-associated protein.

@article{Madejczyk2007AcceleratedUE,
  title={Accelerated urinary excretion of methylmercury following administration of its antidote N-acetylcysteine requires Mrp2/Abcc2, the apical multidrug resistance-associated protein.},
  author={Michael S. Madejczyk and David A. Aremu and Tracey A Simmons-Willis and Thomas W. Clarkson and Nazzareno Ballatori},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={2007},
  volume={322 1},
  pages={378-84}
}
N-Acetylcysteine (NAC) is a sulfhydryl-containing compound that produces a dramatic acceleration of urinary methylmercury (MeHg) excretion in poisoned mice, but the molecular mechanism for this effect is poorly defined. MeHg readily binds to NAC to form the MeHg-NAC complex, and recent studies indicate that this complex is an excellent substrate for the basolateral organic anion transporter (Oat)-1, Oat1/Slc22a6, thus potentially explaining the uptake from blood into the renal tubular cells… CONTINUE READING