the addition of 50 ppm hydroquinone monoethyl ether. The polymerization of MeAN is carried out in tetrahydrofuran (THF) with the disodium salt of polyethylene oxide (PEO). MeAN is also commercially produced by the vapor-phase reaction of isobutylene with ammonia and oxygen in the presence of a catalyst. Acetonitrile, hydrogen cyanide and acrolein are known by-products. It is used in the preparation of homo- and copolymers, elastomers, coatings and plastics. It can be used as a replacement for acrylonitrile in similar reactions. MeAN can also be synthesized by dehydration of methacrylamide or from isopropylene oxide and ammonia. Reactions MeAN can undergo electropolymerization, if it is submitted to electroreduction at metallic cathodes in an organic anhydrous medium, for example; acetonitrile. There are two types of polymers that can be obtained at the end of the synthesis; a physisorbed polymer and a grafted polymer. The mechanism accounting for the non-grafted polymer is pretty well understood: it proceeds via the formation of a radical anion (the product of reduction of the vinylic monomer), which dimerizes in solution because of a radical–radical coupling mechanism (RRC) to deliver a di-anion acting as the initiator of a polymerization reaction in solution. Metabolism There are different metabolizing pathways for methacrylonitrile, that are elaborated here: First of all, methacrylonitrile can be directly conjugated with GSH, which leads to the formation of S-(2-cyanopropyl) GSH, which can be metabolized to N-acetyl-S- (2-cyanopropyl) cysteine (NACPC), which can be excreted in the urine. Due to this, glutathione is depleted to certain degrees after MeAN exposure. After oral exposure to 100 mg/kg MeAN in rats, the maximum depletion was noticed in the liver at 39% of control. This depletion, however, is less than found after AN administration. This is likely because MeAN exists in part bound to red blood cells, and is therefore unavailable for GSH conjugation. Studies using radiolabeled carbon point out that the primary route by which methacrylonitrile left the body is the urine, at 43% of the dose. An additional 18% is excreted in faeces (15%) and exhaled air (2.5%). This means that about 40% of MeAN does not leave the body immediately and is either bound to macromolecules or forms unexcretable conjugates. The red blood cells retained significant amounts of radioactivity: more than 50% of the radioactivity in erythrocytes was detected as covalently bound to hemoglobin and membrane proteins. Secondly, methacrylonitrile can be metabolised in the liver by CYP2E1 (a