At EB 2010, we reported that in perfused rat livers and in live rats (i) levulinate (4-ketopentanoate, LEV) is converted to gamma-hydroxypentanoate (GHP), a new drug of abuse, analog of gamma-hydroxybutyrate, (ii) the formation of GHP from LEV is enhanced by ethanol oxidation, and (iii) the metabolism of LEV and GHP result in substantial accumulation of LEV-CoA, GHP-CoA and 4-phospho-GHP-CoA in the liver leading to CoA trapping. We now report a similar accumulation of LEV-derived CoA esters in (i) the brains of rats gavaged with Ca-LEV and (ii) rat hearts perfused with LEV. We also report new fates of LEV metabolism in liver. First, LEV-CoA is elongated with acetyl-CoA to 3,6-gamma-diketo-heptanoyl-CoA, which is converted to two types of cyclic CoA esters with a cyclopentane ring and with a pyrrole ring. The latter is similar to pyrrole compounds formed in the brain by the binding of toxic gamma-diketones (such as 2,5-diketohexane) to lysine. Such compounds may contribute to the toxicity of GHP derived from LEV. Oral ingestion of Ca-LEV plus ethanol is a public health concern since Ca-LEV is freely available. Supported by NIDDK RoadMap and by NIEHS.