Lung excretion of volatile seleniated compounds is linked with the transmethylation process and the subsequent binding of methyl groups to selenium, in order to form dimethyl selenide; this occurs with selenite but not with selenomethionine or selenocystine. Intravenous injection of selenite is followed by rapid exhalation of dimethyl selenide; the excretion curve is diphasic, with an initial rapid phase followed by a slower component. The amount of exhaled compound is not influenced by administration of methyl donors, but increases after a high protein diet; sub-total hepatectomy induces a slowing down of the first phase of excretion, but the phenomenon disappears rapidly with regeneration of the liver. Stimulation of liver enzymes by phenobarbital produces an increase of lung excretion of dimethyl selenide, while neither inhibition of ribosomal enzymes (by SKF-525 A) nor administration of ethionine influences the rate of exhalation. Administration of toxic doses of selenite results in a diversion of the methyl groups to meet the metabolic challenge and to provoke a considerable acceleration of the liver transmethylation process, at least with regard to the organification of selenite; stimulation with phenobarbital results in a further acceleration, while administration of ethionine is followed by a marked slowing down of the phenomenon. These findings suggest a shift in the transmethylation process in cases of metabolic emergencies; it is not known whether the shift occurs at the expense of the other pathways of transmethylation, especially the proteins and phospholipids. The procedure could be developed into a clinical test of the lipotropic function of the liver, provided that a less toxic compound is employed.