1) 1,4-butanediol is oxidized to gamma-hydroxybutryaldehyde that is then oxidized to gamma-hydroxybutyric acid. This interconverts with succinic semialdehyde which both are oxidized to succinic aldehyde and our mitochondria take care of the rest as it can be thrown into the Kreb's cycle. It's a two step transition, and sorry, no names.
2) I seem to understand that GHB dehydrogenase and/or GHB ketotranshydrogenase converts succinic aldehyde to succinic acid. The reason 1,4-BDO is not oxidized to the corrresponding dicarboxyllic acid, succinic acid, is because there is no single enzyme that can take it that far... it requires five or so steps, and again, sorry, I don't have the name of all of the enzymes involved.
Say, why do you want them? Do you collect enzyme names?
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A quick search on pubmed mentions a paper
Biochem Pharmacol 1982 Dec 1; 31 (23): 3917-23 in which the abstract mentions something about enzymes and BDO being the source of GHB. Maybe you should check out that paper as it might have the answers you were once looking for.
That paper brings up the idea of trying gamma-aminobutyric acid alpha-oxoglutarate aminotransferase inhibitors combined with the administration of GHB to see if it would prolong the effects. I gotta get some rats & a research grant...
Btw, the reason for the interconversion of GHB and succinic semialdehyde is due to the brain's natural pathway of making GHB is from glutamic acid, to GABA to succinic semialdehyde.