Of all the aforementioned metabolites, the toxicity is believed to be due to the metabolic transformation to this γ-diketone.

This suggests induction of microsomal oxidizing enzymes, which results in greater production of toxic metabolites.

Chronic exposure to the compound has been shown to produce a clinical neuropathy, characterized by giant axonal swellings filled with neurofilaments.

The combination of these two compounds increases the neurotoxic effect of 5-nonanone approximately sixfold.

When only exposed to 5-methyl-2-octanone liver swelling was observed, indicating that metabolic activation of hepatic oxidative enzymes may be the cause of the increase in toxicity in co-administration.