AA is well absorbed regardless of the route of administration, and it is metabolized by either conjugation with glutathione and/or oxidation to glycidamide (GA)
Oral exposure has been the primary focus of Acrylamide’s main entry into the human and thus a heavy focus of tissue research into its toxicology upon GI tract tissues has taken place. It is noted in the above-mentioned study by Miller (32) that after administration of Acrylamide, it was absorbed into the GI system.
Another tissue susceptible to Acrylamide absorption is in nervous tissue of the peripheral nervous system. High uptake levels of Acrylamide in the motor nerve terminus and optic nerve are two areas, which have been shown to result in degeneration of the distal axon terminal. Essentially, this process of dying back allows more acrylamide to enter the cell causing further intoxication (27). Earliest neuromuscular changes can be seen in the pacinian corpuscles followed by the muscle spindles and finally the motor nerve terminus.
In the optic nerve, mid diameter axons are most prone to acrylamide absorption in the optic tract allowing for neuronal degeneration in tested primates.