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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: J Neurochem. 2015 Feb 25;133(1):14–25. doi: 10.1111/jnc.13042

Figure 1. Diagram of proposed mechanism for intracellular 3,4-dihydroxyphenylacetaldehyde (DOPAL) buildup.

Figure 1

Several factors might affect DOPAL levels, including release and reuptake of endogenous dopamine (DA), effectively translocating DA from storage vesicles into the cytoplasm; tyrosine hydroxylase (TH), the rate-limiting enzyme in DA synthesis; aldehyde/aldose reductase (AR), aldehyde dehydrogenase (ALDH), cellular uptake of DA from the extracellular fluid and vesicular sequestration of cytoplasmic DA via the vesicular monoamine transporter (VMAT). Based on the present results, the main mechanism of rotenone-induced DOPAL buildup is decreased ALDH activity. This fits with rotenone inhibiting Complex I and thereby reducing the availability of NAD+, a required co-factor for ALDH. Abbreviations: DAV=vesicular dopamine; DOPAC=3,4-dihydroxyphenylacetic acid; DOPET=3,4-dihydroxyphenylethanol; MAO=monoamine oxidase.