ScienceDirect had something else of interest.
Many people talk/write about there being components in a food which can affect the action of components such as toxins.
It seems that the ability of acetogenins in some foods to cause DA cell death (presumably by inhibiting mitochondrial complex I) can be influenced by sugars.
Annonacin caused the death of DA neurons in mesencephalic cultures via a mechanism that mostly resulted from impairment of energy metabolism. Indeed, annonacin-induced DA cell death was prevented by two hexoses, glucose and its glycolyzable isomer mannose, which both operated by partially restoring intracellular ATP levels which were decreased as a consequence of mitochondrial complex I inhibition (Lannuzel et al., 2003). Deoxyglucose, a non-metabolizable glucose/mannose analog, reversed these neuroprotective effects probably by competition, at the glucose transporter sites. Other hexoses such as galactose and fructose were not protective because they were poorly taken up by DA neurons (Lannuzel et al., 2003). Attempts to restore oxidative phosphorylation with substrates of the citric acid cycle, lactate or pyruvate, failed to provide protection to DA neurons whereas idoacetate, an inhibitor of glycolysis, inhibited survival promotion by glucose and mannose indicating that both hexoses acted upstream of the mitochondria by stimulating the glycolytic flux in these neurons (Lannuzel et al., 2003).
https://www.sciencedirect.com/topics/neuroscience/acetogenin
Peterson gives the (ripe?) composition of paw paw fruit as:
Sugars in ripe pawpaw
Fructose 1.3-2.8
Glucose 1.8-4.0
Sucrose 6.0-13.3
I am not finding any information about deoxyglucose in fruits (or pawpaw fruit in particular), but I did run across a research paper where deoxyglucose was used as an internal standard in a fruit extraction. If that extract was then used in a toxicology study, the results could be biased.