Vitamin E acetate, which is used as diluent of Tetrahydrocannabinol (THC), has been reported as the primary causative agent of EVALI (E-cigarette, or Vaping, product Use–Associated Lung Injury). Here, we employ <i>in-vitro</i> assays, docking, and molecular dynamics (MD) computer simulations to investigate the interaction of vitamin E with the membrane-bound Cannabinoid 2 Receptor (CB2R), and its role in modulating the binding affinity of THC to CB2R. Vitamin E interacts with both the CB2R and the membrane phospholipids. Notably, the synchronized effect of these interactions likely facilitates vitamin E acting as a lipid modulator for the cannabinoid system. Specifically, when THC binds to CB2R in the presence of vitamin E, the binding cavity widens facilitating the entry of water molecules into it, leading to a reduced interaction of THC with CB2R. Furthermore, the interaction between THC and vitamin E in solution is stabilized by several H-bonds, which can directly limit the interaction of free THCs with CB2R. Both the MD simulations and the <i>in vitro</i> dissociation assay results suggest THC binding to CB2R is reduced in the presence of vitamin E. Our study discusses the role of vitamin E in limiting the effect of THCs and its implications on reported pathology of EVALI.

Vitamin E's effect on tetrahydrocannabinol binding to the cannabinoid 2 receptor

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ACS Fall 2022

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.