Motivations for understanding the underlying mechanisms
of alcohol
toxicity range from economical to toxicological and clinical. On the
one hand, acute alcohol toxicity limits biofuel yields, and on the
other hand, acute alcohol toxicity provides a vital defense mechanism
to prevent the spread of disease. Herein the role that stored curvature
elastic energy (SCE) in biological membranes might play in alcohol
toxicity is discussed, for both short and long-chain alcohols. Structure–toxicity
relationships for alcohols ranging from methanol to hexadecanol are
collated, and estimates of alcohol toxicity per alcohol molecule in
the cell membrane are made. The latter reveal a minimum toxicity value
per molecule around butanol before alcohol toxicity per molecule increases
to a maximum around decanol and subsequently decreases again. The
impact of alcohol molecules on the lamellar to inverse hexagonal phase
transition temperature (T
H
) is then presented and used as a metric to assess the impact of
alcohol molecules on SCE. This approach suggests the nonmonotonic
relationship between alcohol toxicity and chain length is consistent
with SCE being a target of alcohol toxicity. Finally, in vivo evidence for SCE-driven adaptations to alcohol toxicity in the literature
are discussed.