L-Homocysteine thiolactone hydrochloride is neurotoxic and can induce epilepsy and Alzheimer's disease.

At a concentration of 0.25 mM and after 24 h incubation with L-Homocysteine thiolactone hydrochloride showed around 40% of cell death. Using 1 mM of L-Homocysteine thiolactone hydrochloride and after 24 h incubation up to 80% of cell death was detected.
HUVEC cells were therefore incubated with increasing concentrations of Hcy (1 mM–10 mM) or L-Homocysteine thiolactone hydrochloride (0.25 mM–1 mM) for different times. None of the Hcy or L-Homocysteine thiolactone hydrochloride concentrations tested had an effect on TNF-α or IL-1α secretion. However, Hcy or L-Homocysteine thiolactone hydrochloride promoted the release of IL-8 starting from 3 h and increasing according to a dose-time dependent manner. [3]

L-Homocysteine thiolactone hydrochloride dissolved in PBS was injected i.p., into 4-12-week-old mice (40-600 nmol/g body weight). To determine how Pon1 affects its turnover in vivo, L-Homocysteine thiolactone hydrochloride was injected i.p. into Pon1−/− and Pon1+/+ mice, and Hcy-thiolactone kinetics in plasma were monitored. A non-toxic dose of 600 nmol L-Homocysteine thiolactone hydrochloride /g body weight in most experiments, but similar results were obtained with doses as low as 40 nmol/g body weight. This shows that in Pon1−/− mice Hcy-thiolactone metabolism is not impaired during its transit from the intraperitoneal cavity to the bloodstream and suggests that Pon1 has a negligible contribution to Hcy-thiolactone turnover in membranes surrounding the intraperitoneal cavity. [4]