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In all cell types, from bacterial to human, homocysteine is metabolized to homocysteine thiolactone by methionyl-tRNA synthetase. Elevated levels of homocysteine are an independent risk factor for cardiovascular disease in humans. Homocysteine can be harmful to human cells because of its metabolic conversion to homocysteine thiolactone, a reactive thioester. This conversion occurs in all human cell types, including endothelial cells. Homocysteine thiolactone induces cell death and features of apoptosis including increased phosphotidylserine exposure on the membrane surface, increased apoptotic cells with hypoploid DNA contents, and internucleosomal DNA fragmentation in HL-60 cells. Homocysteine thiolactone is cytotoxic and capable of promoting cell death, as measured by caspase-3 activation and DNA fragmentation. HcyT strongly activates IL-8 release.

Homocysteine thiolactone is toxic, induces epileptic seizures in rodents, and has been implicated in Alzheimer’s disease. Homocysteine thiolactone induces two types of seizures, the coexistence of convulsive and nonconvulsive epilepsy. The grade of seizures is dose dependent.