In silico toxicity investigation of Methaqualone's conjunctival, retinal, and gastrointestinal hemorrhage by molecular modelling approach

Methaqualone was once used to treat insomnia as a hypnotic agent. Methaqualone, like other sedative-hypnotics, is a central nervous system depressant that increases gamma-aminobutyric acid (GABA) activity. Methaqualone toxicity data showed that it inhibits platelet aggregation, increases prothrombin time and partial thromboplastin time, and lowers factors V and VII, all of which can cause retinal, conjunctival, and gastrointestinal hemorrhage. In silico investigation showed that Methaqualone antagonises Vitamin K in the extrinsic and intrinsic pathways of blood clotting, which leads to an increase in prothrombin time and partial thromboplastin time and lowers factors V and VII. Further, a molecular modelling study proved that inhibition of the P2Y12R by Methaqualone is responsible for the inhibition of platelet aggregation. This study systematically correlates all Methaqualone's blood-related toxicity, which results in conjunctival, retinal, and gastrointestinal hemorrhage.

Automated summary

Methaqualone is a central nervous system depressant that increases GABA activity and inhibits blood clotting, leading to decreased platelet aggregation and prolonged prothrombin time and partial thromboplastin time, as well as reduced levels of factors V and VII, resulting in conjunctival, retinal, and gastrointestinal hemorrhage.