Cysteamine (CA), which is an aminothiol drug medically known as Cystagon® was studied in this thesis. Cysteamine was reacted with a binary toxin called peroxynitrite (PN) which is assembled spontaneously whenever nitric oxide and superoxide are produced together and the decomposition of peroxyinitrite was monitored. PN was able to nitrosate CA in highly acidic medium and excess CA to form S-nitrosocysteamine (CANO) in a 1:1 with the formation of one mole of CANO from one mole of ONOOH. In excess oxidant (PN) the following 1:2 stoichiometric ratio was obtained; ONOO- + 2CA → CA-CA + NO2- + H2O . In alkali medium the oxidation of CA went through a series of stages from sulfenic acid, sulfinic acid and then sulfonic acid which was followed by the cleavage of the C-S bond to form a reducing sulfur leaving group, which is easily oxidized to sulfate. The nitrosation reaction was first order in peroxynitrite, thus implicating it as a nitrosating agent in highly acidic pH conditions. Acid catalyzes nitrosation reaction, whitst nitrate catalyzed and increased the amount of CANO product, This means that the nitrosonium cation, NO+ which is produced from the protonation of nitrous acid(in situ) as also contributing to the nitrosation of CA species in highly acidic environments. The acid catalysis at constant peroxynitrite concentrations suggests that the protonated peroxynitrous acid nitrosates at a much higher rate than the peroxynitrite and peroxynitrous acid. Bimolecular rate constants for the nitrosation of CA, was deduced to be 10.23 M-1 s-1. A linear correlation was obtained between the initial rate constants and the pH. The oxidation of CA was modeled by a simple reaction scheme containing 12 reactions.