Reactive oxygen species (ROS) [e.g. hydrogen peroxide (H2O2), hypochlorous acid (HOCl), singlet oxygen (1O2)] can cause oxidative stress, with damage implicated in inflammatory conditions including atherosclerosis. Antioxidants, both enzymatic and non-enzymatic [e.g. glutathione (GSH)], often rely on sulfur or selenium centres for reactivity. Selenium is more nucleophilic than sulfur, so selenocompounds [e.g. selenocysteine (Sec)] typically display higher rate constants than the analogous sulfur species (e.g. Cys). Thus, selenium species may minimise biological damage via removal of oxidants and subsequent rapid reduction of oxidised compounds. Selenols (RSeH, e.g. Sec) are unstable and rapidly auto-oxidise, making therapeutic application problematic. This thesis investigates diselenides (RSeSeR) as shelf-stable alternatives which can be reduced to the reactive selenol in situ. Rate constants were determined for the reactions of low-molecular-mass diselenides [selenocystamine (SeCA), 3,3’-diselenodipropionic acid (DSePA), 2,2’-dipyridyl diselenide (DPDSe), dipyrimidin-2-yl diselenide (DPMSe)], fluorescently-tagged selenocystine (Fmoc-SeCystine; the diselenide of Sec) and the selenium analogue of oxidised GSH [seleno-diglutathione (GSeSeG)] with HOCl, H2O2 and 1O2-generated amino acid/peptide hydroperoxides, with products characterised by LC/MS. Oxidation of diselenides by HOCl (k = 103 – 105 M-1 s-1) was more rapid than with H2O2 (k = 10-4 – 10-2 M-1 s-1). SeCA oxidation was similar between the hydroperoxides (k ~ 10-2 M-1 s-1) but DSePA was oxidised by Trp hydroperoxide (TrpOOH) ca. 50 – 150-fold faster than other diselenides, revealing that the ionisation state of the terminal groups affects the oxidation rate. Product characterisation revealed the major product of oxidation by HOCl, H2O2 and TrpOOH to be the seleninic acid (RSeO2H), postulated to form via an initial transient intermediate and diselenide bond cleavage, as per the pathway of the sulfur species.