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Nitric oxide (NO • ) is a vasodilator compound responsible for different physiological processes and its decrease in vasculature may lead to endothelial dysfunction. The main pathway related to the decrease in NO • bioavailability is its reaction with the superoxide radical (O 2 •- ) with consequent production of peroxynitrite (ONOO - ). Thus, we aim to evaluate the protective effect of diphenyl diselenide (PhSe) 2 on bovine aortic endothelial cells culture (BAEC), clarifying the participation of this compound during nitroxidative stress and mitochondrial modulation. Thus, BAEC were treated at different times and concentrations (1–1000 nM) of (PhSe) 2 and exposed to SIN-1 (ONOO - donor). The treatment with (PhSe) 2 was able to prevent the formation of ONOO - in time and concentration-dependent manner analyzed by the DHR probe test. By high resolution respirometry (Oroboros), the treatment with (PhSe) 2 (1 µM) was able to modulate different respiratory states, such as the increase of the maximum respiratory capacity and the consumption of oxygen coupled to ATP synthesis. Thus, we hypothesized that the activation of transcription factors such as Nrf-2 and FOXO3a by (PhSe) 2 render cells more resistance to oxidative damage and consequent mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]