Peroxynitrite anion (ONOO-) is a potent oxidizing and nitrating agent. A primary effect of ONOO- on proteins is nitration of tyrosine residues. Nitration of tyrosine residues has been implicated in the pathophysiology of various, particularly neurodegenerative, disorders and aging, therefore search for agents preventing or limiting protein modifications by peroxynitrite is of interest. Our previous study has identified compounds, mostly polyphenols, the most reactive with peroxynitrite. However, protective effects in cell-free systems may be not relevant for the cellular effects. The aim of this study was to study the protective effects of chosen compounds, mainly polyphenols, on the nitration of intracellular proteins. MCF-7 cells were preincubated with chosen antioxidants for 1-5 h. Excess of antioxidants was washed off and the cells were exposed to 3-morpholinosydnonimine N-ethylcarbamide (SIN-1) as a source of peroxynitrite at 37oC for 1 h. The concentration of SIN-1 causing a loss of cell viability (estimated with MTT) to 60% in the absence of any antioxidant was chosen (100 µM). From 25 compounds studied, 9 providing the best protection of SIN-1 exposed cells were chosen for protection against nitration of intracellular proteins. The cells were preincubated with the compounds studied at non-cytotoxic concentration of 1 µM for 5 h and subjected to treatment with SIN-1 for 1 h. The level of 3-nitrotyrosine in cellular proteins was estimated by ELISA. The sequence of effectivity in protection against nitration of intracellular proteins was as follows: ferulic acid > uric acid > desferrioxamine > naringin hydrate > luteolin > genistein > quercetin. This sequence is different from that found in a cell-free system of tyrosine nitration, confirming that other factors, apart from reactivity with peroxynitrite alone, related to the cellular behavior of antioxidants, are important for their protective efficiency against nitration in situ.