In this work we have studied the role of the sugar trehalose and its transport in the protection against oxidative stress caused by hydrogen peroxide and menadione, a source of superoxide radical. In the experiments, we used a mutant strain deficient in trehalose synthesis (tps1 strain) and a mutant deficient in trehalose transport (agt1 strain). Exponential sensitive cells, growing on glucose, were adapted with a 10% trehalose solution or with a heat treatment (which leads to trehalose accumulation) and then exposed either to peroxide or menadione. According to our results, the enhancement in tolerance to both oxidative stresses produced by the adaptive treatments (heat shock and external trehalose) was higher in control strain than in tps1 mutant, confirming the importance of this disaccharide in the protection against oxidative damage. The mutant deficient in AGT1 could not uptake external trehalose and was not able of acquiring tolerance to menadione, indicating the necessity of the sugar inside the cell. On the other hand, under hydrogen peroxide stress, trehalose seems to be necessary especially outside of the plasma membrane, since the increasement produced by external trehalose in agt1 strain was almost the half of that found in control strain. Therefore, trehalose plays a role in protecting cells from oxidative injuries. However the mechanism of defense is dependent on the type of oxidative stress to which cells are submitted.