Background. Tabaco cigarette smoke (TCS) was previously demonstrated to affect the innate and adaptive immune responses as a consequence of oxidant generation which play a pivotal role in neutrophilic airway inflammation. Aim of this paper was to investigate whether electronic-cigarette smoke (ECS) generates reactive oxygen species (ROS) similarly to cigarette smoke. Method. By means of a house made apparatus, ECS and TCS were collected in FBS which was used to grow immune cells isolated from rats. As index of oxidative products nitrite and thiobarbituric acid-reactive substances (TBARS) were determined in the medium before and after cell growth. Results. The results showed that i) ECS caused a remarkable increase of nitrites and TBARS although in lesser extension than TCS, ii) the cells grown in ECS and TCS-exposed medium were able to reduce TBARS but not nitrites present in the medium, iii) while all 3 kinds of cells in ECS- exposed medium gave the same levels of ROS, PBMC in TCS-exposed medium were able to reduce nitrites and TBARS more efficiently than spleen and lymph node cells, iiii) TCS and ECS not influence the PBMC and spleen T cell subtype populations (CD4+, CD8+). Conclusions. As ECS nicotine-free gave the same results of unexposed medium, we could conclude that the increase of ROS in ECS exposed medium was prevalently due to nicotine.