Previous results of our group showed that retinol treatment (7uM/24 h) may induce oxidative stress in cultived Sertoli cells. This oxidative stress was caracterized by an increase in biomolecules oxidative damage like lipids, proteins and DNA, and also induction of antioxidant enzymes activities: superoxide dismutase (SOD), Catalase (CAT) and Gluthation peroxidase (GPX). We also showed that retinol treatment can modulate the Sertoli cells cytoskeleton architecture, where its components presented oxidative and phenotipic alterations. In actual work we used Cytochalasin B, a F-actin disruption drug, to investigate the importance of actin architecture on oxidative stress generated by retinol treatment. We quantified carbonyl groups to analyse protein oxidative damage, the TBARS assay was used as index of lipid  oxidative damage and we measured the sulphydril levels (–SH) to analyse the oxidation of this groups on retinol treated cells and co-treated or not with cytochalasin B. We also performed cell viability experiments to demostrate whether retinol or Cytochalasin B treatment were toxic to cells, we mensured extracelular LDH activity, Trypan blue exclusion probe and MTT assay. Our results showed that cytochalasin B co-treatment total reverted or significantly attenuated the oxidative stress indicators increase in a 24h treatment. The cell viability experiments showed that this revetion did not occurr by cell death or by diminuished cell number in culture. Therefore, our results demonstrated that architecture integrity of the F-actin is essencial to lead to oxidative stress in retinol treated culture cells, since the lack of this integrity block retinol oxidative effects. This result  can contribute to a better understanding of how oxidative stress, retinoids and cytoskeleton proteins are interconected, since this three subjects appear to present more correlation than suggested in literacture. (supported by CNPQ, CAPES and FAPERGS)