EVIDENCES OF OXIDATIVE STRESS DURING THE DEVELOPMENT OF EXPERIMENTAL PITUITARY TUMOR: CELL DAMAGE RESPONSE AND ITS POSSIBLE CONTRIBUTION TO CELLULAR SENESCENCE

GRONDONA, E; MONGI BRAGATO B; CARREÑO L; SABATINO ME; SOSA LDV; TORRES A; LATINI A; DE PAUL AL

Buenos Aires

Congreso; REUNIÓN CONJUNTA DE LAS SOCIEDADES DE BIOCIENCIA 2017; 2017

REUNIÓN CONJUNTA DE LAS SOCIEDADES DE BIOCIENCIA

The control of reactive oxygen species (ROS) levels is crucial to guarantee cell survival, since their excessive production is able to promote damages in different cell structures. We have previously demonstrated signs of cellular senescence as mechanism of proliferative arrest and alterations in mitochondrial metabolism and dynamics in experimental pituitary tumors. Since mitochondrial dysfunction has been associated with senescence and this organelle is the main source of ROS, we aimed to analyze the activation of cellular damage response mechanisms to counteract the lesions promoted by oxidative stress.To promote pituitary tumors, estradiol benzoate was implanted subcutaneously in slow releasing silastic brand capsules (10mg) in adult male Wistar rats for 10, 20, 40 and 60 days. Control group: animals were treated with empty capsules. Subsequently, ROS production was determined by flow cytometry, carbonylated proteins by spectrophotometry; γ-H2AX; 8OHdG, total and phosphorylated Nrf2 and HO-1 was assessed by immunohistochemistry and western blot; OGG1 by PCR; and glutathione levels by colorimetry assays. Statistical analysis: ANOVA-Fischer (p