JUAN CARLOS
MAYO BARRALLO

My thesis project was focused on the role of melatonin in preventing neuronal cell death induced by parkinsonian toxins. After the thesis I spent 4 months at the UTHSC in San Antonio under the supervision of Dr. Russel J Reiter, one of the top researchers in the field of melatonin. My thesis project was focused on the role of melatonin in preventing neuronal cell death induced by parkinsonian toxins, and how this pineal product could be useful in Parkinson’s disease (Mayo et al, J Pineal Res 1995; Endocrine, 2005). After a brief stay of 4 months at the UTHSCSA in San Antonio under the supervision of Dr. Russel J Reiter and upon my return to Oviedo, I was directly involved in the research that led us to report the regulation of antioxidant enzymes by melatonin (Mayo et al., Cell Mol Life Sci, 2002; Rodríguez et al, J Pineal Res 2005; both publications have collectively received more than 1400 cites). I moved to UTHSCSA again from 2001 to 2004, working on the antioxidant properties of melatonin in different models including cancer cells and finally we discovered the importance of melatonin in preventing macrophage activation by LPS (Mayo et al, J Neuroimmunol, 2005, >200 cites) After coming back to the University of Oviedo, we decided to extend our research to other fields, centred on the role of free radicals on redox regulation and how they play a role in cell fate. To this aim, we have used cell culture and animal models, as well as patient’s samples, thanks to the association with urologists, pathologists and epidemiologists). This set of collaborations has given us the ability to work in translational research and provide some insights into the role of redox signalling in neuroendocrine differentiation and in tumour progression (Quirós et al, Int J Cancer, 2009 and Free Rad Biol Med, 2011; Rodríguez et al, J Pin Res 2013; Miar et al, Free Rad Biol Med, 2015). The incorporation to our laboratory of modern analytical techniques prompted us to search for additional methodologies for detection and quantification of intracellular concentrations of antioxidants. This led us to discover the role of SLC2A/GLUT transporters in the uptake of melatonin (Hevia et al, J Pineal Res 2015; Mayo et al Cell Mol Life Sci, 2017). More interestingly, this allowed us to study the involvement of these transporter in the progression of prostate cancer (Gonzalez-Menendez et al, Endocrinology, 2014; Gonzalez-Menendez et al, Redox Biol and Int J Cancer, 2018). More recently we started a fruitful collaboration with the ‘Enriched stable isotopes’ group at the Department of Analytical Chemistry in Oviedo, who are currently supporting us to find out the role of metabolic switch in the progression toward androgen independence in prostate cancer (Hevia et al, Int J Mol Sci, 2017). Our collaboration is of particular interest for determining potential metabolites linked to prostate cancer growth (Galilea et al, J Trace Elem Med Biol, 2017). Furthermore, our collaboration with the ‘Multi-case control (MCC) Spanish group, headed in Oviedo by Dr. Tardón, is making possible to study different redox parameters in patients’ samples collected at different Spanish Hospital Institutions, thus allowing us to widen the view of redox regulation throughout the tumour growth. By including either cell culture, transgenic mice and patients’ samples with the collaborations with the groups mentioned above, we plan to approach the study of prostate cancer at different levels.