Federico Mutti
Federico Mutti
*This is an algorithmically generated author record based on publicly available information.
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Federico Mutti has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Aldo Milzani
Department of Biosciences, Università degli Studi di Milano, via Celoria 26, I-20133 Milan, Italy
1 shared publication - Alessandro Miani
Italian Society of Environmental Medicine (SIMA), 20123 Milan, Italy
1 shared publication - Caterina Anna Maria La Porta
Center for Complexity and Biosystems, Department of Environmental Science and Policy, University of Milan
1 shared publication - Emanuela Astori
Department of Biosciences, University of Milan, via Celoria 26, 20133 Milano, Italy
1 shared publication - Emilio Ciusani
Laboratory of Neurological Biochemistry and Neuropharmacology, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milan, Italy
1 shared publication - Erica Soldati
Center for Complexity and Biosystems, Department of Environmental Science and Policy, University of Milan, via Celoria 26, 20133 Milano, Italy
1 shared publication
Latest Publications
- Open Access
- 23 February 2019
- Published by MDPI AG in International Journal of Environmental Research and Public Health
- Vol. 16 (4) , 657
Sulforaphane Cannot Protect Human Fibroblasts From Repeated, Short and Sublethal Treatments with Hydrogen Peroxide
A delicate balance of reactive oxygen species (ROS) exists inside the cell: when the mechanisms that control the level of ROS fail, the cell is in an oxidative stress state, a condition that can accelerate aging processes. To contrast the pro-aging effect of ROS, the supplementation of antioxidants has been recently proposed. Sulforaphane (SFN) is an isothiocyanate isolated from Brassica plants that has been shown to modulate many critical factors inside the cells helping to counteract aging processes. In the present work, we exposed human dermal fibroblast to short, sublethal and repeated treatments with hydrogen peroxide for eight days, without or in combination with low concentration of SFN. Hydrogen peroxide treatments did not affect the oxidative status of the cells, without any significant change of the intracellular ROS levels or the number of mitochondria or thiols in total proteins. However, our regime promoted cell cycle progression and cell viability, increased the anti-apoptotic factor survivin and increased DNA damage, measured as number of foci positive for -H2AX. On the other hand, the treatment with SFN alone seemed to exert a protective effect, increasing the level of p53, which can block the expansion of possible DNA damaged cells. However, continued exposure to SFN at this concentration could not protect the cells from stress induced by hydrogen peroxide.- 23 February 2019
- Published by MDPI AG in International Journal of Environmental Research and Public Health
- Vol. 16 (4) , 657
Open AccessSulforaphane Cannot Protect Human Fibroblasts From Repeated, Short and Sublethal Treatments with Hydrogen Peroxide
A delicate balance of reactive oxygen species (ROS) exists inside the cell: when the mechanisms that control the level of ROS fail, the cell is in an oxidative stress state, a condition that can accelerate aging processes. To contrast the pro-aging effect of ROS, the supplementation of antioxidants has been recently proposed. Sulforaphane (SFN) is an isothiocyanate isolated from Brassica plants that has been shown to modulate many critical factors inside the cells helping to counteract aging processes. In the present work, we exposed human dermal fibroblast to short, sublethal and repeated treatments with hydrogen peroxide for eight days, without or in combination with low concentration of SFN. Hydrogen peroxide treatments did not affect the oxidative status of the cells, without any significant change of the intracellular ROS levels or the number of mitochondria or thiols in total proteins. However, our regime promoted cell cycle progression and cell viability, increased the anti-apoptotic factor survivin and increased DNA damage, measured as number of foci positive for -H2AX. On the other hand, the treatment with SFN alone seemed to exert a protective effect, increasing the level of p53, which can block the expansion of possible DNA damaged cells. However, continued exposure to SFN at this concentration could not protect the cells from stress induced by hydrogen peroxide.