Mitochondria and lysosomes: lords of life and death in cells?

by Mauricio da Silva Baptista

An important aim of our CEPID-Redoxoma is to develop diagnostic and therapeutic applications of redox processes. In this context, antioxidant therapies are at the frontline of our interests as a group. In parallel, however, a smaller but nonetheless significant group of strategies aim to explore prooxidant and stress-enhancing effects of distinct interventions, mainly to achieve selective toxicity towards damaged or tumor cells. The group of Prof. Mauricio S. Baptisata, from our CEPID-Redoxoma, has been exploring for more than a decade photo-induced compounds as a means to achieve such type of effects. Interestingly, this group recently provided a significant contribution


Mitochondria can dictate your fate, especially if you’re a stem cell

Redoxoma Highlights | Mitochondria can dictate your fate, especially if you’re a stem cell  Maria F. Forni

by Maria F. Forni*

Known for over a century, mitochondria have become, during the last four decades, an important subject of research within several disciplines. This is mostly due to the fact that this organelle comprises the site of oxidative phosphorylation, the citric acid cycle, fatty acid oxidation, the urea cycle and the biosynthesis of iron-sulphur centres and haem. Moreover, mitochondria are an important redox-signaling node. Indeed, the bioenergetic status of a cell is dependent on the overall quality and relative abundance of the mitochondrial population it harbors. Recent evidence suggests that the control of mitochondrial mass and morphology occurs through the processes of fusion


Mitochondria-to-nucleus communication controls mitochondrial activity and stress resistance in yeast

Redoxoma Highlights | Mitochondria-to-nucleus communication controls mitochondrial activity and stress resistance in yeast by Fernanda M. Cunha

by Fernanda M. Cunha

Mitochondria are believed to be former free living bacteria that established a successful symbiotic relationship with eukaryotic cells in such a way that today, besides being crucial for the biosynthesis of intermediary metabolites, calcium homeostasis, coordination of apoptosis and ATP synthesis, most mitochondrial proteins are encoded by nuclear rather than mitochondrial DNA. In that scenario, communication pathways that relay signals from the nucleus to mitochondria as well as from mitochondria to the nucleus (the retrograde way) are mandatory to secure energetic and metabolic homeostasis. In yeast, the best characterized retrograde signaling pathway, activated whenever


Is cholesterol bad for mitochondria?


by Sayuri Miyamoto

Cholesterol is an important component of cell membranes and plays essential structural and signaling roles. It is synthesized in the endoplasmic reticulum and distributed to other cell membranes/compartments through a tightly regulated trafficking system involving vesicular and non-vesicular processes [1]. Cholesterol distribution among intra-cellular membranes is not homogeneous. Mitochondria are cholesterol-poor organelles (less than 5 %). However, mitochondrial cholesterol is increased in cancer cell lines and treatment of these cells with statins (cholesterol lowering drugs) increases their susceptibility to chemotherapy [2].

How mitochondrial cholesterol could influence


Succinate accumulates during ischemia forcing mitochondrial complex I to operate in reversal, while producing oxidant species during reperfusion

by José Carlos Toledo

Ischemia-reperfusion (IR) is a process where blood supply (thus oxygen supply) to an organ is interrupted and then restored. While reperfusion is essential for survival, it is accompanied by a burst of mitochondrial generation of redox species and intermediates such as superoxide and hydrogen peroxide. Such species associate with derived ischemic tissue injury, underling disorders such as heart attack and stroke [1]. Nonetheless, IR mitochondrial ROS production has been considered a nonspecific consequence of a dysfunctional interaction of mitochondrial redox


The new roles of cardiolipin in ROS-mediated signalling

Cytochrome c

by Alberto Lévano-Martinez

Cardiolipin, the signature phospholipid of mitochondria, has been extensively studied as this organelle’s main structural and regulatory lipid. It exerts influential roles in the catalytic activity of key components of the oxidative phosphorylation under physiological conditions. However, recents advances in mitochondrial physiology have uncovered roles of this phospholipid in pathophysiological situations such as apoptosis, or in Barth syndrome. Cardiolipin anchors cytochrome c to the outer face of the inner mitochondrial membrane, which favors the electron transfer to the terminal component of the respiratory chain (Complex IV). However, during oxidative


Mitochondrial metabolism and central nervous system dysregulation govern an overeating but low energy conversion efficiency response to intermittent-feeding

The ideal type of diet is a long-sought goal that has not been fulfilled so far, both for preventive as well as therapeutic purposes. At the same time, caloric restriction has been well demonstrated to afford increase in lifespan in several species. Intermittent feeding has been used as a substitute for caloric restriction both by overweight or obese individuals (frequently without medical supervision) or, experimentally, as a mechanistical tool to understand the physiology of lifespan extension. These intermittently-fed animals, indeed display decreased body mass, but surprisingly overall caloric intake is similar to that of ad libitum-fed animals. Work performed by the CEPID-Redoxoma