Associate ProfessorT: 514-398-2515 | ryan.mailloux [at] mcgill.ca (Email) | Macdonald-Stewart Bldg MS2-042a
BSc (Honours) - Biochemistry/Laurentian University
PhD - Biomolecular Sciences/Laurentian University
After receiving his PhD in Biomolecular Sciences, Dr. Ryan Mailloux conducted his postdoctoral work from 2008-2013 at the University of Ottawa where he studied mitochondrial bioenergetics and redox signaling in the contexts of brown fat thermogenesis, obesity, insulin secretion, heart disease, and chemotherapeuetic resistance in cancer cells. He then continued his postdoctoral work at Carleton University/Health Canada and the University of Ottawa, respectively, from 2013-2015 in toxicology and redox biology. In 2015, Dr. Mailloux joined the Department of Biochemistry at Memorial University, Newfoundland, as an assistant professor. His research focused on decoding how mitochondria generate reactive oxygen species and maintain cell redox balancing whilst assessing the impact of sex, mouse strain, and diet on these processes. Dr. Mailloux also became a leader in the study of mitochondrial glutathionylation reactions, demonstrating these redox signals are vital for controlling energy metabolism in response to alterations in diet and that there are sex differences in these pathways. He has also pioneered work into understanding the function of these reactions in serving as a negative feedback loop to control ROS production. Dr. Mailloux was successfully recruited by the School of Human Nutrition and started at McGill University September 1st, 2019. His work continues to focus on understanding the function of mitochondrial ROS and redox signals in physiology and disease.
Human cells need a lot of energy to drive various physiological functions (e.g. heartbeat). This is mostly supplied by specialized cell structures called mitochondria, which extract energy from nutrients to make a more usable form of energy called ATP. These structures also make another molecule called reactive oxygen species (ROS), which can be dangerous in high enough quantities but are essential for cell health when kept at low amounts. ROS are kept in check by antioxidants, which are produced by the same pathways in mitochondria that make ATP. A complex interplay exists between ATP, ROS, and antioxidants which can have a significant impact on cell fate decisions. In addition, various environmental/physiological factors such as diet, exercise, gender, toxins and pollutants, and changes in temperature influence how much ATP, ROS, and antioxidants are made which can lead to changes in cell behavior. Dr. Mailloux’s work aims to decode how mitochondria can tailor the metabolic pathways that make ATP, ROS, and antioxidants in response to environmental and physiological cues. This includes delineating the effect of sex and gender as well as changes in diet affect these cell pathways.
How do mitochondria serve as cell reactive oxygen species (ROS) stabilizers?
- Studying the contribution of the “unconventional” ROS sources to total mitochondrial ROS production for cell signaling.
- Contribution of the unconventional ROS sources towards the induction of oxidative distress and the development of heart and fatty liver disease and obesity.
- Impact of nutritional interventions and sex differences on ROS production.
- Understanding the capacity of mitochondria to quench ROS produced in the cytoplasm using different antioxidant mechanisms.
- Adaptations of the C57BL/6J strain to maintain mitochondrial ROS buffering capacities.
Role of reversible protein S-glutathionylation reactions in the regulation of mitochondrial and cellular bioenergetics
- Understanding the basic underlying biochemical mechanisms of S-glutathionylation, identification of new targets for modification, and its capacity to modulate various mitochondrial proteins in response to changes in diet.
- Function of S-glutathionylation reactions in the regulation of respirasome and supercomplex assemblies.
- Role of S-glutathionylation in serving as a negative feedback loop for the control of ROS production.
- Delineating how manipulation of these pathways can protect from heart disease and the development of diet-induced obesity and related disorders (e.g. type 2 diabetes mellitus and fatty liver disease).
- Investigation into sexual dimorphisms in S-glutathionylation and its impact on mitochondrial bioenergetics, ROS production, and the response of mitochondria towards dietary interventions.