Oxidative stress in myelin sheath: The other face of the extramitochondrial oxidative phosphorylation ability

Oxidative phosphorylation (OXPHOS) is not only the main source of ATP for the cell, but also a major source of reactive oxygen species (ROS), which lead to oxidative stress. At present, mitochondria are considered the organelles responsible for the OXPHOS, but in the last years we have demonstrated that it can also occur outside the mitochondrion. Myelin sheath is able to conduct an aerobic metabolism, producing ATP that we have hypothesized is transferred to the axon, to support its energetic demand. In this work, spectrophotometric, cytofluorimetric, and luminometric analyses were employed to investigate the oxidative stress production in isolated myelin, as far as its respiratory activity is concerned. We have evaluated the levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), markers of lipid peroxidation, as well as of hydrogen peroxide (H2O2), marker of ROS production. To assess the presence of endogenous antioxidant systems, superoxide dismutase, catalase, and glutathione peroxidase activities were assayed. The effect of certain uncoupling or antioxidant molecules on oxidative stress in myelin was also investigated. We report that isolated myelin produces high levels of MDA, 4-HNE, and H2O2, likely through the pathway composed by Complex I-III-IV, but it also contains active superoxide dismutase, catalase, and glutathione peroxidase, as antioxidant defense. Uncoupling compounds or Complex I inhibitors increase oxidative stress, while antioxidant compounds limit ROS generation. Data may shed new light on the role of myelin sheath in physiology and pathology. In particular, it can be presumed that the axonal degeneration associated with myelin loss in demyelinating diseases is related to oxidative stress caused by impaired OXPHOS

The Double Bind of Communicating About Zoonotic Origins: Describing Exotic Animal Sources of COVID‐19 Increases Both Healthy and Discriminatory Avoidance Intentions

Many novel diseases are of zoonotic origin, likely including COVID‐19. Describing diseases as originating from a diverse range of animals is known to increase risk perceptions and intentions to engage in preventative behaviors. However, it is also possible that communications depicting use of exotic animals as food sources may activate stereotypes of cultures at the origin of a disease, increasing discriminatory behaviors and disease stigma. We used general linear modeling and mediation analysis to test experimental data on communications about zoonotic disease origins from the critical first two months leading up to the declaration of a global pandemic. Results suggest that communications about potential familiar food origins (pigs) affected people's risk perceptions, health behaviors, and COVID‐19 stigma compared to more exotic food sources (e.g., snakes). Participants (N = 707) who read descriptions of exotic origins viewed the virus as riskier and reported stronger intentions to engage in preventative behaviors than those who read about familiar origins (pigs). However, reading exotic origin descriptions was also associated with stronger intentions to avoid Asian individuals and animal products. These results are critical for both theory and public policy. For theory, they are the first to experimentally demonstrate that zoonotic origin descriptions can impact intentions to engage in discriminatory behaviors for cultures viewed as the origin of a novel infectious disease. For policy, they offer clear, actionable insights on how to communicate about risks associated with a novel zoonosis while managing the potential impact on discriminatory behaviors and stigma