The Activation of Prosurvival Pathways in Myotis lucifugus during Torpor

AbstractHibernation is a strategy used by some mammals to survive harsh winter conditions. Many small mammals, such as the little brown bat, Myotis lucifugus, enter a long-term state of hibernation characterized by a period of deep torpor that can range from days to weeks. Torpid bats undergo metabolic rate depression that not only results in physiological changes but also promotes biochemical changes that favor survival. The present study utilizes multiplex technology to assess key early apoptosis markers and a select group of antioxidant enzymes in muscle, heart, and liver in euthermic controls and torpid bats. Muscle showed a significant decrease in the proapoptotic c-Jun N-terminal kinase and p53 and the antioxidant enzyme catalase but a significant increase in peroxiredoxin 2 levels. The heart responded similarly, with most proapoptotic proteins (caspase 8/9 and p53) remaining at low levels, while the antiapoptotic Bcl-2 protein significantly increased during torpor. There was no significant change in the antioxidant enzymes measured during torpor in the heart compared with the controls. The liver showed increases in catalase and Mn superoxide dismutase 2 enzymes during torpor, which correlated with activation of select antiapoptotic proteins and suppression of levels of proapoptotic ones. Overall, our data demonstrate that antiapoptotic and antioxidant defense responses have organ-specific regulation during torpor in bats. The induction of key antioxidant enzymes and antiapoptotic proteins may function as protective mechanisms that are necessary for surviving torpor.