The effect of hyperbaric oxygen on mitochondrial and glycolytic energy metabolism: the caloristasis concept

Abstract

We present new data on the effects of HBOT on human kidney (HK-2) cell metabolism using a SeaHorse XF Analyzer to evaluate separately the state of mitochondrial and glycolytic energy metabolism. The data are discussed in the context of the concept of cellular caloristasis networks. The information on the changes in cellular energy metabolism stimulated by HBOT presented here provides new insights into the cellular energy state and mitochondrial environment in which sHSPs function. These data will be useful in forming testable hypotheses about the functions of translocated sHSPs in human mitochondria responding to stressors.

The interaction of heat shock proteins with cellular membranes: a historical perspective

“…It is frequently said that tumor cells are "addicted" to HSP and that they have highjacked a normal defensive maneuver of stressed cells, the acquisition of cytoprotection. This defensive response involves conversion of energy transduction from oxidative phosphorylation to glycolysis to drive biosynthesis for the repair and replacement of damaged molecules, similar to why tumor cells are thought to switch to aerobic glycolysis to drive biosynthesis to support rapid proliferation, known as the Warburg Effect (Tezgin et al 2020). Thus, mortalin could fulfill its role as a multifunctional integrator of caloristasis and proteostasis through its functions as a regulator of oxidative phosphorylation, as a central component of the mitochondrial protein import machinery, and as part of a damaged protein disaggregating complex (Iosefson et al 2012).…”

“…Dai and colleagues proposed that this antagonism creates a third mechanism to balance cellular homeostasis (Dai, et al 2015). Tezgin and coworkers have postulated that this new mechanism is actually the caloristasis network, in which HSF1 acts as a master proximal integrator (Tezgin et al 2020). The term caloristasis was coined to pair with proteostasis, and like the latter, it emphasizes the integrative regulatory interactions by molecules like HSF1, which is necessary to understand cellular energy homeostasis in normal and stressed cells.…”

Can hyperbaric oxygen safely serve as an anti-inflammatory treatment for COVID-19?

“…HBO 2 allows the delivery of oxygen at high partial pressure reaching tissues rapidly at elevated concentrations, which could reverse the hypoxic condition and preserve cellular metabolism [22] . Indeed, HBO 2 has been shown to preserve mitochondrial activity [23] . Moreover, HBO 2 improved kidney function after infection [24] , protected organs from ischemia/reperfusion injury [25] , [26] , reduced UV skin damage [27] , and avoided kidney damage in diabetic patients [28] .…”

COVID-19, acute respiratory distress syndrome (ARDS), and hyperbaric oxygen therapy (HBOT): what is the link?

“…The elevated supply of oxygen is likely to preserve cellular metabolism and organ function. Indeed, HBOT has been reported to improve mitochondrial function (Tezgin et al 2020). Moreover, HBOT alters the balance between glycolysis and mitochondrial respiration, possibly countering an effect of viral infection on cellular caloristasis networks (Tezgin et al 2020) and improving hypoxia in COVID-19 patients.…”

“…Indeed, HBOT has been reported to improve mitochondrial function (Tezgin et al 2020). Moreover, HBOT alters the balance between glycolysis and mitochondrial respiration, possibly countering an effect of viral infection on cellular caloristasis networks (Tezgin et al 2020) and improving hypoxia in COVID-19 patients. An additional advantage of HBOT is its capacity to reduce the inflammatory response (Buras et al 2006;Halbach et al 2019).…”