Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that exerts diverse biological effects across tissues and organs. At high concentrations, it is recognized as toxic because of harmful effects such as tissue hypoxia, oxidative stress, peroxynitrite formation, inflammation, apoptosis, and immune damage. However, the endogenous production of CO suggests that it may confer protective mechanisms to the host. These protective effects include inhibition of platelet activation, smooth muscle relaxation, vasoactive properties, anti-inflammatory and anti-apoptotic actions, and beneficial influences on neurotransmission. Despite its toxic potential, low-concentration endogenous CO may provide protection linked to the body's defense mechanisms. In this study, we aimed to investigate the anti-apoptotic effects of carbon monoxide at low concentrations. To this end, the relationships between COHb levels and plasma levels of NF-κB, NRF2, and PGC-1α were analyzed statistically.
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Blood COHb, NF-kB, NRF2, and PGC-1α levels during Low-Flow and Normal-Flow Anesthesia
Timeframe: 24 HOUR
Blood COHb, NF-kB, NRF2, and PGC-1α levels during Low-Flow and Normal-Flow Anesthesia
Timeframe: 24 HOUR
Blood COHb, NF-kB, NRF2, and PGC-1α levels during Low-Flow and Normal-Flow Anesthesi
Timeframe: 24 HOUR
Blood COHb, NF-kB, NRF2, and PGC-1α levels during Low-Flow and Normal-Flow Anesthesi
Timeframe: 24 HOUR