Role of melatonin in carbon monoxide-induced hypoxemia.
Melatonin (MEL) works in tandem with serotonin (5HT), where an equilibrium exists in perfect health. Under stress or in crisis, it may be that the production of MEL predominates in conjunction with ever increasing production of reactive oxygen species (ROS), may lead to hypoxemia and consequently, to metabolic disruption. The Melatonin Hypothesis could offer an explanation towards certain clinical observation and may support the Catacholamine Hypothesis in the development of depression but it is the role played by carbon monoxide (CO) in inducing hypoxemia which may result in the Cascade Effect that could in turn explain the development of neurodegenerative, neurodevelopmental as well as immune dysfunctional type disorders, prevalent today. CO-induced hypoxemia is an important aspect in any discussion of cell integrity as CO is formed endogenously from the degradation of erythrocytic heme, any hemolytic disturbance or lipid peroxidation, may increase the level in blood. CO, in inducing hypoxemia, causes the generation of large quantities of hydroxyl (-OH) which could damage specific amino acid and disorder protein metabolism that may result in the creation of toxic metabolites. Hydroxyl damage is emerging as the precursor to low-grade inflammation in the presence of C Reactive Protein (CRP) that is currently speculated in the etiology of many known disorders. As disordered protein metabolism may play a crucial role in the formation of the cascade, the hypothesis aims to address the issues of cell viability and the process of cell replication in the event where cell integrity is severely compromised in the face of apoptotic and/or necrotic damage, as the intra-cellular and extra-cellular environments are becoming increasingly hostile. Where -OH damage to specific amino acid in protein may contribute to the Cascade Effect, the hypothesis goes further to explain the importance of the Circardian Cycle and the role of paradoxical sleep, by taking into consideration the need for repair and for regeneration in order to maintain morphology as any cellular event that depends on a redox state is likely to be compromised in an event of hypoxemia. As MEL enters a cell readily because of its high lipid solubility, the role of MEL becomes clear as in its diversity, MEL is a potent oxygen radical scavenger that operates throughout the cell.
Nicholls
June Cheah
JC
3 St. Peters Road, Oundle, Petersborough Cambridgeshire PE8 4PH, UK. junecnicholls@aol.com
D002248:Carbon Monoxide / Q000378:metabolism / Q000633:toxicity*; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000378:metabolism*; D008550:Melatonin / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D002248:Carbon Monoxide; D008550:Melatonin