Vitamin C Modes of Action in Calcium-Involved Signaling in the Brain.
Ludmila ZylinskaMalwina LisekFeng GuoTomasz BoczekPublished in: Antioxidants (Basel, Switzerland) (2023)
Vitamin C (ascorbic acid) is well known for its potent antioxidant properties, as it can neutralize ROS and free radicals, thereby protecting cellular elements from oxidative stress. It predominantly exists as an ascorbate anion and after oxidation to dehydroascorbic acid and further breakdown, is removed from the cells. In nervous tissue, a progressive decrease in vitamin C level or its prolonged deficiency have been associated with an increased risk of disturbances in neurotransmission, leading to dysregulation in brain function. Therefore, understanding the regulatory function of vitamin C in antioxidant defence and identification of its molecular targets deserves more attention. One of the key signalling ions is calcium and a transient rise in its concentration is crucial for all neuronal processes. Extracellular Ca 2+ influx (through specific ion channels) or Ca 2+ release from intracellular stores (endoplasmic reticulum, mitochondria) are precisely controlled. Ca 2+ regulates the functioning of the CNS, including growth, development, myelin formation, synthesis of catecholamines, modulation of neurotransmission and antioxidant protection. A growing body of evidence indicates a unique role for vitamin C in these processes. In this short review, we focus on vitamin C in the regulation of calcium-involved pathways under physiological and stress conditions in the brain.
Keyphrases
- oxidative stress
- endoplasmic reticulum
- white matter
- cerebral ischemia
- induced apoptosis
- anti inflammatory
- resting state
- dna damage
- reactive oxygen species
- multiple sclerosis
- functional connectivity
- blood brain barrier
- cell death
- protein kinase
- working memory
- diabetic rats
- ischemia reperfusion injury
- transcription factor
- ionic liquid
- nitric oxide
- heat shock protein
- heat stress
- visible light