Vitamin c as sodium ascorbate
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The Role and Impact of Vitamin C as Sodium Ascorbate
Stability and Degradation of Sodium Ascorbate in Polymer Matrices
Sodium ascorbate, a common form of vitamin C, exhibits varying stability depending on its physical state and environmental conditions. Research indicates that sodium ascorbate is more labile than ascorbic acid (AA) when in an amorphous state, particularly in low moisture food products produced by rapid dehydration. Both forms of vitamin C degrade significantly in storage environments that maintain the products in a glassy amorphous state, with sodium ascorbate degrading faster when present at lower proportions in polymer matrices.
Anticancer Properties of Sodium Ascorbate
Sodium ascorbate has shown promising anticancer properties, particularly in high doses administered intravenously. In vitro studies have demonstrated its effectiveness against various human tumor cell lines, although clinical trials have yet to replicate these results consistently. Factors such as the pharmaceutical preparation, administration schedule, and tumor tissue oxygenation may influence the efficacy of sodium ascorbate in vivo. Despite these challenges, sodium ascorbate remains a potential anticancer agent due to its safety, minimal contraindications, and selective action against cancer cells.
Mechanisms of Sodium Ascorbate-Induced Apoptosis
Iron Uptake and Apoptosis in Melanoma Cells
Sodium ascorbate induces apoptosis in melanoma cells by down-regulating transferrin receptor (TfR) dependent iron uptake. This reduction in intracellular iron levels triggers apoptosis, a process enhanced by iron chelators and inhibited by iron donors. The down-regulation of TfR expression precedes apoptosis, suggesting a specific mechanism by which sodium ascorbate mediates cell death in melanoma cells.
Cell Cycle Arrest and Apoptosis
In human malignant melanoma A375.S2 cells, sodium ascorbate induces cell cycle arrest and apoptosis in a dose-dependent manner. This process involves increased expressions of p53 and p21, decreased expressions of cyclin A, cyclin E, CDK2, and CDK4, and changes in mitochondrial membrane potential and caspase 3 activation. These molecular changes culminate in apoptosis, highlighting the potential of sodium ascorbate as a therapeutic agent against melanoma.
Prooxidant Activity and Mitochondrial Pathways
Sodium ascorbate also induces apoptosis in B16F10 murine melanoma cells through a prooxidant mechanism, increasing intracellular reactive oxygen species (ROS) levels. This process is independent of caspase-8 and involves a reduction in mitochondrial membrane potential and cytochrome-c release from mitochondria. These findings suggest that sodium ascorbate's prooxidant activity and its impact on mitochondrial pathways are crucial for its apoptotic effects in melanoma cells.
Transport Mechanisms of Ascorbate and Dehydroascorbic Acid
Ascorbate and its oxidized metabolite, dehydroascorbic acid, are transported into human cells via distinct mechanisms. Ascorbate is transported by a sodium-dependent carrier-mediated active transport, while dehydroascorbic acid is transported and accumulated as ascorbate through a sodium-independent process. Once inside the cells, dehydroascorbic acid is rapidly reduced to ascorbate, ensuring its availability for intracellular utilization.
Conclusion
Sodium ascorbate, a form of vitamin C, plays a significant role in various biological processes, including its potential as an anticancer agent. Its stability in different environments, mechanisms of inducing apoptosis, and distinct transport pathways highlight its multifaceted nature. Further research is needed to optimize its clinical applications and fully harness its therapeutic potential.
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