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Combining the analysis of GSH, GSSG, and conjugates would be beneficial in pinpointing the role of contaminants within the plethora of causes that could lead to the toxic effects of reactive oxygen species

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The Ca 2+ overloading-mediated neuronal excitotoxicity is a well-known mechanism for the pathogenesis of cerebral ischemia, during which the abnormal increase in intracellular Ca 2+ contributes largely to neuronal loss (Kobayashi and Mori, 1998)

Cellular uptake of riboflavin occurs through the actions of the SLC transporters encoded by the SLC52A1 and SLC52A2 genes