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This effect is independent of its anti-inflammatory activity, it is exerted on both peripheral and central-spinal nociceptive terminals, and it involves the impairment of nociceptive-induced intracellular signaling (protein kinase A, calcium, and Akt/ERK activation) and the expression and release of pronociceptive peptides and neurotransmitters [22]
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![Separating Intravenous Ascorbic Acid [IV Ascorbate] and Glutathione on the same Day in Oxidative Therapies. Rationale and limitations of clinical timing](https://www.consultdranderson.com/wp-content/uploads/2019/01/iv-ascorbic.png)
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