Ascorbic Acid (80, 100, 200, 300mesh Fine Powder)

Fowler, Alpha A., et al. Journal of translational medicine, 2014, 12, 1-10.

This work aimed to determine whether intravenous ascorbic acid is safe in patients with severe sepsis. The results showed that intravenous ascorbic acid is safe and well tolerated and may have a positive effect on the degree of multiorgan failure and biomarkers of inflammation and endothelial injury.
· Evaluation methods
In this study, 24 patients diagnosed with severe sepsis in the medical intensive care unit were randomly assigned to three groups in a 1:1:1 ratio. Each group received intravenous infusions every six hours over a four-day period: the first group received low-dose ascorbic acid (Lo-AscA) at 50 mg/kg/24 h, the second group received high-dose ascorbic acid (Hi-AscA) at 200 mg/kg/24 h, and the third group was given a placebo consisting of 5% dextrose in water.
· Results
At the start of the study, the mean plasma ascorbic acid level among all participants was 17.9 ± 2.4 μM, which is below the normal range of 50-70 μM. Infusions of ascorbic acid led to a rapid and significant increase in plasma levels. Ascorbic acid patients showed no safety issues. Ascorbic acid patients showed no safety issues. Furthermore, the ascorbic acid group rapidly reduced SOFA scores while the placebo group did not improve. The administration of ascorbic acid also significantly lowered proinflammatory biomarkers such as C-reactive protein and procalcitonin. Additionally, patients receiving ascorbic acid did not experience a significant increase in thrombomodulin levels, indicating a reduction in vascular endothelial damage, unlike the placebo group.

Ajith, T. A., et al. Clinica chimica acta, 2007, 375(1-2), 82-86.

This work compared the protective effects of ascorbic acid (vitamin C) and α-tocopherol (vitamin E) against cisplatin-induced nephrotoxicity in mice. Higher doses of the vitamins were effective in preventing oxidative renal injury, and vitamin C was a better renal protector than vitamin E. This protective effect was achieved in part by preventing a decline in the renal antioxidant status.
· Evaluation methods
A comparative study was conducted to assess the nephroprotective effects of antioxidant vitamins (vitamin C and vitamin E) against cisplatin-induced oxidative renal damage in mice. Mice were administered cisplatin (10 mg/kg, intraperitoneal) to induce renal damage. To counteract this, mice were treated with either 250 mg/kg or 500 mg/kg of the antioxidant vitamins orally. Renal function was evaluated by measuring serum urea and creatinine levels, while antioxidant status was assessed in kidney homogenates.
· Results
Both vitamin C and vitamin E at a dose of 500 mg/kg significantly (P < 0.01) protected against cisplatin-induced nephrotoxicity. Treatment with either vitamin at both doses reduced the cisplatin-induced increases in serum urea and creatinine levels. However, the cisplatin-induced decline in renal antioxidant enzyme activities, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), was only reversed by the 500 mg/kg dose of the vitamins. Both vitamins, at both doses, were able to increase reduced glutathione (GSH) levels and prevent the cisplatin-induced increase in lipid peroxidation.