We're sorry, but we could not fulfill your request for /high-dose-vitamin-c-protocol-for-cancer/ on this server. An invalid request was received from your browser. This may be caused by a malfunctioning proxy server or browser privacy software. Your technical support key is: af29-b8ee-1756-6707 You can use this key to fix this problem yourself. and be sure to provide the technical support key shown above.Cancer researchers in the US are currently studying the effects of treatment combining chemotherapy or radiotherapy with high doses of vitamin C administered intravenously. The first results, focusing on lung cancer and pancreatic cancer -- the two of the disease's most deadly forms -- appear to be encouraging. Vitamin C levels in the blood can be 100 to 500 times higher when administered intravenously, researchers from the University of Iowa, USA, explain in a study published in Redox Biology. This super-high concentration of vitamin C in the blood is understood to be crucial in its ability to fight cancer cells.
Vitamin C, or ascorbic acid, is an antioxidant compound found in a wide range of fruit and vegetables (oranges, grapefruits, lemons, cabbages). It can also be taken as a dietary supplement, either alone or as part of a multivitamin complex. A preliminary clinical trial, involving lung cancer and pancreatic cancer patients, saw initial encouraging results when combining high-dose intravenous vitamin C with chemotherapy or radiotherapy. The overall health of patients was found to improve and the treatment was well tolerated. The scientists established that vitamin C breaks down to form hydrogen peroxide (H2O2) that can damage DNA and tissue. The study reveals that unlike "normal" cells, cancer cells have difficulty removing hydrogen peroxide, and can struggle to survive its effects. This phenomenon explains how very high levels of vitamin C, used in the clinical trials, can effectively attack cancer cells. According to the study, hydrogen peroxide doesn't appear to be harmful to healthy, non cancerous cells, which contain an enzyme called catalase that allows them to keep levels of hydrogen peroxide, caused by the decomposition of vitamin C, very low by removing it.
"Our results suggest that cancers with low levels of catalase are likely to be the most responsive to high-dose vitamin C therapy, whereas cancers with relatively high levels of catalase may be the least responsive," said Garry Buettner, professor of radiation oncology at the University of Iowa. The researchers now hope to establish whether this kind of treatment can improve survival rates for cancer patients.Your action has resulted in an error. Please click the Back button in your browser and try again.The requested URL /scielo.php?script=sci_arttext&pid=S1807-59322016000800470 was not found on this server.We have found that open AAA repair caused significant changes in markers of systemic endothelial dysfunction as well as an increase in systemic and pulmonary inflammation, and a reduction in a marker of pulmonary function. However ascorbic acid therapy did not attenuate changes in these biomarkers following open AAA repair.Our findings are in keeping with previous data showing increased urinary ACR and inflammation and with a decrease in PaO2:FiO2 ratio following open AAA repair [12,38].
In contrast to these findings however we did not see an increased serum CRP or increased plasma vWF. An increasing proportion of participants now receive treatment for co-morbid conditions such as statins. Statins have anti-inflammatory effects [28,39] and may modulate endothelial function modifying responses to open AAA surgery. We found no increase in pulmonary dead space fraction. It is possible that the injury was not sufficient to induce pulmonary endothelial dysfunction or that the time to post operative assessment was of insufficient duration. As part of the standardized anaesthetic protocol, maintenance was with sevoflurane which has been shown to protect the endothelium from ischaemia-reperfusion injury [40] and might have further attenuated any potential pulmonary endothelial injury.The fall in EBC pH as a marker of alveolar neutrophilic inflammation was an interesting finding. This was associated with a decrease in the PaO2:FiO2 ratio. The fall in EBC pH in this study may reflect pulmonary inflammation given that there was no correlation found with this decrease and changes in systemic pH.Ischaemia-reperfusion injury has been used to provoke acute lung injury (ALI) in animal models [41].
The obligate ischaemia-reperfusion injury of open AAA repair is associated with post operative pulmonary dysfunction [42]. A recent observational study found that post-operative respiratory failure was associated with increased mortality [43]. Reflecting findings in ALI, we have shown open AAA repair is associated with local alveolar inflammation as well as systemic endothelial dysfunction and inflammation. Elevated plasma IL-6 and -8 levels are predictive of outcome in patients with ALI [44]. As a marker of systemic vascular permeability, urinary ACR has been shown to have an inverse relationship with PaO2:FiO2 ratio in a cohort of trauma patients [45]. These findings support the use of open AAA repair as a human model of ALI induced by systemic inflammation. However, in the present study mediators implicated in ALI such as vWF [11] were not elevated. It is possible that endothelial injury was not caused to a measurable level. In a murine model of ALI the administration of parenteral ascorbic acid (200 mg/ml) 30 minutes after a septic insult attenuated the inflammatory response and was associated with improved survival, pulmonary function and coagulation [21].
In this study Fisher and colleagues suggested that the protective effects of ascorbic acid are due to its pleotropic actions on multiple pathways and it is possible in the current study, a lack of benefit may be related to the limitations in biomarkers used.We investigated a single 2 g bolus of intravenous ascorbic acid following induction of anaesthesia in this study. This dose was informed by previous research where pre-treatment with 2 g ascorbic acid was found to modulate the adverse haemodynamic effects of experimentally induced hyperglycaemia [46]. In addition ascorbic acid (2 g) has been shown to prevent hyperglycaemia-induced endothelial dysfunction in healthy human volunteers [47].In the present study a decrease in plasma adhesion molecules was found. Haemodilution as part of intra-operative management could be potential mechanism for the reduction in soluble adhesion molecules as well as the lack of increase in serum hsCRP. However, as plasma IL-6 and IL-8 both increased, haemodilution is less likely.
Co-morbid treatment may also have influenced adhesion molecules expression. Both statins and β blockers may modify adhesion molecules expression. Human coronary endothelial cells treated with nebivolol in vitro have a decrease in VCAM-1, ICAM-1, E- and P-Selectin expression [48]. Interestingly in another study of open AAA repair there was a non-significant fall in both ICAM-1 and VCAM-1 [49]. This has been mirrored in an in vitro study of human aortic endothelial cells which showed exposure of these cells to hypoxia and subsequent reoxygenation did not upregulate surface expression or shedding of adhesion molecules [50].There was no increase in markers of oxidative stress in the placebo group unlike in other studies. Prosaglandin F2α is increased both on hospital arrival and during the perioperative period in patients with ruptured AAA repair [51]. Malondialdehyde, another marker of oxidative damage was increased at one and 24 hours post open AAA repair [52]. In a recent small observational study derivatives of reactive oxygen metabolites were used to define post-operative oxidative stress in patients undergoing aortic surgery.
This showed that in those having open AAA repair this marker was no different at 24 hours after surgery, but was significantly elevated 1 week later [53]. This study had an earlier sampling time, older cohort of patients and aortic clamp times contributing to the different data between studies.Ascorbic acid did not improve markers of endothelial function or attenuate the inflammatory response markers in this study. In previous research pretreatment with 2000mg parenteral ascorbic acid prevented arterial stiffness secondary to induced hyperglycaemia in healthy male volunteers [23]. In a study of 37 critically ill patients with burns the use of high dose ascorbic acid (66 mg/kg/hr) for 24 hours reduced fluid requirements, wound oedema, and severity of pulmonary dysfunction [25]. In a double-blind randomized placebo-controlled trial of 216 critically ill patients, enteral ascorbic acid (500 mg/day) and tocopherol (400 IU/day) was associated with a decrease in 8-isoprostane. The anti-oxidant treated group had improved 28-day mortality and more ventilator free days [54].
We found lipid hydroperoxides were increased with ascorbic acid. This increase in lipid peroxides was not seen in plasma 8-isoprostanes, another measure of oxidative stress. Lipid hydroperoxides can be affected by dietary factors not accounted for in the current study. Isoprostane levels however, are not affected by diet [55] and may be a better measure of oxidative stress [56]. Previous studies utilizing the FOX assay have indicated its lack of specificity for hydroperoxides [57]. However, in keeping with our findings, Bailey at al found 2000 mg ascorbic acid orally two hours before operation in patients undergoing major vascular surgery increased both lipid peroxides and plasma IL-6 [58]. Possible reasons for increased oxidative stress markers in this current study may relate to the timing of sampling and range of ischaemic times. It is possible that at the dose used in this study, ascorbic acid acted as a pro-oxidant with no beneficial effects on either the endothelium or measured mediators of inflammation.