scholarly journals Exploring the Pivotal Neurophysiologic and Therapeutic Potentials of Vitamin C in Glioma

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Seidu A. Richard ◽  
Marian Sackey ◽  
Nii Korley Kortei
Keyword(s):  
Vitamin C ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Diagnostic Techniques ◽  
Vital Role ◽  
Water Soluble ◽  
Reduced Form ◽  
High Dose ◽  
Enzymatic Reactions ◽  
Primary Glioblastoma

Gliomas represent solely primary brain cancers of glial cell or neuroepithelial origin. Gliomas are still the most lethal human cancers despite modern innovations in both diagnostic techniques as well as therapeutic regimes. Gliomas have the lowest overall survival rate compared to other cancers 5 years after definitive diagnosis. The dietary intake of vitamin C has protective effect on glioma risk. Vitamin C is an essential compound that plays a vital role in the regulation of lysyl and prolyl hydroxylase activity. Neurons store high levels of vitamin C via sodium dependent-vitamin C transporters (SVCTs) to protect them from oxidative ischemia-reperfusion injury. Vitamin C is a water-soluble enzyme, typically seen as a powerful antioxidant in plants as well as animals. The key function of vitamin C is the inhibition of redox imbalance from reactive oxygen species produced via the stimulation of glutamate receptors. Gliomas absorb vitamin C primarily via its oxidized dehydroascorbate form by means of GLUT 1, 3, and 4 and its reduced form, ascorbate, by SVCT2. Vitamin C is able to preserve prosthetic metal ions like Fe2+ and Cu+ in their reduced forms in several enzymatic reactions as well as scavenge free radicals in order to safeguard tissues from oxidative damage. Therapeutic concentrations of vitamin C are able to trigger H2O2 generation in glioma. High-dose combination of vitamin C and radiation has a much more profound cytotoxic effect on primary glioblastoma multiforme cells compared to normal astrocytes. Control trials are needed to validate the use of vitamin C and standardization of the doses of vitamin C in the treatment of patients with glioma.

scholarly journals Making sense of early high-dose intravenous vitamin C in ischemia/reperfusion injury

Critical Care ◽  
2018 ◽  
Vol 22 (1) ◽  
Author(s):  
Angelique M. E. Spoelstra-de Man ◽  
Paul W. G. Elbers ◽  
Heleen M. Oudemans-van Straaten
Keyword(s):  
Vitamin C ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Dose ◽  
Making Sense ◽  
Intravenous Vitamin

scholarly journals The Effect of High Dose Melatonin on Cardiac Ischemia-reperfusion Injury

2008 ◽  
Vol 49 (5) ◽  
pp. 735 ◽  
Author(s):  
Hakan Ceyran ◽  
Figen Narin ◽  
Nazmi Narin ◽  
Hülya Akgün ◽  
A. Bahar Ceyran ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
High Dose

scholarly journals NEUROPROTECTIVE ROLE OF ASCORBIC ACID: ANTIOXIDANT AND NON-ANTIOXIDANT FUNCTIONS

2018 ◽  
Vol 11 (10) ◽  
pp. 30 ◽  
Author(s):  
Arun Kumar ◽  
Reena V Saini ◽  
Adesh K Saini
Keyword(s):  
Ascorbic Acid ◽  
Vitamin C ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glutamate Toxicity ◽  
Cellular Functions ◽  
Dietary Antioxidant ◽  
The Central Nervous System

Ascorbic acid (AA) or Vitamin C is an important antioxidant which participates in numerous cellular functions. Although in human plasma its concentration is in micromolars but it reaches millimolar concentrations in most of the human tissues. The high ascorbate cellular concentrations are generated and maintained by a specific sodium-dependent Vitamin C transporter type 2 (SVCT2, member of Slc23 family). Metabolic processes recycle Vitamin C from its oxidized forms (ascorbate) inside the cells. AA concentration is highest in the neurons of the central nervous system (CNS) of mammals, and deletion of its transporter affects mice brain and overall survival. In the CNS, intracellular ascorbate serves several functions including antioxidant protection, peptide amidation, myelin formation, synaptic potentiation, and protection against glutamate toxicity. SVCT2 maintains neuronal ascorbate content in CNS which has relevance for neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s disease. As ascorbate supplements decrease infarct size in ischemia-reperfusion injury and protect neurons from oxidative damage, it is a vital dietary antioxidant. The aim of this review is to assess the role of the SVCT2 in regulating neuronal ascorbate homeostasis in CNS and the extent to which ascorbate affects brain function as an antioxidant.

Intramuscular Administration of Very High Dose of a-Tocopherol Protects Liver from Severe Ischemia/Reperfusion Injury

2002 ◽  
Vol 26 (7) ◽  
pp. 872-877 ◽  
Author(s):  
Dimitrios Giakoustidis ◽  
Georgios Papageorgiou ◽  
Stavros Iliadis ◽  
Nicholas Kontos ◽  
Evanthia Kostopoulou ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Intramuscular Administration ◽  
High Dose ◽  
Very High ◽  
Severe Ischemia

scholarly journals Production of Hydrogen Sulfide by Fermentation in Rumen and Its Impact on Health and Production of Animals

Processes ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 1169
Author(s):  
Ali Mujtaba Shah ◽  
Jian Ma ◽  
Zhisheng Wang ◽  
Rui Hu ◽  
Xueying Wang ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Animal Health ◽  
Rumen Fermentation ◽  
Intestinal Wall ◽  
Vital Role ◽  
The Body ◽  
Sulfide Concentration ◽  
Production Of Hydrogen

Hydrogen sulfide is a Janus-faced molecule with many beneficial and toxic effects on the animal health. In ruminants, rumen fermentation plays a vital role in the digestion and absorption of nutrients. During rumen fermentation, the production of hydrogen sulfide can occur, and it can be rapidly absorbed into the body of the animals through the intestinal wall. If the production of hydrogen sulfide concentration is higher in the rumen, it can cause a toxic effect on ruminants known as poliomyelitis. The production of hydrogen sulfide depends on the population of sulfate-reducing bacteria in the rumen. In rodents, H2S maintains the normal physiology of the gastrointestinal tract and also improves the healing of the chronic gastric ulcer. In the gut, H2S regulates physiological functions such as inflammation, ischemia–reperfusion injury and motility. In this review article, we summarize the toxicity occurrence in the body of animals due to high levels of hydrogen sulfide production and also recent progress in the studies of physiological function of H2S in the gut, with a special emphasis on bacteria-derived H2S is discussed in this review.

scholarly journals Insulin-Like Growth Factor and Epidermal Growth Factor Treatment: New Approaches to Protecting Steatotic Livers against Ischemia-Reperfusion Injury

Endocrinology ◽  
2009 ◽  
Vol 150 (7) ◽  
pp. 3153-3161 ◽  
Author(s):  
Araní Casillas-Ramírez ◽  
Amine Zaouali ◽  
Susagna Padrissa-Altés ◽  
Ismail Ben Mosbah ◽  
Anna Pertosa ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Dose ◽  
Igf Binding Proteins ◽  
Igf I ◽  
Epidermal Growth ◽  
Sites Of Action

Hepatic steatosis is a major risk factor in ischemia-reperfusion (I/R). IGF-binding proteins (IGFBPs) modulate IGF-I action by transporting circulating IGF-I to its sites of action. Epidermal growth factor (EGF) stimulates IGF-I synthesis in vitro. We examined the effect of IGF-I and EGF treatment, separately or in combination, on the vulnerability of steatotic livers to I/R. Our results indicated that I/R impaired IGF-I synthesis only in steatotic livers. Only when a high dose of IGF-I (400 μg/kg) was given to obese animals did they show high circulating IGF-I:IGFBP levels, increased hepatic IGF-I levels, and protection against damage. In lean animals, a dose of 100 μg/kg IGF-I protected nonsteatotic livers. Our results indicated that the combined administration of IGF-I and EGF resulted in hepatic injury parameters in both liver types similar to that obtained by IGF-I and EGF separately. IGF-I increased egf expression in both liver types. The beneficial role of EGF on hepatic I/R injury may be attributable to p38 inhibition in nonsteatotic livers and to PPARγ overexpression in steatotic livers. In conclusion, IGF-I and EGF may constitute new pharmacological strategies to reduce the inherent susceptibility of steatotic livers to I/R injury.

scholarly journals Administration of a CO-releasing molecule at the time of reperfusion reduces infarct size in vivo

2004 ◽  
Vol 286 (5) ◽  
pp. H1649-H1653 ◽  
Author(s):  
Yiru Guo ◽  
Adam B. Stein ◽  
Wen-Jian Wu ◽  
Wei Tan ◽  
Xiaoping Zhu ◽  
...  
Keyword(s):  
At Risk ◽  
Infarct Size ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Effective Means ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Water Soluble ◽  
Arterial Blood

Although carbon monoxide (CO) has traditionally been viewed as a toxic gas, increasing evidence suggests that it plays an important homeostatic and cytoprotective role. Its therapeutic use, however, is limited by the side effects associated with CO inhalation. Recently, transition metal carbonyls have been shown to be a safe and effective means of transporting and releasing CO groups in vivo. The goal of the present study was to test whether a water-soluble CO-releasing molecule, tricarbonylchloro(glycinato) ruthenium (II) (CORM-3), reduces infarct size in vivo when given in a clinically relevant manner, i.e., at the time of reperfusion. Mice were subjected to a 30-min coronary artery occlusion followed by 24 h of reperfusion and were given either CORM-3 (3.54 mg/kg as a 60-min intravenous infusion starting 5 min before reperfusion) or equivalent doses of inactive CORM-3, which does not release CO. CORM-3 had no effect on arterial blood pressure or heart rate. The region at risk did not differ in control and treated mice (44.5 ± 3.5% vs. 36.5 ± 1.6% of the left ventricle, respectively). However, infarct size was significantly smaller in treated mice [25.8 ± 4.9% of the region at risk ( n = 13) vs. 47.7 ± 3.8% ( n = 14), P < 0.05]. CORM-3 did not increase carboxyhemoglobin levels in the blood. These results suggest that a novel class of drugs, CO-releasing molecules, can be useful to limit myocardial ischemia-reperfusion injury in vivo.

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