Administration of Vitamin C and Vitamin E in Severe Head Injury: A Randomized Double-blind Controlled Trial

Razmkon, Ali; Sadidi, Ahmad; Sherafat-Kazemzadeh, Ehsan; Mehrafshan, Ali; Jamali, Mohammad; Malekpour, Babak; Saghafinia, Masoud

doi:10.1227/neu.0b013e3182279a8f

Cited by 60 publications

(63 citation statements)

References 14 publications

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“…The only published RCT of Vitamin E (at a dose of 400 IU/d IM for 7 days) in severe TBI showed decreased hospital mortality and improved 6 month Glasgow Outcome Scale Score (GOS) vs. placebo in adults (Razmkon et al, 2011). Due to the small size of this trial (n = 23–27 patients/group), known antiplatelet effects of Vitamin E, and associated risk of hemorrhagic stroke with Vitamin E supplementation (Schurks et al, 2010), a multicenter RCT is necessary before Vitamin E can be recommended for routine use in severe TBI .…”

Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

“…Similarly, plasma ascorbate levels are decreased after stroke (Yokoyama et al, 2000), intracranial hemorrhage and head trauma (Polidori et al, 2001). Razmkon and colleagues (Razmkon et al, 2011) compared treatment with low-dose (500 mg/d IV for 7 days) and high-dose Vitamin C (10 g IV on the 1 st and 4 th days followed by 4 g/d IV for 3 days) with placebo after severe TBI in adults. While high-dose Vitamin C decreased the diameter of perilesional hypodense region on head CT (defined as edema), low-dose Vitamin C increased the diameter of this region compared with placebo.…”

Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

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Therapies targeting lipid peroxidation in traumatic brain injury

2016

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Lipid peroxidation can be broadly defined as the process of inserting a hydroperoxy group into a lipid. Polyunsaturated fatty acids present in the phospholipids are often the targets for peroxidation. Phospholipids are indispensable for normal structure of membranes. The other important function of phospholipids stems from their role as a source of lipid mediators – oxygenated free fatty acids that are derived from lipid peroxidation. In the CNS, excessive accumulation of either oxidized phospholipids or oxygenated free fatty acids may be associated with damage occurring during acute brain injury and subsequent inflammatory responses. There is a growing body of evidence that lipid peroxidation occurs after severe traumatic brain injury in humans and correlates with the injury severity and mortality. Identification of the products and sources of lipid peroxidation and its enzymatic or non-enzymatic nature is essential for the design of mechanism-based therapies. Recent progress in mass spectrometry-based lipidomics/oxidative lipidomics offers remarkable opportunities for quantitative characterization of lipid peroxidation products, providing guidance for targeted development of specific therapeutic modalities. In this review, we critically evaluate previous attempts to use non-specific antioxidants as neuroprotectors and emphasize new approaches based on recent breakthroughs in understanding of enzymatic mechanisms of lipid peroxidation associated with specific death pathways, particularly apoptosis. We also emphasize the role of different phospholipases (calcium-dependent and -independent) in hydrolysis of peroxidized phospholipids and generation of pro- and anti-inflammatory lipid mediators.

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Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

Section: Therapeutic Strategies Targeting Lipid Peroxidationmentioning

confidence: 99%

Therapies targeting lipid peroxidation in traumatic brain injury

2016

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“…The search of other gray literature only produced duplicate or nonrelevant material. Of the 37 articles, 6 articles met our inclusion criteria and were included in the final review (Aquilani et al, 2008;Hoffer, Balaban, Slade, Tsao, & Hoffer, 2013;Ma, Huang, Qin, & You, 2012;Maas et al, 2006;Razmkon et al, 2011;Theadom et al, 2013).…”

Section: Search Strategymentioning

confidence: 99%

“…Accurately assessing the adequacy of sample size of the studies was challenging as only one of the six studies provided details of power analysis (Maas et al, 2006). Based on the reported findings, it appeared that majority of the studies (Hoffer et al, 2013;Ma et al, 2012;Maas et al, 2006;Razmkon et al, 2011;Theadom et al, 2013) had appropriate sample size ranging from 60 to 861. The study by Aquilani et al (2008) was a much smaller RCT with only 41 patients.…”

Section: Critical Appraisalmentioning

confidence: 99%

Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes

Shen

Hiebert

Hartwell

et al. 2016

Worldviews Ev Based Nurs

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Background: Traumatic brain injury (TBI) is an acquired brain injury that occurs when there is sudden trauma that leads to brain damage. This acute complex event can happen when the head is violently or suddenly struck or an object pierces the skull or brain. The current principal treatment of TBI includes various pharmaceutical agents, hyperbaric oxygen, and hypothermia. There is evidence that secondary injury from a TBI is specifically related to oxidative stress. However, the clinical management of TBI often does not include antioxidants to reduce oxidative stress and prevent secondary injury.

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“…The antioxidant compounds PEG-SOD and tirilazad, an inhibitor of lipid peroxidation, have both been tested in multicenter phase III trials with no significant benefit in the overall TBI population, although post hoc analysis demonstrated potential benefit in certain subsets of patients [34,37,38]. In a small study, vitamin C and vitamin E each had mixed results [39]. Dexanabinol, a mixed glutamate antagonist and antioxidant drug, also failed to show therapeutic benefit in a randomized, placebo-controlled clinical trial in severe TBI [40].…”

Section: Peg-hccs As Potential Therapeutic Agents In Experimental Modelsmentioning

confidence: 99%

Hydrophilic carbon clusters as therapeutic, high-capacity antioxidants

Samuel

Duong

Bitner

et al. 2014

Trends in Biotechnology

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Oxidative stress reflects an excessive accumulation of reactive oxygen species (ROS) and is a hallmark of several acute and chronic human pathologies. While many antioxidants have been investigated, the majority have demonstrated poor efficacy in clinical trials. Here, we discuss limitations of current antioxidants and describe a new class of nanoparticle antioxidants, poly(ethylene glycol)-functionalized hydrophilic carbon clusters (PEG-HCCs). PEG-HCCs show high capacity to annihilate ROS such as superoxide and hydroxyl radicals, show no reactivity toward nitric oxide, and can be functionalized with targeting moieties without loss of activity. Given these properties, we propose that PEG-HCCs offer an exciting new area of study for treatment of numerous ROS-induced human pathologies.

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Administration of Vitamin C and Vitamin E in Severe Head Injury: A Randomized Double-blind Controlled Trial

Cited by 60 publications

References 14 publications

Therapies targeting lipid peroxidation in traumatic brain injury

Therapies targeting lipid peroxidation in traumatic brain injury

Systematic Review of Traumatic Brain Injury and the Impact of Antioxidant Therapy on Clinical Outcomes

Hydrophilic carbon clusters as therapeutic, high-capacity antioxidants

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