Plasma Vitamin C Levels Are Decreased and Correlated With Brain Damage in Patients With Intracranial Hemorrhage or Head Trauma

Abstract

Background and Purpose-Free radical hyperproduction may play an important role in brain hemorrhage and ischemia/reperfusion injury. The aims of this study were to assess whether antioxidant depletion occurs after intracranial hemorrhage (ICH) and head trauma (HT) and to evaluate the relation between the diameter of the brain lesion, the degree of the neurological impairment, and any observed antioxidant changes. Methods-We measured plasma levels of vitamin C (ascorbic acid, AA), uric acid (UA), vitamin E (␣-tocopherol), and ubiquinol-10 in 13 patients with ICH and 15 patients with HT on the day of the brain injury and subsequently every other day up to 1 week. Patients were compared with 40 healthy control subjects. Results-ICH and HT patients had significantly lower plasma levels of AA compared with healthy subjects, in contrast to plasma levels of UA, ␣-tocopherol, and ubiquinol-10. AA levels were significantly inversely correlated with the severity of the neurological impairment as assessed by the Glasgow Coma Scale and the National Institutes of Health Stroke Scale. AA levels were also significantly inversely correlated with the major diameter of the lesion. In addition, mean plasma AA levels were lower in jugular compared with peripheral blood samples obtained from 5 patients. Conclusions-These findings suggest that a condition of oxidative stress occurs in patients with head trauma and hemorrhagic stroke of recent onset. The consequences of early vitamin C depletion on brain injury as well as the effects of vitamin C supplementation in ICH and HT patients remain to be addressed in further studies. Key Words: antioxidants Ⅲ brain hemorrhage Ⅲ head trauma Ⅲ oxidative stress Ⅲ vitamin C I ncreased production of free radicals and reactive oxygen species (ROS) leading to oxidative stress 1 appears to play an important role in the pathogenesis of ischemic, 2,3 hemorrhagic, 4,5 and traumatic brain injury. 6,7 Studies in animal models of focal cerebral ischemia and reperfusion have demonstrated the presence of increased levels of ROS. 8 -11 ROS also probably contribute to brain injury in head trauma (HT) and intracranial hemorrhage (ICH) in humans, because hemorrhage is associated with the release of hemoglobinbound heme iron, which can participate in free radical reactions to produce ROS. 4,5,12 One possible consequence of excess ROS formation is lipid peroxidation. The brain appears to be particularly vulnerable to oxidative lipid damage because of its high content of polyunsaturated fatty acids. 13 Lipid peroxidation may alter the fluidity and permeability of neuronal membranes and thus, cellular functioning, or damage membranebound receptors and enzymes. 13 In brain hemorrhage, the presence of "free" iron 14 may favor the conversion of lipid hydroperoxides to lipid alkoxyl radicals, which can "reinitiate" lipid peroxidation and hence further expand the radical chain reaction. 13 In addition, tissue lactic acidosis can dramatically enhance ROS formation and lipid peroxidation in brain tissue, which in turn ca...

Two Grams BID Is an Oral Dosage of Vitamin C to Reduce the Risk of Recurrence of Superficial Bladder Carcinoma

“…Other documented effects of AA are beneficial. These include a minor reduction in blood pressure [26], a reduction in cortisol levels [27], and a reduction in the risk of stroke damage [28]- [30].…”

Antioxidant Strategies in Neurocritical Care

“…The role of OS in patients with ICH has been investigated in a small study of 13 patients with spontane-ous ICH and 15 patients with traumatic ICH, compared to 40 healthy controls [38]. ICH patients had significantly lower plasma levels of vitamin C and vitamin C levels inversely correlated with the severity of neurological impairment, as assessed by Glasgow Coma Scale and the NIHSS, and the diameter of the hematoma.…”

“…The levels of nutrients with antioxidant properties are decreased in critical illness. For example, patients with ICH have lower plasma levels of vitamin C compared with healthy volunteers [38]. Other studies have shown a reduction in muscle glutamine and glutathione and muscle protein synthesis in intensive care patients [81].…”

Revisión del traumatismo craneoencefálico

“…Este ion hidroxilo altera la configuración espacial de los fosfolípidos de las neuronas, astrocitos y probablemente del endotelio, pasando sucesivamente de una molécula lipídica a otra a lo largo de la membrana hasta alterar la totalidad de las mismas (peroxidación lipídica). La vitamina E es capaz de interponerse entre cada dos moléculas de fosfolípidos, inactiván-dose por oxidación, a la vez que convierte al OH -en agua, y reactivándose ulteriormente gracias a la vitamina C, a la que oxida y consume en el proceso 32 . A este respecto, uno de los autores ha observado en modelos de isquemia cerebral que, siempre que la concentración plasmática de vitamina C se encuentra dentro de un determinado rango, no es necesario aportar vitamina E pues ésta se mantiene en concentraciones adecuadas simplemente con el aporte que supone la ingesta normal.…”