Oxidative Stress In Brain Tissue Research Articles

Developmental exposure to trichloroethylene promotes CD4 + T cell differentiation and hyperactivity in association with oxidative stress and neurobehavioral deficits in MRL+/+ mice

The non adult immune system is particularly sensitive to perinatal and early life exposures to environmental toxicants. The common environmental toxicant, trichloroethylene (TCE), was shown to increase CD4+ T cell production of the proinflammatory cytokine IFN-γ following a period of prenatal and lifetime exposure in autoimmune-prone MRL+/+ mice. In the current study, MRL+/+ mice were used to further examine the impact of TCE on the immune system in the thymus and periphery. Since there is considerable cross-talk between the immune system and the brain during development, the potential relationship between TCE and neurobehavioral endpoints were also examined. MRL+/+ mice were exposed to 0.1 mg/ml TCE (~ 31 mg/kg/day) via maternal drinking water or direct exposure via the drinking water from gestation day 1 until postnatal day (PD) 42. TCE exposure did not impact gross motor skills but instead significantly altered social behaviors and promoted aggression associated with indicators of oxidative stress in brain tissues in male mice. The immunoregulatory effects of TCE involved a redox-associated promotion of T cell differentiation in the thymus that preceded the production of proinflammatory cytokines, IL-2, TNF-α, and IFN-γ by mature CD4+ T cells. The results demonstrated that developmental and early life TCE exposure modulated immune function and may have important implications for neurodevelopmental disorders.

Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice

Conditional double knock-out of presenilin-1 (PS1) and presenilin-2 (PS2) (PS cDKO) in forebrain of mice led to progressive memory dysfunction and forebrain degeneration. These changes in the brain recapitulated most of the neurodegenerative phenotypes of Alzheimer's disease (AD). Oxidative stress in brain tissues is intimately related to AD. In this report, we examined oxidative stress status in cerebral cortex in 2-, 4- and 7-month PS cDKO and the age- and gender-matched control mice (WT). Lipid peroxidation (MDA as the measure) and protein oxidation (protein carbonyl as the measure) were found to be significantly increased in PS cDKO mice over the age points examined, notably in those at 2-month, suggesting that oxidative stress is an early event in response to PS loss-of-function. The oxidative modification of cortical proteins was further confirmed by Oxyblot assay. The investigations into endogenous antioxidant defense (CAT, SOD and GSH-px as measures) revealed a compensatory defense against oxidative stress, particularly at the early age stage, in PS cDKO mice. The expression level of cortical glial fibrillary acidic protein (GFAP) increased in an age-related manner, in particular in 2-month PS cDKO mice, suggesting that the interaction relationship between oxidative stress and inflammatory response may be closely associated with the underlying loss-of-function pathogenesis of AD.

Effects of 900-MHz electromagnetic field emitted from cellular phone on brain oxidative stress and some vitamin levels of guinea pigs

This study was designed to demonstrate the effects of 900-MHz electromagnetic field (EMF) emitted from cellular phone on brain tissue and also blood malondialdehyde (MDA), glutathione (GSH), retinol (vitamin A), vitamin D 3 and tocopherol (vitamin E) levels, and catalase (CAT) enzyme activity of guinea pigs. Fourteen male guinea pigs, weighing 500–800 g were randomly divided into one of two experimental groups: control and treatment (EMF-exposed), each containing seven animals. Animals in treatment group were exposed to 890- to 915-MHz EMF (217-Hz pulse rate, 2-W maximum peak power, SAR 0.95 w/kg) of a cellular phone for 12 h/day (11-h 45-min stand-by and 15-min spiking mode) for 30 days. Control guinea pigs were housed in a separate room without exposing EMF of a cellular phone. Blood samples were collected through a cardiac puncture and brains were removed after decapitation for the biochemical analysis at the end of the 30 days of experimental period. It was found that the MDA level increased ( P < 0.05), GSH level and CAT enzyme activity decreased ( P < 0.05), and vitamins A, E and D 3 levels did not change ( P > 0.05) in the brain tissues of EMF-exposed guinea pigs. In addition, MDA, vitamins A, D 3 and E levels, and CAT enzyme activity increased ( P < 0.05), and GSH level decreased ( P < 0.05) in the blood of EMF-exposed guinea pigs. It was concluded that electromagnetic field emitted from cellular phone might produce oxidative stress in brain tissue of guinea pigs. However, more studies are needed to demonstrate whether these effects are harmful or/and affect the neural functions.

Effects of iloprost on visual evoked potentials and brain tissue oxidative stress after bilateral common carotid artery occlusion

Effects of iloprost on visual evoked potentials and oxidant/antioxidant status were evaluated after bilateral carotid artery occlusion. There were three experimental groups; Sham (S) group ( n=10), bilateral common carotid artery occluded (BCCAO) group ( n=10) and after bilateral common carotid artery occlusion, iloprost-treated (BCCAOI) group ( n=10). Iloprost was administered (0.5 ng/kg/day) for 10 days by intraperitoneal injection. N 2 and P 2 latencies (millisecond) and N 2–P 2 (μV) amplitudes were recorded 10 days after operation for evaluating VEPs. The rats were sacrificed by decapitation immediately after recording of VEPs. Malondialdehyte (MDA), glutathione (GSH), Cu–Zn superoxide dysmutase (SOD) were studied spectrophotometricly. After BCCAO, MDA levels were increased, GSH and Cu–Zn SOD levels were decreased significantly, and abnormal VEPs parameters were observed. Iloprost treatment after BCCAO decreased MDA and increased GSH levels significantly. Low Cu–Zn SOD levels and impaired VEPs remained after iloprost treatment. Iloprost treatment may protect the brain tissue from oxidative damage during cerebral hypoperfusion.

Acute Hypertension Induces Oxidative Stress in Brain Tissues

Arterial hypertension is not only a major risk factor for cerebrovascular accidents, such as stroke and cerebral hemorrhage, but is also associated to milder forms of brain injury. One of the main causes of neurodegeneration is the increase in reactive oxygen species (ROS) that is also a common trait of hypertensive conditions, thus suggesting that such a mechanism could play a role even in the onset of hypertension-evoked brain injury. To investigate this issue, we have explored the effect of acute-induced hypertensive conditions on cerebral oxidative stress. To this aim, we have developed a mouse model of transverse aortic coarctation (TAC) between the two carotid arteries, which imposes acutely on the right brain hemisphere a dramatic increase in blood pressure. Our results show that hypertension acutely induced by aortic coarctation induces a breaking of the blood-brain barrier (BBB) and reactive astrocytosis through hyperperfusion, and evokes trigger factors of neurodegeneration such as oxidative stress and inflammation, similar to that observed in cerebral hypoperfusion. Moreover, the derived brain injury is mainly localized in selected brain areas controlling cognitive functions, such as the cortex and hippocampus, and could be a consequence of a defect in the BBB permeability. It is noteworthy to emphasize that, even if these latter events are not enough to produce ischemic/hemorrhagic injury, they are able to alter mechanisms fundamental for maintaining normal brain function, such as protein synthesis, which has a prominent role for memory formation and cortical plasticity.

Enhanced maze performance and reduced oxidative stress by combined extracts of zingiber officinale and ginkgo biloba in the aged rat.

Here we assessed the effects of i.g. administration of Zingicomb (ZC), a mixture of zingiber officinale and ginkgo biloba extracts, on learning and memory, and on indicators of oxidative stress in aged rats. Effects of ZC (1 and 10 mg/kg) were investigated in 22-24 months old Wistar rats using the Morris water maze, in which they show deficient performance as compared to 3 months old rats in the undrugged state (days 1 and 2). Treatment was administered on days 3 and 4 of training, then over 7 days with training discontinued, and again on days 5 and 6 when training was resumed. Thereafter chronic treatment was maintained over 5 months. 1 mg/kg ZC improved escape learning in the water maze. The two capital indicators of oxidative stress in brain homogenates, the amount of oxidized proteins (assessed as carbonyl group containing proteins) and lipid peroxidation, were significantly reduced in ZC treated animals. Thus, ZC, which had previously been shown to improve inhibitory avoidance learning and to have anxiolytic properties in adult animals, might also facilitate spatial learning in aged animals, and reduces indices of oxidative stress in brain tissue after chronic treatment.

Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-<i>p</i>-dioxin

Acute acidosis elevates malonaldehyde in rat brain in vivo

Oxidative stress in brain tissue was measured experimentally in situ using microdialysis to sample the extracellular environment for a lipid peroxidation breakdown product and antioxidants. The extracellular concentrations of the lipid peroxidation product malonaldehyde (MDA) and the antioxidants ascorbic acid (AA) and uric acid (UA) were measured in rat cortex and striatum in vivo using microdialysis coupled to HPLC with UV detection. Tissue acidosis following ischaemia and epileptic seizures may contribute to neuronal damage, which may be mediated by reactive oxygen species. Perfusion of microdialysis probes with acidic artificial cerebrospinal fluid (pH 6) led to a significant increase in the sampled concentration of MDA and the antioxidant ascorbic acid. Simultaneous perfusion of ascorbate (5 mM) with acidic ACSF (pH 6) completely attenuated the rise in lipid peroxidation. This study provides in vivo evidence for acidosis induced oxidative stress in brain tissue and an antioxidant action of ascorbate. The methodology described here can provide direct in vivo information in respect of oxidative stress in experimental situations. The method could equally be applied to the assessment of oxidative stress in a number of pathological models not necessarily confined to the CNS