Trace Element, Antioxidant Activity, and Lipid Peroxidation Levels in Brain Cortex of Gerbils After Cerebral Ischemic Injury

Abstract

Proper trace element level and antioxidant enzyme activity are crucial for the brain in maintaining normal neurological functions. To our knowledge, alteration of lipid peroxidation status, trace element level, and antioxidant activity in the homogenates of brain cortex after cerebral ischemia in gerbil, however, has not been investigated so far. Male Mongolian gerbils were divided into control and ischemic subjects. Cerebral ischemia was induced by occlusion of the right middle cerebral artery and right common carotid artery for 1 h. Experimental results showed that a significant increase (P < 0.01) of the malondialdehyde level was found in the ischemic brain as compared with the control group. Trace element analysis indicated that a remarkable elevation (P < 0.01) of the level of iron (Fe), chromium (Cr), and a statistical decrease of selenium (Se) and zinc (Zn) (P < 0.05) concentration were observed in the ischemic brain as compared with the control subject. No significant change (P > 0.05) of the copper (Cu) level was found in both experimental groups. Additionally, antioxidant activity of superoxide dismutase (P < 0.01) and catalase (P < 0.05) was significantly decreased in the ischemic brain as compared with the control subject. Taking all results together, it is conceivable to manifest the experimental findings that cerebral ischemia not only may result in an enhanced oxidative stress but also may lead to further oxidative injury. Moreover, disturbance of trace element level combined with declined antioxidant activity seems to play a significant role in responsible for the etiology of cerebral ischemia.

Selenium in the therapy of neurological diseases. Where is it going?

“…SelP−/−knockout mice display a neurological phenotype with subtle disruption of memory processes and spatial learning [60]. Moreover, other researchers have shown reduction in brain Se levels followed by a decrease in Se-dependent enzyme activity and impaired motor coordination in the same model [52,61,62]. Burk et al confirmed that the knock-out of SelP or apoER2 significantly depleted the brain's Se pool [63].…”

“…SelPs are an unusual family that can incorporate multiple Sec residues, while other selenoproteins can integrate only one. Therefore, SelP has been postulated as being involved in both Se intercellular transport and storage [52,53]. The N-terminal domain of SelP contains one Sec residue, while the other nine are located in the C-terminal.…”

“…The primary source of plasma SelP is the liver, from where SelP is transported to peripheral tissues, including brain [54,55]. Its role in the CNS is unique, because brain tissue can take up tracer Se in a form of SelP and is unable to take up directly radioactive molecule 75 Se [52]. Yet, recent data show that a deficiency of hepatic SelP does not affect brain Se levels, which indicates that this protein could be produced locally.…”

The Role of Selenium in the Multivariate Etiopathogenesis of Ischemic Stroke

“…При окислительном стрессе, сопровождающим развитие инсульта, истощение Se с последующим снижением активности селензависимых фермен-тов является важным фактором этиопатогенеза этой патологии (Fang et al, 2013;Zangieva, 2013;Bhowmick et al, 2014;Loscalzo, 2014). Известно, что во время мозгового ишемического каскада фактором, который приводит к митохондриаль-ной дисфункции, является недостаток кислорода, сопровождающийся снижением продукции АТФ.…”

Trace Elements Tolerance Modulated by Antioxidant System in Plants

“…Trace element toxicity has also been attributed to their generation of ROS (Meharg and Hartley-Whitaker, 2002;Fang et al, 2013) that cause oxidative damage to biomolecules and eventual cell death (Gunes et al, 2007). Plants have evolved mechanisms to protect cells and subcellular systems from the effects of ROS (e.g.…”