Oxidative stress in developmental brain disorders

Abstract

Oxidative stress is one of the predisposing factors in adult neurological disorders. We have examined the involvement of oxidative stress in child-onset neurodegenerative disorders, and here we review the findings from our analysis. In cases of Cockayne syndrome, the oxidative products of lipids and proteins were increased in the globus pallidus; however, oxidative nucleotide damage that coincided with reduced copper/zinc superoxide dismutase (Cu/ZnSOD) expression was observed in cases of xeroderma pigmentosum, and these patients also presented increased oxidative stress markers in urine samples. In spinal muscular atrophy, lipid peroxidation in conjunction with oxidative DNA damage was observed in motor neurons. Cases of subacute sclerosing panencephalitis presented oxidative nucleoside damage in cerebral cortical neurons at early disease stages, which were subsequently replaced by lipid peroxidation in glial cells of cerebral white matter. In relation to progressive myoclonic epilepsy, oxidative damage to DNA, proteins, and lipids appeared to coincide with cerebral and cerebellar cortical lesions of neuronal ceroidlipofuscinosis. Patients with Lafora disease also presented an increase in oxidative stress markers for DNA and/or lipids in the brain and urine. These findings imply involvement of oxidative stress in developmental brain disorders; antioxidant agents could prove to be useful for treating patients with those disorders.

Oxidative stress in children affected by epileptic encephalopathies

“…In alternative, the high oxidative stress markers detected in serum of these patients may describe an epiphenomenon of unspecific stress adaptation to epileptic attacks. It has been reported that structural anomalies of brain may play a role in increasing oxidative stress markers [3]. That pathogenetic hypothesis cannot be evoked in our series of patients since all of them had normal brain MRI.…”

“…Lipid peroxidations originating from oxidative degeneration of polyunsaturated fatty acids can migrate to different regions of cells leading to destructive processes. In addition, the loss of fatty acids results in membrane damage [3,4]. The defense mechanisms against oxidation include: (i) antioxidant enzymes such as glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase; and (ii) low-molecular-weight antioxidant compounds such as albumin, uric acid, ascorbic acid, alfa-tocopherol, beta-carotene, metal chelators, glutathione, and ubiquinones [5].…”

Changes in Cerebrospinal Fluid Biomarkers in Human Herpesvirus-6-Associated Acute Encephalopathy/Febrile Seizures

“…Oxidative stress originates from an imbalance between the production of reactive oxygen species (ROS) and, to a lesser extent, reactive nitrogen species (RNS), and the antioxidant capacities of cells and organs [5]. Recently, oxidative stress was confirmed to play a role in adult-onset neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis [6, 7].…”

Estimate of consumption of phenolic compounds by Brazilian population

“…Several studies have highlighted the inverse association between the consumption of plant foods and the prevalence of noncommunicable chronic diseases such as cancer, diabetes, cardiovascular diseases and degenerative diseases [1][2][3][4][5][6] . The benefits are related to the presence of bioactive compounds with antioxidant activity, which are capable of neutralizing the so-called free radicals.…”