The brain is particularly susceptible to oxidative stress being the most aerobically active organ in the body due to its high metabolic demands. There is evidence that neuronal hyperexcitability and oxidative injury produced by an excessive production of free radicals may play a role in the initiation and progression of epilepsy. Understanding the role of oxidative stress in epileptogenesis is essential to delineate appropriate therapeutic strategies. Neuroprotectant or antioxidant compounds may exert positive effects when associated with antiepileptic drugs (AEDs). Areas covered: This review aims to outline the current state of knowledge on the relationship between oxidative stress and epilepsy. The role of neuroprotectants in the therapeutic strategy to prevent or treating epilepsy is also discussed. PubMed/Medline database was searched for relevant articles on the relation between oxidative stress and epilepsy and on antioxidant strategies for epilepsy management. Expert commentary: Therapeutic intervention with antioxidants may represent a key strategy to counteract the epilepsy-related neurodegenerative process. However, in spite of the incredible development of new drugs for epilepsy treatment, definitive evidence about the neuroprotective ability of the existing compounds is still lacking. Therefore, there is great need for clinical trials to evaluate new antioxidant compounds specifically on epileptic patients.

Postnatal age and mode of delivery significantly influence CRP values. Reliable reference values are crucial in order to obtain an adequate diagnostic accuracy.

Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients.

Oxidative stress (OS) is involved in several human diseases, including obesity, diabetes, atherosclerosis, carcinogenesis, as well as genetic diseases. We previously found that OS occurs in Down Syndrome as well as in Beckwith-Wiedemann Syndrome (BWS). Here we describe the clinical case of a female patient with Prader Willi Syndrome (PWS), a genomic imprinting disorder, characterized by obesity, atherosclerosis and diabetes mellitus type 2, pathologies in which a continuous and important production of free radicals takes place. We verified the presence of OS by measuring a redox biomarkers profile including total hydroperoxides (TH), non protein-bound iron (NPBI), thiols (SH), advanced oxidation protein products (AOPP) and isoprostanes (IPs). Thus we introduced in therapy an antioxidant agent, namely potassium ascorbate with ribose (PAR), in addition to GH therapy and we monitored the redox biomarkers profile for four years. A progressive decrease in OS biomarkers occurred until their normalization. In the meantime a weight loss was observed together with a steady growth in standards for age and sex.

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