Oxidative Stress in Metabolic and Non-metabolic Diseases

Dear Colleagues,

Mitochondria are a major source of reactive oxygen species (ROS) generation within the cell. Electron leakage from complexes I and III of the mitochondrial respiratory chain (MRC) causes the partial reduction of molecular oxygen to the superoxide, which is then dismutated to hydrogen peroxidase by superoxide dismutase. Both superoxide and hydrogen peroxide are considered mitochondrial ROS. Under physiological conditions, ROS act as potential secondary messengers which could be used to specifically modulate distinct cellular pathways, including the innate immunity signalling cascade. However, once the level of ROS production exceeds the scavenging capacity of the cellular antioxidant defence system, a condition known as oxidative stress (OS) arises, which can induce a secondary mitochondrial dysfunction as opposed to a primary mitochondrial dysfunction which is an inherited genetic disorder. OS can induce DNA mutations, impair MRC activity, alter membrane permeability, and influence Ca²⁺ homeostasis and mitochondrial internal defence mechanisms leading to an impaired mitochondrial function and contributing to disease pathophysiology. OS and mitochondrial dysfunction have been implicated in the progression of a number of diseases, including the neurodegenerative disorders of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, metabolic diseases such as MRC disorders and lysosomal storage disorders, diabetes, cardiovascular diseases and cancer. The use of appropriate antioxidant adjunct therapies may be particularly important in the treatment of diseases associated with mitochondrial dysfunction and OS, although treatment protocols have yet to be fully established or standardised. Since mitochondria are a major contributor to cellular OS in the disease state, antioxidant strategies targeting this organelle may offer particular therapeutic potential. However, an excessive administration of antioxidants may inhibit ROS-dependent signalling pathways and prevent the induction of endogenous antioxidant defence systems. In order to detect evidence of OS in patients and to ensure appropriate levels of antioxidant therapy, non-invasive assessments of plasma or white blood cell antioxidant status or the stable end products of lipid, DNA or protein oxidation may be appropriate, although, as yet, these procedures may only be available at specialist centres or on an ad hoc basis. Therefore, it is particularly important to engender some consensus with the aim of establishing a unified approach to monitor evidence of OS in patients, together with the development of appropriate therapeutic strategies that can target OS in disease.

This Special Issue aims to highlight appropriate antioxidant therapeutic strategies to mitigate OS in disease and target the mitochondria. This Special Issue will also focus on suitable low-invasive methods to assess evidence of OS in patients and their application to disease monitoring.

Dr. Iain P. Hargreaves
Guest Editor

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• mitochondria
• reactive oxygen species (ROS)
• oxidative stress
• mitochondrial respiratory chain (MRC)
• mitochondrial dysfunction
• neurodegenerative disorders
• metabolic diseases