Mitochondria and free radical studies on health, disease and pollution

Recent developments in free radical research have shown that many neuronal diseases such as Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis as well as other conditions such as aging, diabetes, cardiovascular disease, prematurity in babies and cancer, result from, or are associated with, oxidative stress. The production of reactive oxygen species (ROS) from electron transport chains may result in oxidative stress in cells, leading to apoptotic cell death. Majima et al. reported the first evidence of a relationship between ROS generated from mitochondria and apoptosis [1]. In addition, an increase in intracellular ROS generation was reported in mitochondrial DNA (mtDNA)-damaged cells [2]. This special issue of Free Radical Research focuses on the fusion of, and innovation occurring in, the fields of “Free Radical Research” and “Mitochondrial Research”, and includes five original and seven review papers that present new insights into mitochondria and free radical research.

The 5th Biennial Meeting of Society for Free Radical Research-Asia (SFRR-Asia), the 8th Conference of the Asian Society for Mitochondrial Research and Medicine (ASMRM) and the 11th Conference of the Japanese Society of Mitochondrial Research and Medicine (J-mit) were jointly held at the Kagoshima Citizen’ Culture Hall in Kagoshima City, Japan from August 31 to September 4, 2011. This collective event (The Kagoshima Congress) was the first such joint meeting held by the respective societies. This special issue consists of seven review papers and five original papers, representing the highlights of this joint Kagoshima Congress.

With regard to the effects and mechanisms of air pollution on health, Shiraiwa et al. [3] point out that air pollution and associated chemical reactions are also linked to free radical effects. They summarize data that indicate that polycyclic aromatic compounds (PACs) and allergenic proteins are efficiently oxygenated and nitrated upon exposure to ozone and nitrogen dioxide, which leads to an enhancement of their toxicity and allergenicity. Chen et al. [4] review the function of sphingolipids in Alzheimer's disease. Mynocycline provides the anti-apoptotic and anti-oxidative functions against sphingomyelinases/ceramides- induced neurotoxicity. Huang [5] reviews the functions of three superoxide dismutases on the related functions of learning in hippocampal neurogenesis and memory under normal conditions and following cranial irradiation. Yin and Zhu [6] focus on the detection of the chemical mechanisms of free radical oxidation of cardiolipin. They show that cardiolipin works as an important mediator of apoptosis, mitochondrial dysfunction and human diseases. Pattison et al. [7] discuss the roles of myeloperoxidase (MPO) in the immune system and during the development of numerous human pathological conditions. The major reactive species produced by MPO under physiological conditions are hypochlorous acid (HOCl) and hypothiocyanous acid (HOSCN) and the ratio of these oxidants critically depends on the concentration of thiocyanate (SCN⁻) ions. They show that SCN ⁻ ions have the potential to modulate both the extent and nature of oxidative damage in vivo. Mellier and Pervaiz [8] review the potential of TRAIL as a therapeutic modality. They present evidence suggesting that intracellular reactive oxygen species are critical to regulating the response of cancer cells to TRAIL. Ichikawa and Yasukawa [9] introduce the topic of Overhauser-enhanced magnetic resonance imaging (OMRI), a recently developed free radical imaging technique. In vivo imaging of redox-status with the OMRI/aminoxyl radical technique allows data to be obtained regarding redox status of tissues in animal models of diseases. This technique will provide new insights into the involvement of oxidative stress in vivo.

It is still unclear how loss of function of Parkin protein leads to dopaminergic cell death in Parkinson's disease. Relevant to these mechanisms, Siddiqui et al. [10] report that induction of the enzyme monoamine oxidase B (MAO-B) can interfere with mitochondrial quality control through losses in Parkin activity that processes mitochondrial turnover. They show that rapamycin, which independently enhances autophagic removal of damaged mitochondria, can alleviate these effects. Mukai et al. [11] report on the mechanisms of protective effects of quercetin on Parkin. They provide evidence that quercetin metabolites are converted to their aglycone forms to exert preventive effects of damage on neuronal cells. Relevant to radiation-induced apoptosis, Indo et al. [12] report that ROS generated from mitochondria play important roles in the induction of apoptosis by X-irradiation, suggesting that mitochondria are the critical sites of X-ray-induced cellular oxidative injuries. S-nitrosylation plays an important role in the regulation of protein function and signal transduction. Zhang et al. [13] introduce a new technique to detect S-nitrosothiol (SNO) proteins by spectral counting. This proteomic method has the potential to be widely applied for the fast screening of SNO-containing proteins. Furthermore, in relation to the effects of oestrogen, Park et al. [14] report on the inhibitory effects of resveratrol on 4-dydroxyestradiol-induced transformation of human breast epithelial MCF-10A cells. They provided evidence that resveratrol blocks the activation of IKKβ-NF-κB signalling and the induction of COX-2 expression in 4-hydroxyestradiol-treated MCF-10A cells. We hope that you will find this special issue to be a useful guide to current mitochondrial and free radical research.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.