Abnormal Production Of Reactive Oxygen Species Research Articles

Dietary Antioxidants and the Mitochondrial Quality Control: Their Potential Roles in Parkinson's Disease Treatment.

Advances in medicine and dietary standards over recent decades have remarkably increased human life expectancy. Unfortunately, the chance of developing age-related diseases, including neurodegenerative diseases (NDDs), increases with increased life expectancy. High metabolic demands of neurons are met by mitochondria, damage of which is thought to contribute to the development of many NDDs including Parkinson’s disease (PD). Mitochondrial damage is closely associated with the abnormal production of reactive oxygen species (ROS), which are widely known to be toxic in various cellular environments, including NDD contexts. Thus, ways to prevent or slow mitochondrial dysfunction are needed for the treatment of these NDDs. In this review, we first detail how ROS are associated with mitochondrial dysfunction and review the cellular mechanisms, such as the mitochondrial quality control (MQC) system, by which neurons defend against both abnormal production of ROS and the subsequent accumulation of damaged mitochondria. We next highlight previous studies that link mitochondrial dysfunction with PD and how dietary antioxidants might provide reinforcement of the MQC system. Finally, we discuss how aging plays a role in mitochondrial dysfunction and PD before considering how healthy aging through proper diet and exercise may be salutary.

Endogenous and Exogenous Antioxidants As a Tool to Ameliorate Male Infertility Induced by Reactive Oxygen Species.

Significance: Antioxidants are essential for the maintenance of cellular redox homeodynamics in the male reproductive tract, playing a key role in fertilizing potential. Reactive oxygen species (ROS), at physiological levels, are essential for sperm function and fertilization. Under pathological conditions, abnormal production of ROS may occur. Redox control is primarily regulated by the inner antioxidant system. However, these endogenous antioxidants may be present at abnormal amounts or may be insufficient. Exogenous antioxidants obtained through the diet may have an important role, particularly in specific pathological conditions. This review addresses the regulation of redox homeodynamics in the male reproductive tract by endogenous and exogenous antioxidants and the importance of their cooperation for the maintenance of fertility. Recent Advances: Many studies have shown the importance of antioxidants for the preservation of male fertility, mostly under pathological conditions. Excessive antioxidants can inhibit ROS-induced signaling pathways that are essential for the reproductive system. The challenge is to keep the balance between oxidants and antioxidants to maintain ROS-amount at physiological concentration. Critical Issues: Although antioxidant therapies are gaining popularity and showing promising results in the improvement of male fertility, there is a lack of knowledge regarding the type of exogenous antioxidant, the doses and time to be administered. Future Directions: It would be of great importance to find a way to restore redox homeostasis under stress conditions. Understanding the poorly studied mechanisms by which exogenous antioxidants cooperate with the inner cellular antioxidant system to counteract free radicals may help in the development of new fertility therapies.

Redox Biology Poster Prize Winner P55 - Role of Oxidized Protein Repair in Human Skeletal Muscle

There is now increasing evidence that reactive oxygen species (ROS) are signalling molecules that regulate growth, differentiation, proliferation and apoptosis, at least in physiological concentration. However, when ROS levels overcome the capacity of cellular antioxidant systems, they damage cellular components such as nucleic acids, lipids and in particular proteins, inflicting alterations to cell structure and function. Oxidation of sulfur-containing aminoacids, like cysteine and methionine, within proteins, can be repaired by specific enzymatic systems. Indeed methionine sulfoxide is catalytically reduced back to methionine by the methionine sulfoxide reductase (Msr) system. We showed that this Msr system is involved in cellular protection against oxidative stress by preventing apoptosis and limiting irreversible protein oxidative damage. Furthermore, it has been demonstrated that the Msr system is no longer efficient during ageing and senescence as well as that Msr modulates longevity in animal models. In this work we analysed Msr expression in human skeletal muscle. We showed, using both primary and immortalized skeletal muscle cell lines, that the expression of the Msr system increases during differentiation, suggesting a role of this antioxidant system on myofibres formation. Since myoblasts senescence associated with less differentiation capacity and an abnormal production of ROS have been observed in some muscular dystrophies, we wondered about the state of the Msr system in late-onset myopathies, such as oculopharyngeal muscular dystrophy (OPMD). In OPMD we confirmed, at the transcription level, an increased expression of Msr with differentiation, both on immortalized and primary cell cultures, similarly to what we observed on control cell lines. Our aim is to characterize for the first time the role of a major oxidized protein repair system (Msr) in human skeletal muscle homeostasis and, in particular, in myotubes protection during oxidative stress conditions.

Current Concepts in the Use of Antioxidants for the Treatment of Preeclampsia

Preeclampsia is a leading cause of maternal and neonatal mortality and morbidity. It is a complex syndrome of undetermined etiologic origin, usually diagnosed during the second half of pregnancy, with clinical features of hypertension, proteinuria, and edema. No cure for preeclampsia exists, except premature delivery. There is increasing evidence that oxidative stress is an important contributing factor to the pathogenesis of preeclampsia. Oxidative stress is defined as an imbalance between reactive oxygen species (ROS), such as nitric oxide(NO·), superoxide anion (O2·↔), and hydrogen peroxide (H2O2), and antioxidants, favouring an overabundance of ROS. The consequence of an overproduction of ROS can be observed as increased levels of markers of oxidative stress, such as lipid peroxides.Pregnant women affected by preeclampsia may have abnormal ROS production, particularly NO· and O2·↔, abnormal levels of antioxidant defences, and increased placental lipid peroxidation. Several observations suggest that decreased bioavailability of endothelium-derived NO·, due to oxidative destruction of NO· by ROS, might contribute to the impaired endothelium-dependent vasodilatory responses and multisystemie pathology of preeclampsia, a phenomenon in which antioxidant vitamins may play a beneficial role. This review focuses on the rationale for vitamins C and E supplementation toward prevention of preeclampsia, with an emphasis on the limit of our scientific knowledge concerning the deleterious oxidative events taking place in this pathology.