Topic
Oxidative stress
About: Oxidative stress is a research topic. Over the lifetime, 86513 publications have been published within this topic receiving 3845790 citations. The topic is also known as: oxydative stress.
Papers published on a yearly basis
Papers
More filters
TL;DR: JunD, a member of the AP-1 family of transcription factors, reduces tumor angiogenesis by limiting Ras-mediated production of ROS and provides new insights into the regulation of PHD activity, allowing immediate reactive adaptation to changes in O2 or iron levels in the cell.
547 citations
TL;DR: The impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS are reviewed and the emerging concept of utilizing OS as a tool of contraception is highlighted.
Abstract: Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.
547 citations
TL;DR: A considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta of PD patients is illustrated and the important need for further research in this area is highlighted.
Abstract: Parkinson's disease (PD) is a progressive, neurodegenerative condition that has increasingly been linked with mitochondrial dysfunction and inhibition of the electron transport chain. This inhibition leads to the generation of reactive oxygen species and depletion of cellular energy levels, which can consequently cause cellular damage and death mediated by oxidative stress and excitotoxicity. A number of genes that have been shown to have links with inherited forms of PD encode mitochondrial proteins or proteins implicated in mitochondrial dysfunction, supporting the central involvement of mitochondria in PD. This involvement is corroborated by reports that environmental toxins that inhibit the mitochondrial respiratory chain have been shown to be associated with PD. This paper aims to illustrate the considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta (SNpc) of PD patients and to highlight the important need for further research in this area.
546 citations
TL;DR: The administration to aged mice of agents capable of activating the α isoform of the peroxisome proliferator-activated receptor (PPARα) was found to restore the cellular redox balance and suggest that PPARα and the genes under its control play a role in the evolution of oxidative stress excesses observed in aging.
546 citations
TL;DR: Increased levels of chelatable zinc have been shown to be present in cell cultures of immune cells undergoing apoptosis, very reminiscent of the zinc staining of neuronal perikarya dying after an episode of ischemia or seizure activity.
546 citations