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.

Calcium, mitochondria and reperfusion injury: a pore way to die.

Abstract: When mitochondria are exposed to high Ca2+ concentrations, especially when accompanied by oxidative stress and adenine nucleotide depletion, they undergo massive swelling and become uncoupled. This occurs as a result of the opening of a non-specific pore in the inner mitochondrial membrane, known as the MPTP (mitochondrial permeability transition pore). If the pore remains open, cells cannot maintain their ATP levels and this will lead to cell death by necrosis. This article briefly reviews what is known of the molecular mechanism of the MPTP and its role in causing the necrotic cell death of the heart and brain that occurs during reperfusion after a long period of ischaemia. Such reperfusion injury is a major problem during cardiac surgery and in the treatment of coronary thrombosis and stroke. Prevention of MPTP opening either directly, using agents such as cyclosporin A, or indirectly by reducing oxidative stress or Ca2+ overload, provides a protective strategy against reperfusion injury. Furthermore, mice in which a component of the MPTP, CyP-D (cyclophilin D), has been knocked out are protected against heart and brain ischaemia/reperfusion. When cells experience a less severe insult, the MPTP may open transiently. The resulting mitochondrial swelling may be sufficient to cause release of cytochrome c and activation of the apoptotic pathway rather than necrosis. However, the CyP-D-knockout mice develop normally and show no protection against a range of apoptotic stimuli, suggesting that the MPTP does not play a role in most forms of apoptosis.

Reactive oxygen species and oxidative burst: Roles in stress, senescence and signal transduction in plants

Abstract: The oxidative burst, during which large quantities of reactive oxygen species (ROS) like superoxide, hydrogen peroxide, hydroxyl radicals, peroxy radicals, alkoxy rad icals, singlet oxygen, etc. are generated, is one of the earliest responses of plant cells under various abio tic and biotic stresses and natural course of senescence. In fact, reactions involving ROS are an inherent fe ature of plant cells and contribute to a process of oxidative deterioration that may lead ultimately to cell death. Sources of ROS include leakage of electrons from electron transport systems, decompartmentalization of iron which facilitates generation of highly reactive h ydroxyl radicals, and also various biological reactions. The imposition of both abiotic and biotic stresses causes overproduction of ROS, which ultimately imposes a secondary oxidative stress in plant cells. Degradation of membrane lipids, resulting in free fatty acids, initiates oxidative deterioration by providing a substrate for enzyme lipoxygenase, causing membrane lipid peroxidation. Since lipid peroxidation is known to produce alkoxy, peroxy radicals as well as singlet oxygen, these reactions in the membrane are a major source of ROS in plant cells. Regulatory mechanisms function both at gene and protein level to coordinate antioxidant responses. Superimposed upon our understanding of ROS-induced oxidative damages and their protection by antioxidative system, is the newly discovered role of ROS in signalling processes. ROS like H2O2 act as a signalling molecule, second messenger, mediating the acquisition of tolerance to both biotic and abiotic stresses. ROS as ubiquitous messengers of stress responses likely play a signalling role in various ada ptive processes. Plants can sense, transduce and translate ROS signal into appropriate cellular responses with the help of some redox-sensitive proteins. Hydrogen peroxide has been implicated as a key factor mediating programmed cell death. Plants exposed to abiotic stresses can produce a systemic signal, a component of which may be H 2O2 which sets up an acclimatary response in unstressed regions of plants. ROS is also found to communicate with other signal molecules and the pathways forming part of signa lling network that controls responses downstream of ROS.

Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF

Abstract: Neuroinflammation and mitochondrial dysfunction are common features of chronic neurodegenerative diseases of the central nervous system. Both conditions can lead to increased oxidative stress by excessive release of harmful reactive oxygen and nitrogen species (ROS and RNS), which further promote neuronal damage and subsequent inflammation resulting in a feed-forward loop of neurodegeneration. The cytokine tumor necrosis factor (TNF), a master regulator of the immune system, plays an important role in the propagation of inflammation due to the activation and recruitment of immune cells via its receptor TNF receptor 1 (TNFR1). Moreover, TNFR1 can directly induce oxidative stress by the activation of ROS and RNS producing enzymes. Both TNF-induced oxidative stress and inflammation interact and cooperate to promote neurodegeneration. However, TNF plays a dual role in neurodegenerative disease, since stimulation via its second receptor, TNFR2, is neuroprotective and promotes tissue regeneration. Here we review the interrelation of oxidative stress and inflammation in the two major chronic neurodegenerative diseases, Alzheimer's and Parkinson's disease, and discuss the dual role of TNF in promoting neurodegeneration and tissue regeneration via its two receptors.