Information on Disorders
Both types of diabetics display increased levels of reactive oxygen species such as free radicals; for this reason, the onset of diabetes is closely associated with oxidative stress. The precise mechanism by which oxidative stress accelerates diabetes complications is only partly understood, but damaged protein is recognized to be one contributing factor. Additionally, it appears that oxidative stress byproducts contribute to insulin resistance, the basis of diabetes.
Oxidative stress causes protein damage and plays a major role in the development of diabetes. It causes excessive formation of free radicals which weaken defense mechanisms against further oxidation and that increases the likelihood of more cell damage, insulin resistance, and further complications of diabetes.
Diabetics exhibit an increase in oxidative stress, which contributes to the development of oxidative protein damage. Additionally, the dialysis procedure contributes to oxidative stress. Study show that plasma proteins suffer damage, too.
“Oxidative stress damages and impairs the functioning of several kinds of proteins, harming lung physiology in ways that can induce COPD. The harmful effects include oxidative inactivation of antiproteases and surfactants, excessive secretion of mucus, membrane lipid peroxidation, mitochondrial respiration, alveolar epithelial injury, remodeling of the extracellular matrix, and apoptosis. The importance of the restoration of the faulty protein functions, including protein-controlled antioxidant management, is discussed.
Exercise causes increased oxidative stress in COPD patients, as in healthy people. But additional oxidative stress occurs in COPD patients, because oxidative stress causes inflammation, and inflammation in turn causes more oxidative stress. This cycle occurs because oxidation causes various protein dysfunctions, and that hinders the operation of functions that restore a healthy oxidant/antioxidant balance.
Conditions found in COPD patients, such as protein glycation and other forms of COPD-related protein damage, all make each other worse. This suggests that protein-controlled processes for antioxidant management may help in the treatment of COPD to restore correct cellular activity.
Oxidative stress has been associated with diverse diseases, including cancer, renal disease, and neurodegeneration. Forty years of research also shows that all vascular cells produce reactive oxygen species, the byproducts of oxidative stress, and that that contributes to many of the abnormalities associated with vascular diseases, including atherosclerosis and hypertension.
Reactive oxygen species (ROS) influence many physiological processes including host defense and cellular signaling, and their increased production through oxidative stress plays a role in such pathologies as hypertension, atherosclerosis, diabetes, and kidney disease. The article considers various possible major sources of vascular and renal reactive oxygen species, and discusses their physiological role in vascular regulation – for example, how they can cause endothelial dysfunction, inflammation, hypertrophy, apoptosis, and other disorders. Decreasing ROS generation and increasing nitric oxide availability and antioxidants may prevent or repair organ damage by reducing vascular injury and renal dysfunction.
The article highlights current developments in the field of reactive oxygen species (ROS) and hypertension, focusing on the role of oxidative stress in hypertension-associated vascular damage. Experimental evidence indicates that increased oxidative stress and associated oxidative damage are mediators of renovascular injury in cardiovascular pathologies. Research suggests possible therapies that, for example, decrease ROS generation and increase nitric oxide availability to minimize vascular injury and renal dysfunction.
Oxidative DNA modifications are frequent in mammalian DNA and appear to be important mechanisms in carcinogenesis, diabetes, and ageing. This is indicated by, for example, high levels of oxidative lesions in cancer tissue, and reduced cancer incidence in populations with high dietary antioxidant intake. Some evidence conflicts with this theory, such as unchanged cancer rates after antioxidant interventions in large clinical trials. But excreted repair products exhibit levels of DNA oxidation that indicate life-threatening damage.
Cancer almost certainly stems from damage in the form of DNA mutation due to oxidative stress. The authors describe structural, chemical, and biochemical aspects of free radicals, the damage that free radicals inflict on lipids and proteins, the formation of free radicals, and the phenomenon of oxidative stress, cancer, and imbalance within cells.
Oxidative stress plays a multistep role in carcinogenesis, through a process of both cell mutation and proliferation. Oxidative stress can occur through overproduction of reactive oxygen and nitrogen species and the unregulated production of cellular oxidants damages DNA, causing mutations and modification of gene expression. Reactive protein species, the results of oxidative stress, activate signal transduction pathways, leading to the transcription of genes involved in cell growth regulatory pathways.
Researchers are investigating the role that an imbalance of oxidants and antioxidants – oxidative stress – plays in the development of chronic airway inflammation in asthma.
In asthma, oxidative stress plays a strong role in the inflammation of airways and hyperreactivity. This insight from studies of mice could throw light on how asthma develops and could also suggest ways to use antioxidants to lessen the severity of the disease.
The protein aP2, which regulates allergic inflammation of airways, has for the first time been detected in epithelial cells, which line the airways. That demonstrates that aP2 is associated with the immune-system condition, asthma – a startling finding, given that aP2 had previously been considered to be a specific marker for fat cells and had been shown to be associated with metabolic-system conditions such as obesity, diabetes type 2 (including insulin resistance), and atherosclerosis (hardening of the arteries). The discovery of its link to asthma marks the first demonstrated link between the immune and metabolic systems of the human body, and emphasizes the close link between the regulation of inflammation and metabolism. It also calls into question the “hygiene hypothesis” that has been the preferred explanations of asthma, and that holds that childhood infection and environmental factors such as diet and airborne pollution bring on the condition.
In asthma patients, a type of protein cells known as eosinophil cationic protein (ECP), which originate in plasma or inflamed tissue, severely alter the structure and function of brochoalveolar lavage fluid, which helps to flush the lungs. The finding could explain airway obstruction in asthma.