Introduction
Oxidative stress is essentially defined as the imbalance in the equilibrium of antioxidants systems in the human body. Oxidative damage in aerobic organisms can be caused by certain molecules known as reactive oxygen species (ROS). These reactive species are ones that cause oxidative damage in biomolecules. In order to maintain equilibrium of these substances, the human body has various endogenous antioxidants and phase 2 proteins which have evolved to defend against any harmful effects of ROS or any other reactive species. In normal physiological conditions, a balance is maintained between the ROS production and their detoxification by the appropriate antioxidants and phases 2 proteins. (Uttara, Singh, Zamboni & Mahajan, 2009). Oxidative stress can occur due too many pathological conditions, when the balance of prooxidants and antioxidants is disturbed oxidative damage could accumulate in proteins, lipids, carbohydrates and nucleic acids. In severe cases these events can lead to cell death. The process can directly alter the antioxidant systems by either inducing or inhibiting the proteins which take part in these systems. Moreover it can also cause the depletion of storage of antioxidants such as glutathione, vitamin E and many more in cells. (Thomas 2006). Antioxidants are defined as any substance which has the ability to inhibit, reduce or repair the damage as a result of an ROS in a biomolecule. The general three mechanisms that are used by antioxidants include the inhibition of ROS generation, the repair of damage induced by ROS and scavenging for ROS molecules. Since ROS plays a precarious role in both physiology and pathophysiology in the human body, it is vital that the endogenous antioxidants and phase prote...
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Thomas, J.A. (2006). Oxidant Defense in Oxidative and Nitrosative stress. In M.E. Shils, M. Shike, A.C. Ross, B. Caballero & R.J Cousins (Eds.), Modern nutrition in health and disease. (10th ed.). (pp. 685-687). Philadelphia: Lippincott Williams & Wilkins.
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Uttara, B., Singh, A.V., Zamboni, P. & Mahajan, R.T. (2009). Oxidative stress and neurodegenerative diseases: A review of upstream and downstream therapeutic options. Current neuropharmacology, 7(11), 65-74.
Zhu, H., Wang, J., Santo, A. & Li, Y. (2013). Downregulation of antioxidants and phase 2 proteins. In F.A. Villamena (Ed.), Molecular basis of oxidative stress. (pp. 113-118). New Jersey: John Wiley & Sons.
Dr. Janis Eells presented a study that was accomplished by her and her students under the title “UNBLINDED BY THE LIGHT: Photobiomodulation for the Treatment of Retinal Degenerative Disease”. The purpose of this study is to determine whether photobiomodulation with near-infrared is able to treat retinal degeneration diseases. Thus, they hypothesis that the exposure of a rodent model of methanol toxicity to photobiomodulation (PBM) with near-infrared (NIR) could play a potential role in protecting the retina against the toxic actions of the methanol- derived formic acid. What is known about the topic is that if a small amount of methanol is injected it will rapidly cause permanent blindness. The methanol is metabolized to a mitochondrial toxin, and it is formic acid that can inhibit Cytochrome c Oxidase. This formic acid is able to interrupt mitochondrial function and increases oxidative stress in the retina and optic nerve which eventually leads to blindness. In order to fully test their hypothesis, the rats were randomly divided into four treatment groups: untreated control, LED-treated control, methanol-intoxicated, and LED-treated, methanol-intoxicated rats. they used electroretinogram as a sensitive indicator of retinal function, the experimental rats under methanol intoxication were exposed to three ...
The gaseous free radical nitric oxide is an abundant intracellular messenger molecule that plays a central role in maintenance of health, and is heavily involved in signal transduction in various cells of the body [1]. This molecule acts as a mediator in the regulation of cardiac function as well as having an important role in regulating contractility of the heart and maintenance of vascular tone in the cardiovascular system. As one of the most significant individuals in our discovery of nitric oxide, Dr. Robert Furchgott pioneered our understanding of this molecule through his experiments on the vasorelaxant properties of acetylcholine and the subsequent proposal of the presence of the endothelium derived relaxing factor, which was later identified to be nitric oxide [7]. Given the observation that cardiovascular disorders are the number one cause of death in many nations around the world, research into the vasorelaxant properties seems particularly relevant in order to help combat rising rates of vascular hypertension and high blood pressure. In this paper, the properties of nitric oxide are discussed largely with respect to the cardiovascular system. This paper focuses on the synthesis and characteristics of nitric oxide, the mechanisms of action by which nitric oxide works and the regulation of nitric oxide in the body, and finally a short summary of Robert Furchgott’s contributions to the discovery of nitric oxide and its properties.
AGEs alter the mechanical properties of cells and tissues by crosslinking intracellular and extracellular proteins. They also bind to cell surface receptors called receptor for AGEs (RAGE), thus interrupting various cellular processes. Through laboratory experiments, scientists have shown that glycation of mitochondrial proteins, lipids and DNA may induce mitochondrial dysfunction due to a decrease in ATP production and increased free radical formation. The mitochondria are specialized...
Varanese, S., Birnbaum, Z., Rossi, R., & Di Rocco, A. (2010). Treatment of Advanced Parkinson's Disease. Parkinson's Disease.
Goldmann, David R., and David A. Horowitz. American College of Physicians Home Medical Guide to Parkinson's Disease. New York: Dorling Kindersley Pub., 2000. Print.
With more than 200,000 US cases per year, Parkinson’s disease has become a major part
The path physiology of Parkinson’s disease is the pathogenesis if Parkinson disease is unknown. Epidemiologic data suggest genetic, viral, and environmental toxins as possible causes. Nigral and basal loss of neurons with depletion of dopamine, an inhibitory neurotransmitter, is the principal biochemical alteration in Parkinson disease. Symptoms in basal ganglia disorders result from an imbalance of dopaminergic (inhibitory) and cholinergic (excitatory) activity in the caudate and putamen of the basal ganglia.
Thomas, C. G. (2013, November 25). National Institute of Neurological Disorders and Stroke. Gene-silencing study finds new targets for Parkinson's disease, pp. 1-2. Retrieved December 13, 2013, from http://www.nih.gov/news/health/nov2013/ninds-24.htm
Most signs and symptoms of Parkinson disease correspond to one of three motor deficiencies: bradykinesia, akinesia, tremor, and rigidity. The first two qualities are usually present before tremor, but often attributed to aging by the patient and even the physician, and thus the disease is rarely diagnosed until tremor becomes evident much later. An average of 80% of the nigrostriatal neurons may have already degenerated by the time Parkinsonism is diagnosed, which complicates treatment (Fitzgerald, 130). Bra...
Another study proposed that CR slowed aging process by increasing resistance to hyperoxidation. As aging progressed in yeast and other animals, the presence of free radicals increased in the cells. Usually, the levels of the...
...inoic acid is a possible way to decrease the oxidative stress levels in the brain.
There are numerous theories regarding what causes Parkinson’s disease, such as Lewy bodies; these are proteins that are abnormal and aged, accumulated together. Another theory is pointing towards oxidative stress; this is when there is a loss of ability with the Dopaminergic neurons in processing excess amounts of toxic free radicals, leading to their death. Mitochondrial dysfunction and inflammation in ...
...t one has it. Many scientists hypothesize that there is an inflammatory response in the brain when there is an extensive B-42 amassing. To slow or stop this, scientists theorize that the use of anti-inflammatory drugs, such as aspirin, could delay the swelling in the brain. Also, as scientists have known that taking a multi-vitamin tablet each day is good for you, there has been recent research demonstrating that the use of antioxidants may protect neurons, not just the immune system and keeping the body healthy by providing vitamins and minerals. These special supplements protect the neurons from the effects of the accruing B-Amyloid that would likely cause the plaque that causes AD.
As a person ages, the thymus of that person begins to age as well. The phenotype of this aging is seen as withering or shrinkage. This withering or shrinkage is due in part to the stromal cell deficiency. This deficiency is a result of elevated levels of H2O2 and several types of oxidative damage. Dr. Griffith and other researchers discovered that the genetic complementation of catalase in stromal cells can be preserved with antioxidants. By finding this, the conclusion was drawn that there is a direct correlation between antioxidants, metabolism, and normal immune function. To further test this theory, Dr. Griffith is currently following up with this phenomenon in the
The human body is very complex. It is like a job. You have to do a million things in one day to make it through the day. The body uses nine systems to do all of those jobs. They all have separate functions, but some work together. Each system is also made up of organs. There are many ways to care and protect the systems from the many different problems they can have. There are also many interesting facts about each system.