Protandim Research Paper

A recent study was done at McMaster University in Ontario to see whether the signs of ageing were unavoidable. This study involves mice as test subjects that they were designed to age prematurely. The mice was put on a regimen of exercises, where the results have showed that it prevented the signs of ageing and even reverse the early ageing in the mice. The mice that remained inactive have grown with signs of weakened, ill, wizened, and bald. In contrast, mice that were provided with running wheels, they maintained in healthy muscles, brains, hearts, reproductive

Scientist have seen that telomerase expressing clones have no difference in karyotype but have a long lifespan by 20 doublings. With this research, cells have been seen to have a very youthful looking state for much longer. A last area of study is the hypothalamus of the brain. This part of the brain controls reproduction, growth, metabolism, and aging. This is where many of the age related diseases occur. The study of this area can lead to many advancements in age related diseases that can help people live longer. Though this area of study does not have many advancements it holds promising results. Though there have been numerous advancements, many people ask the question whether people need to live longer because of an already over populated Earth.

When we’re young, our cells have a very strong defense system known as superoxide dismutase (SOD) that kicks free radical butt. But as we get older, SOD doesn’t work as well. Without SOD keeping the peace, the free radicals have a field day and wreak as much damage as they possibly can causing our cells, and eventually us, to die. Free radicals have also been linked to a number of diseases such as cancer, dementia and heart disease.

In the course of evolution man has lost his ability to produce some powerful antioxidants such as beta carotene and vitamin C in your body. Are preserved, however, other antioxidants (Eg melatonin) That inactivate free radicals and thus form a powerful defense system against them.

Based from observations made in the early 1950s, Denham Harman proposed that functional decline in cells and tissues was due to cumulative effects of macromolecular damage caused by oxygen radicals produced by respiratory enzymes (Harman 1956). This theory proposes that superoxide and other free radicals cause damage to the macromolecular components of the cell, resulting in accumulated damage to cause cells, and eventually organs, to stop functioning, leading to the aging phenotype (Sohal and Weindruch 1996, Clancy and Birdsall 2013). Oxidative damage is thought to occur from an imbalance when the antioxidant systems are unable to counter all the free radicals continuously generated during the life of the cell.

As you may know, antioxidants promote good health as they help avoid diseases. More specifically, antioxidants help slow down the oxidation of cells in our body. When cells oxidize, they generate free radicals, which are also known as cellular bi-products. It is perfectly safe to have a manageable amount of these free radicals in the body. However, when the free radicals are in excess, they can wreak havoc on our organism's cellular

It specifically focuses on two strategies: the role of physical exercise and Vitamin E in overcoming oxidative damage in normal aging of the brain. However, for the purposes of this research synthesis, I will only focus on the effect of exercise on oxidative damage in the normal aging of the rat and human brains.

studied mice that were growing 48 different kinds of human cancers and treated them with the 12

The research was done by Sabry M. El-Bahr at the Department of Biochemistry, Faculty of Veterinary Medicine, P.O. Box 22758, Alexandria University, Egypt. The overall purpose of this experiment was to study the causes of oxidative stress that is caused by free radical. It is known that the free radicals and the Reactive Oxygen Species (ROS) are used interchangeably. ROS can damage DNA, biomembrane lipids, proteins and other macromolecules. The primary source of ROS is the leakage of electron from the respiratory chain during the reduction of molecular oxygen to water generating superoxide anion. The classification of ROS includes oxygen centered radicals and oxygen centered non- radicals. Moreover,

Polyphenols are a naturally occurring compound in apples that have recently been found equally as effective as antioxidants in preventing free radicals from damaging the cells due to their ability to fight oxidation of low density lipoproteins and scavenge reactive oxygen species (Rana, Boyer and Liu, Bellion et al.). They are known as a stronger protector for the organism against oxidative stress-mediated damage (Bellion et al.) Humans and animals have complex antioxidant defense systems, but they cannot prevent every oxidative stress from occurring. Both cardiovascular disease and cancer are thought to be the most dangerous results of oxidative stress, both of which can lead to damage of the larger biomolecules, such as DNA, lipids, and proteins

Superoxide dismutase (SOD) is an enzyme that alternately catalyzes the partitioning of superoxide anion O2− to convert it to hydrogen peroxide H2O2 and molecular oxygen O2 [79, 80]. SOD plays significant protective roles versus cellular and histological damage that occur by ROS. It facilitates the transformation of superoxide radicals to hydrogen peroxide H2O2, and in the existence of other enzymes it converts H2O2 to O2and H2O [81]. In mammalian tissues there are three forms of SOD: Cu-Zn-SOD, Mn-SOD, and EC-SOD, and each form of them are having a special gene [82, 83]. Cu-Zn-SOD called SOD is centralized in cytosol, Mn-SOD also known SOD 2 found in mitochondria, and EC-SOD or SOD 3 localized in extracellular space [84, 85]. Superoxide interacts rapidly with nitric oxide (NO), decrease the activity of NO and generating the oxidative peroxy nitrite radical [86].

Oxidative stress has been implicated in various pathophysiological conditions either directly or indirectly. They are cardiovascular disease, cancer (1), neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s diseases (AD) (2,3), Amyotrophic lateral sclerosis (ALS), Huntington’s disease, and multiple sclerosis, Diabetes Mellitus (4), ischemia/reperfusion, fibrosis, Kidney disease, impairment via cochlear damage induced by elevated sound levels, ototoxicity of drugs such as cisplatin, and in congenital deafness in both animals and humans, obstructive sleep apnea, obesity, hypertension, diseases of prematurely and other diseases related to ageing (5). These diseases fall into two groups.

The best known function of mitochondria is the generation of ATP from food sources. Pyruvate, converted from glucose, is consumed by mitochondria to produce ATP. As mitochondria produce ATP, they release reactive oxygen species (ROS) locally that must be detoxified as they can induce oxidative damage to mitochondrial DNA (mtDNA). This damage results in mutations and deletions of mtDNA. The relative absence of repair enzymes for mtDNA may explain its sensitivity to oxidative stress-induced damage [8]. The 10- to 20-fold higher mutation rate in mitochondrial DNA compared with nuclear DNA is believed to be due to its proximity to ROS generation and the limited DNA repair capacity [9, 10]. As the organism, tissue, and cells age, exposure of the

These reactions will likely produce chronic inflammation, which is thought to contribute to many chronic, and terminal diseases such as alzheimer 's or cancer. This theory allows us to focus on the immune system, more specifically areas in which cells deteriorate or diversify too much. Once we are able to target which specific parts of the immune system causes it to deteriorate, cell repair potential is likely. If immune cell deterioration is due to diversification of human cells, one will one day be able to either slow the process or stop specific areas to allow the immune system to be strong and thus the likeliness of diseases such as alzheimer 's or diabetes will decrease. Another theory of aging is the Wear- and Tear Theory. This theory describes the aging process as the general deterioration of our body over time, whether it be environmental factors or just degeneration of our body 's structure and core. Like a car, over time we become less functional exposure to “radiation, toxins, and ultraviolet light can damage our genes,” as well as our own body 's functioning. Some nerve cells of the brain do not replicate or replace themselves as we age, so function will be lost as well. As our cells divide, it shortens the “telomeres of the chromosomes,” which will ultimately not be able to divide anymore as well. This theory allows one to understand the general

Antioxidants are bioactive molecules in foods which inhibit the oxidation of other molecules. Antioxidant capacity refers to an individual’s overall antioxidant level and activity in the body (Van Duyn and Pivonka 2000). A higher antioxidant capacity leads to a decrease in free radicals. Free radicals cause oxidative stress. Therefore, a higher antioxidant capacity leads to a decrease in plasma membrane, protein and DNA damage (Valko et al 2007). Increased levels and chronic levels of oxidative stress have been shown to be contributors in inflammatory and cardiovascular related diseases such as atherosclerosis, coronary heart disease, stroke and some cancers also (Grimble 1994) (Conner and Grisham 1996).