ROS and Free Radicals

Reactive Oxygen Species and Free Radicals

Aging is a conjectured process of deterioration, which occurs after reproductive maturity (Held 2002). It comes as a result of various processes and interactions, such as reactive oxygen species and glycosylation. It differs from longevity in that longevity is influenced by genetic and environmental factors. Physiological reserves are evolutionarily selected as they enhance the probability of survival in order to produce. Longevity is a consequence of the selection. But aging cannot be selected by evolution. The Institute for Human Genome Research has embarked on the search for the minimum set of genes needed to sustain life. When this is achieved, the riddle of what life is would be answered. The answer would unlock the secret of creating life and, therefore, extending it. It may also provide the clue on how aging can be stopped. There is at present negligible understanding of the aging process. Reducing death rates, controlling disease and extending life expectancy are the best approaches to increasing life span. But scientific knowledge continues to advance in that direction. There is every indication that 21st century medicine will cure more diseases and increase life span. With more knowledge, these ends can be achieved. Some pharmaceutical and biotech companies conduct tests towards these ends. Laboratories and universities are constantly in search for new discoveries. More and more research has been coming up with new knowledge about life processes, which can slow down the aging process. Director Francis Collins of the Institute predicted that major genes behind the aging process could be discovered by 2030. This discovery would enable clinical trials on drugs that would retard the aging process (Collins 2000 as qtd in Held), a most exciting probability worth looking forward to. (Merz 1992)

Experts describe aging as the autonomous deterioration with increasing chronological age (Merz 1992). Gerontology is a 20th century development, a new science. The aging process was not a preoccupation in earlier centuries, which focused on the young on their way to middle age. It was only in the early 1900s when antibiotics and maternal health increased the life span into the sixth decade of life. Gerontology would explore all the aspects of the aging process and help physicians distinguish normal aging from the effects of sickness. Gerontologists at present agree that the major organ systems change some way as a result of age. Many of them attribute such changes as the effects of the death of some or many cells. Until 1960, most scientists believed that the body determined when cells should die. In 1960, Leonard Hayflick proved that normal cells divide indefinitely and then die. He also discovered that connective-tissue cells from a fetus divided twice faster than those of adults. Scientists agreed that the life span of a cell was genetically predetermined and environmentally influenced. They theorized that these agents are reactive oxygen species or ROS, which includes oxygen free radicals or OFRs (Merz).

OFRs are oxygen molecules or compounds seek to pair off with the first possible molecule but impair its function (Merz 1992). That body's internal network of antioxidants comes to the rescue throughout its life span. But it becomes less and less effective as the cell ages or becomes overworked. When this happens, OFRs can gain a foothold and disturb cellular processes. In this condition, the once normal glucose molecules can disturb and disrupt proteins. These molecules behave like OFRs. It sticks strongly with the proteins and difficult to separate. It interferes with cellular processes and resists the enzymes, which try to break them up. A host of other disruptions accompanies it. Sugars, fats, proteins and RNA increase and the amount of DNA decreases. The shape of mitochondria cells becomes distorted and the number of ribosomes also decreases. With this disorder in the mitochondria, there is cellular collapse. Molecular waste collects. Lysosomes, which clean up wastes, consume proteins faster than body cells can produce them. The visible result of this scavenging riot is the decline in the number of cells in the body of an average 75-year-old to as much as 30% and affecting almost all major body systems (Merz).

The Population Reference Bureau projected that 21% of the U.S. population would be 65 years old or older by the year 2050 (Hood 2003). This would intensify the interest on aging and the factors, which bring it on. In 1916, the National Institute for Environmental Health Sciences documented the first evidence that aging of in vitro cells is an inherently and genetically controlled process. The Institute explored the mitochondrial theory of aging, which suggests that the aging process itself is the result of a lifetime of oxidative damage to proteins, DNA and lipids in mitochondria. Scientists believe that the oxidative stress, resulting from the overproduction of free radicals or the decreased protective mechanisms, is involved in the development of disease and aging. Environmental factors, such as exposures, contribute to the production of these oxidants. Professor Colleen Jackson-Cook of the Virginia Commonwealth University suggested that acquired genomic changes could have a role in aging and disease, such as cancer, ulcerative colitis and AD. Professor of occupational and environmental medicine Howard Hu at the Harvard School of Public Health suggested that adult patients with a high body burden of lead had a greater risk of developing anxiety, depression, myocardial infarction, hearing loss and cataract. Most importantly, they tended to suffer from reduced cognitive function with aging. In 1999, researchers also discovered that exposure to increased air pollution depleted cardiovascular functioning in 27 Boston adults aged 60 to 90. Older persons of lower socioeconomic classes and older Blacks faced greater risks of disability on account of greater exposure to biological risk factors and inclement social and environmental conditions (Hood).

Chronic damage to the retina is a leading cause of blindness in advanced countries (King 2004). It is called age-related macular degeneration or AMD. The condition involves oxidative stress and the death of the pigment epithelium of the retina, mainly brought about by the action of mitochondria-derived reactive oxygen species or ROS. Findings of laboratory research suggested that this can be counteracted by using antioxidants, which will block ROS and cell death by inhibiting the mitochondrial electron transport chain. The experiment was based on the free radical theory of aging, which states that changes in biological function, which turn up in time, are due to cumulative cellular damage created by reactive oxygen species or ROS. This oxidative condition of injury is linked with diseases, including age-related macular degeneration or AMD. AMD usually begins at past 65 and is disabling. The disease process is not very well understood and no effective cure or prevention has been established. In vivo experiments may likewise lead to mitochondria damage and cell dysfunction in time, partly from accumulated ROS-mediated mtDNA linked with aging and other age-related diseases and conditions, such as Alzheimer's disease. This study showed that cell damage in AMD can be triggered by blue light, which induces ROS and cell death by interacting the mitochondria's electron transport chain. Sufferers of AMD may, thus, benefit from the use of antioxidants, which will shield them from this mitochondrial action and inhibit the progress of the disease (King).

In vivo theories expound that many specific mitochondrial DNA mutations accumulate in many tissues as one ages (Diamond et al. 2002). These tissues are the brain, heart and skeletal muscles. Mitochondrial DNA mutations are believed to induce the progressive decrease in the production of energy in the mutated cells. Experiments on the human larynx showed this change. Advocates of these theories isolate and identify free radicals as the main cause of aging. The human body constantly produces free-radical oxygen species through adulthood. Gradually, the body's ability to cleanse itself of these free radicals slows down and they begin to accumulate. The accumulation can lead to oxidative stress and damage to DNA, protein and lipids. Among the by-products of oxidative damage are DNA injury, lipid peroxidation and protein oxidation (Diamond et al.).

Free radicals are atoms with unpaired electrons and blamed as the primary cause of cell damage and aging (Nelson 2000). The free radical theory says that these radicals injure cells in an organism and that this results in the condition known as aging. Free radicals are produced in the mitochondria, cell areas which produce chemical energy. They perform the task through an electron transport chain. The mechanism passes electrons between molecules to produce useful chemical energy. At times, the electron incorrectly interacts with oxygen and produces a changed or radical oxygen form. This happens primarily at the mitochondrial DNA or mgDNA. When there is extensive mtDNA damage through time, it stops mitochondria. As a result, the cells die and the organism ages (Nelson).

Genetically and nutritionally, the action of these free radicals can be prevented or altered.

A fruit flies. These labs genetically altered fruit flies to produce more of the natural antioxidants in their body. Antioxidants are molecules, which remove free radicals. They reduce mtDNA damage caused by these radicals. Other experiments restricted feeds given…