The Biology of Aging

The Biology of Aging

Aging shouldn’t be viewed as a negative consequence of being alive, after all, it means you have been fortunate enough to make it this far. With that said, the best way to celebrate aging is to do so gracefully, and for that to happen, it is paramount to understand how and why we age.

by Wendy Ouriel

 


Aging Begins Within Our Cells

 Image Credit: USF Department of Cell Biology, Microbiology and Molecular Biology

Image Credit: USF Department of Cell Biology, Microbiology and Molecular Biology

 

Aging that we see at the surface is the culmination of aging at the cellular and molecular level. Aging of our cells is referred to as ‘senescence’ and occurs to some degree in all living organisms (with a few notable exceptions). Senescence comes from the latin, senescere, which means “to grow old,” and is the natural consequence of DNA damage that occurs with the passage of time. DNA damage manifests in a loss of cellular function and the inability of cells to replicate. For example, around age 40 skin cells cease producing collagen, leading to a loss of skin firmness, and the formation of wrinkles. Fortunately, senescence can be delayed due environmental and genetic factors. However, senescence can be accelerated by environmental and genetic factors too. 

Aging Can Be Examined at the Genetic Level

 DNA is so long that it must be compacted into chromosomes so it can all fit within the cell's nucleus.

DNA is so long that it must be compacted into chromosomes so it can all fit within the cell's nucleus.

DNA is the Blueprint for Making You

The instructions to make all living things is encoded in DNA. DNA is the long, double helical strands that, when read, encode proteins. Proteins make up a significant portion of our body, from hair, to muscle, to organs. DNA is housed in the nucleus of the cell, and all of the DNA within a single nucleus can be stretched to over 6ft ( ~3meters ) long. Since DNA is so long it must be condensed to fit into the nucleus, which is why we have our DNA packaged in the form of chromosomes.


Telomeres Protect our DNA from Aging

 Telomeres are similar to the plastic caps protecting your shoelaces. When telomeres become too short, they can no longer protect DNA, and senescence occurs.

Telomeres are similar to the plastic caps protecting your shoelaces. When telomeres become too short, they can no longer protect DNA, and senescence occurs.

When we examine a chromosome, there are two components to note: the DNA, and the telomere. The telomere exists on the ends of the chromosome to provide structural integrity so that the DNA does not unravel. Think of telomeres like the plastic cap (aglet) on the end of a shoelace. When shoes are new, not having a cap on the end of the lace will not cause fraying, but with each wear the shoe lace is exposed to the environment, which adds up over time, leading to physical damage. Telomeres become damaged as we age because whenever the cell divides, the telomere is nicked. Therefore, with each divide the telomere gets short and shorter. Cellular division is a natural biological process, and after approximately 50 divisions, the cell reaches what is known as the “Hayflick limit” and senescence begins.

 

Cancer cells and stem cells do not have a Hayflick limit, and are not subject to telomere shortening.


Reactive Oxygen Species

 Antioxidants scavenge for ROS

Antioxidants scavenge for ROS

 

Damage to DNA can occur in many ways, and skin care formulations have focused on one culprit in particular: Reactive Oxygen Species (ROS). For the last decade or so, the superstar in cosmetic formulations has been antioxidants. Antioxidants can be found in seed oils, and botanical extracts to name a few, and they function to scavenge for radicals, known as Reactive Oxygen Species, or ROS.

 

 Generation of ROS from UV exposure  Image Credit: Wolfle et al., 2013.

Generation of ROS from UV exposure

Image Credit: Wolfle et al., 2013.

ROS are formed as a byproduct of normal biochemical reactions, however when ROS are generated in mass or in uncontrolled quantities, they can disrupt normal biological function and cause cellular damage. Examples of causes for ROS overproduction include

-   Exposure to ionizing radiation (X-rays and Gamma rays)

-   Exposure to UV radiation

-   Taking drugs that cause cellular oxidation

 Image Credit: Health Plexus, Theory of Aging

Image Credit: Health Plexus, Theory of Aging

ROS has been implicated for its role in biological aging, in what is known as the Free Radical Theory of Aging. According to the Free-radical theory of aging, the accumulation of free radical damage is the primary culprit for biological aging. For example, an excess of the ROS, superoxide, was found to cause endothelial dysfunction in elderly patients with hypertension.

ROS accumulation may also be partly responsible for many of the classic hallmarks of aging, such as sagging skin and loss of elasticity. However, topical application of skin care products containing vitamin E and C have been found to reverse some of the damage caused by UV-induced ROS accumulation.

 

References

 

Bowen, R., 2003. Free radicals and reactive oxygen. http://www.vivo.colostate.edu/hbooks/pathphys/misc_topics/radicals.html

Campisi, J. and di Fagagna, F.D.A., 2007. Cellular senescence: when bad things happen to good cells. Nature reviews Molecular cell biology8(9), pp.729-740.

Dreher, F. and Maibach, H., 2001. Protective effects of topical antioxidants in humans. In Oxidants and antioxidants in cutaneous biology (Vol. 29, pp. 157-164). Karger Publishers.

Bowen, R., 2003. Free radicals and reactive oxygen. http://www.vivo.colostate.edu/hbooks/pathphys/misc_topics/radicals.html

Wendy O