Aging and the Cellular Human Body

In this section, we will explore the types of cells in the human body and the aging sequences associated with them.

Human cells

Within the human body there are two types of cells: 1-somatic cells and 2-germ cells also referred to as reproductive cells. Somatic cells are cells of all living organisms with the exclusion of gametes (sperm or egg cells). In the human body, somatic cells are any cell outside of the reproductive organ cells such as germ cells; sperm cells and egg cells. Examples of somatic cells are connective tissue cells(cartilage, bone, blood, lymph, and fibrous cells) skin cells, muscle cells, vascular cells, and all cells of the internal organs. Normal somatic cells have a finite number of divisions and irreversible arrested growth. This phenomenon is thought to be the main intrinsic mechanism for the cause of our aging body. 

Telomeres

Each somatic cell has telomeres at the terminal portions of their corresponding chromosomes (end caps) which protect the chromosome. A popular analogy is a plastic wrap at the tip of shoelaces. Without these plastic tips, a shoelace will become unraveled and considerably damaged over time. Telomeres are structural compounds (end caps) of the repetitive nucleotide sequence (TTAGGG) designed to protect the chromosome from damage during cell division, organize our chromosomes within the nucleus, keep the replicated DNA intact without loss of information, and protect us from premature death. These telomeres determine the number of times that somatic cells can divide, thus determining the consequential age of that somatic cell and globally our bodies. With each cellular division of the somatic cell, the enzyme DNA polymerase that repairs and produces the chromosomes cannot replicate the telomere zones (end caps) which leads to shorter telomeres and in-turn a shorter cell life. This shortening inevitably signals the cellular senescence (apoptosis). Lifestyle choices such as smoking, poor dietary habits, over-exposure to UVA & UVB, and uncontrolled psychological health lead to one of the main causes of telomere shortening; Oxidative stress.

Senescence

Senescence (aging or growing old) cells inevitably are in an irreversible state of arrested proliferation. Therefore, going into a phenotypic (observed characteristic) alteration leading to cell death from the absence of continuous division and a finite somatic cell lifespan. In Vivo skin samples from many donors across a cultural, genetic, and chronological age span, showed an age-dependent increase in dermal fibroblast and epidermal keratinocytes. 95% of epidermal cells are keratinocytes designed to produce keratin for structural dermal support. Early studies showed that cellular senescence was first responsible for inhibition of proliferation in tumor cells; tumor suppression by the aging body. However, continued research showed a positive attribute of cellular senescence: cancer promotion and tissue repair as well. More studies are necessary to truly understand the importance of cellular senescence besides the known hypothesis of apoptosis.

Mitochondria DNA

Degeneration and aging of tissue are further propagated by the major role of the cells' mitochondrial. Mitochondria are the cells' power generators. Life and continued existence are dependent upon the body's' ability to harness the energy generated by mitochondria. Mitochondria DNA (mt-DNA) the DNA located within mitochondria is small and circular and is passed predominantly from mother to offspring in mammalian cells. Mutations and deletions of mt-DNA occur at times causing inherited developmental and health-related problems of the body secondary to faults in energy production. Specifically, mt-DNA deletions are suggested to play a prominent role in aging and these deletions were determined to occur during the repair phase as opposed to the replication phase of mitochondria DNA. The mt-DNA 4,977bp deletion is a common mutation occurring in cancerous and also healthy tissue, which shows us the complexity of this common mt-DNA deletion. Oxidative stresses account for large amounts of mutations in the mt-DNA 4,977 and have been accounted for in many cancerous tissues such as breast cancer, colorectal cancer, gastric cancer, lung cancer, etc. The mt-DNA frequencies may be altered by healthier habits, however, there are still further large-sample studies necessary for absolute conclusions on the role mt-DNA has to play in tissue aging.

Recommended Articles

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Taylor, R. W., & Turnbull, D. M. (2005). Mitochondrial DNA mutations in human disease. Nature Reviews Genetics, 6(5), 389-402.

Nie, H., Shu, H., Vartak, R., Milstein, A. C., Mo, Y., Hu, X., ... & Bai, Y. (2013). Mitochondrial common deletion, a potential biomarker for cancer occurrence, is selected against in cancer background: a meta-analysis of 38 studies. PloS one, 8(7), e67953.