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Gene & Protein in Disease Buccal mucosa and aging

dysfunction, and altering protein and lipid content in the same chronological age. At the individual level, different
body (Figure 2). Aging has also been linked to changes in cells, tissues, and organs age at different trajectories.
DNA methylation levels and epigenetic modifications, both Biological aging can be affected by exposure to chemical
of which are influenced by environmental factors such as hazards, particularly through DNA damage in cells such as
occupational exposures. The effects of ROS on aging are buccal cells, which serve as the first line of defense against
thought to be mediated through histone modification foreign particles entering the body. 9
and DNA methylation, processes that contribute to the DNA damage resulting from both internal and external
regulation of gene expression. 68 factors poses a significant threat to living cells. Genotoxic
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Molecular modifications in immune cells, such as NK agents derived from exogenous or endogenous sources
cells, can play a critical role in the initiation and progression – including UV light, ionizing radiation, chemicals,
of senescence and age-related diseases, including infection, and the intrinsic biochemical instability of DNA – can
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malignancies, and inflammatory disorders. These changes disrupt cellular homeostasis by causing DNA damage 74,75
are consequences of decreased immune system function and altering its chemical structure. DNA damage, along
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and a process known as inflammaging, which refers to the with chromosomal changes caused by mutations, DNA
chronic, low-grade inflammation associated with aging. adducts, DNA breaks, and alkali-labile sites, can trigger
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Therefore, NK cells in the buccal mucosa provide an and accelerate the aging process. The effects of chemical
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interesting resource for assessing aging in the body. 8 exposure on genotoxic materials can be monitored using
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Exposure to environmental hazards can transform biomarkers, which assess molecular and cellular events
79,80
normal cells into abnormal ones by interacting with in biological systems. These biomarkers, as listed in
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genetic material and changing DNA and/or RNA in cells. Table 2, are categorized into three groups: exposure,
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24,81
These genetic alterations can affect cellular functions, susceptibility, and early effects (Figure 3).
including those of immune system cells such as NK cells. Exposure biomarkers measure substances, metabolites,
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This transformation may occur within a latency period of or products resulting from the interaction of target
4 – 40 years following initial exposure. As aging is a time- molecules with tissue, reflecting external and/or internal
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related process resulting from life-long exposure to low and
natural levels of environmental agents, regular exposure to Table 2. Types of biomarkers
chemicals in daily occupational activities poses a higher
risk of premature aging, health damage, and decreased Biomarkers Description
productivity. Biomarkers of aging and biological aging can Exposure Biomarkers of internal dose, biomarkers of biologically
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assess these risks, reflecting individual-specific age-related effective dose (e.g., DNA adducts)
vulnerabilities, physiological function, and overall health. 3 Effect DNA breaks, chromosome aberrations, micronuclei,
sister chromatic exchange, biochemical effects,
5. Related molecular biological markers of oxidative damage, DNA repair enzymes, metal-binding
proteins
aging Susceptibility Single nucleotide polymorphisms, telomere length,
Aging is a heterogeneous process, with significant epigenetics, metabolism enzyme induction, varying
variability in health outcomes among individuals of the DNA repair capacity

Figure 2. A schematic representation of reactive oxygen species effects on cellular senescence

Volume 3 Issue 4 (2024) 4 doi: 10.36922/gpd.4418