Page 39 - GPD-3-4

Gene & Protein in Disease Buccal mucosa and aging

Moreover, changes in biomarkers related to NK cells,
such as cytokines, including interferon (IFN)-γ, IFN-β,
and interleukins (IL-2), as well as alterations in NK cell
types, are associated with aging. NK cells may also exhibit
telomere shortening, a marker of aging, which can be
70
investigated using buccal cells. This approach enhances
our understanding of aging and age-related diseases
and aids in designing future immune therapies targeting
NK cells in the elderly population. Identifying reliable
69
biomarkers is crucial for accurate risk stratification and
exploring antiaging interventions. Given the challenge of
3
pinpointing a single biomarker that reflects the intricate
interaction between environmental exposures and
aging, further studies are needed to identify biomarkers
Figure 3. Biomarkers associated with environmental exposure
sensitive to mixed or low-dose exposures. In addition, a
combination of biomarkers reflecting various levels of
exposures. 24,82,83 These biomarkers indicate short-term cellular organization, such as DNA, RNA, and proteins,
DNA or chromosomal damage in cytogenetic analyses may provide the most effective approach.
30
and serve as sensitive indicators of recent human
exposures to hazards. Consequently, the potential risk 6. Interaction between molecular
84
posed by hazards and their ability to induce long-term biomarkers and aging
health problems can be determined. Biomarkers of effect
30
show early health effects, such as health impairment and Genomic damages after exposure to chemicals can occur
critical and clinical effects. 24,82,83 Biomonitoring the effects in two forms: (i) point mutations at the nucleotide level in
of exposure through various cytogenetic tests enables the a gene and (ii) structural changes in chromosomes, such
90
evaluation of genotoxic effects by detecting DNA damage, as chromosomal aberrations. Two major perspectives
on senescence include: (i) a specific genetic program
such as sister chromatid exchange and micronuclei. for senescence and (ii) evolutionary forces, particularly
46
Micronuclei, an example of such biomarkers, are formed
84
due to chromosomal damage, typically arising from reproductive success, that suggest a genetic basis for
85
58
chromosomal fragmentation or lagging. This biomarker senescence. Senescence results from the coordinated
86
is evaluated in cells, such as buccal cells, and reflects actions of multiple genes, and mutations in these genes can
67
genotoxic damage in the dividing basal cell layer of target lead to premature aging.
46
organs 1 – 3 weeks earlier. Micronucleus levels tend to Genetic analysis of aging helps identify regulatory links
increase with age. The first effective biomarkers used to between gene expressions and lifespan, involving pathways
91
86
assess the aging process were micronuclei, sister chromatid such as insulin/IGF-1 signaling, PI3K, TOR, MAPK,
exchange, and chromosome aberrations. 77 AMPK, PKC, NF-κb, TGF-β, Notch, WNT, S6K, 92-96 and the
64
Biomarkers of susceptibility indicate an individual’s p53/p21 and p16INK4A/pRb pathways. The p16INK4A/
increased sensitivity to specific target molecules or pRb pathway can lead to premature senescence or stress-
metabolic processes, leading to a higher dose of the target induced premature senescence. Oncogene-induced
compound upon exposure. 24,82,83 These biomarkers reveal senescence is characterized by the activation of pathways
the inherent or acquired capability of an organism to involving p53 and DNA damage and is marked by tumor
64
metabolize xenobiotic substances upon chemical exposure, progression restriction without telomere shortening.
resulting in variations in metabolic pathways and toxic DNA repair pathways play an important role in
responses among individuals. Examples of susceptibility correcting damage caused by mutagens, such as DNA
biomarkers include cytochrome P-450 (CYPs) and damage and chromosomal alterations, which pose
79
73
glutathione transferases (GSTs). Telomere shortening and significant threats to living cells. These repair processes
87
epigenetic modifications are also included in this group. involve cell cycle regulation and mechanisms such as
88
97
Epigenetic biomarkers reflect stable changes to the genome the SOS response, utilizing ATP and NADH to remove
76
3,89
that affect gene expression or silencing. Factors such DNA lesions. It is estimated that over 130 genes in the
62
98
as DNA methylation levels, cell metabolism, and signal human genome are involved in DNA repair, with more
transmission control through epigenetic mechanisms play than 70 genes contributing directly to the major nuclear
significant roles in human longevity. 68 DNA repair pathways. Mutations in these repair genes
99
Volume 3 Issue 4 (2024) 5 doi: 10.36922/gpd.4418