Skin Aging &
Ultra-Violet (UV)-Induced Skin Aging
Aging
Genetic Environment
Chromosomes Free radical/ Cellular
structure reactive oxygen mechanisms
shortening telomeres species
Intrinsic Skin Aging
Normal physiology
process.
A slow process
Caused partly by reactive
oxygen species produced
in metabolism.
UV-induced Skin Aging
!
Direct UV effects on skin
Caused partly by reactive
oxygen (ROS) induced by
UV.
ROS induce cellular
damage.
Photoaging and Pigmentary Changes of the Skin Chapter 3 33
Kang recently demonstrated that the genera- prominent thinning after the eighth decade [23,
tion of free radicals by UV light was impaired 24]. Additionally, melanocytes also decrease
by the antioxidant genistein and the antioxi- during adulthood, with an estimated decrease
dant precursors n-acetyl cysteine [22]. of 10% per decade [25]. As expected, pigmen-
tary changes are not a prominent feature of in-
trinsically aged skin compared with photoaged
skin (Fig. 3.2). Environmental factors that con-
3.3 Clinical Characteristics tribute to aging, such as pollution and smok-
of Photoaging ing, produce marked wrinkling of the skin but
and Pigmentary Changes not pigmentary abnormalities. There are sever-
al different manifestations of pigmentary alter-
The clinical characteristics of photoaged skin ations associated with photoaged skin. These
are more pronounced compared with those ob- include mottled hyperpigmentation, solar len-
served in intrinsic aging (Table 3.1). It is these tigines, diffuse hyperpigmentation, pigmented
changes that are of cosmetic concern to many seborrheic keratoses, and guttate hypopigmen-
individuals as they overshadow those associat- tation. Some manifestations of photoaging are
ed with intrinsic aging. In intrinsic aging, the more prominently displayed in certain racial
skin has a pale appearance with fine wrinkling. groups compared with others. These differenc-
It has been demonstrated that the dermis thins es will be discussed below and are highlighted
by 20% with intrinsic aging, with the most in Table 3.2.
Clinical Characteristics of Aged Skin VS Photoaged Skin
Table 3.1. Clinical characteristics of intrinsic aging and photoaging
Clinical characteristic Intrinsic aging Photoaging
Pigmentation Pale, white, hypopigmentation Mottled, confluent, and focal hyperpigmentation
Wrinkling Fine lines Deep furrows
Hydration Dry and flakey Dry and rough
Growths Benign Cancerous and benign
Fig. 3.2.
Pigmentary changes are not a
prominent feature of intrinsi-
cally aged skin as seen on the
sun-protected flexor arm
compared with the pigmen-
tation displayed on the sun
exposed extensor arm of the
same woman
Acute UV-induced Skin Damage
UVB
DNA damage
Pigment changes (suntan)
Sunburn cells
Epidermal thickening
Melanogenesis
Minimal Erythema Dose (MED)
Index pengukur sensitivitas kulit pada sinar UV.
Dosis terkecil sinar UVB yang menyebabkan reaksi eritema pada kulit
24 jam setelah pemaparan.
Chronic UV-induced Skin Damage
Collagen
Dermal alterations (elasticity & firmness)
Elastin
Photoaging
Fungsi fibroblast
sel jumlahnya
berkurang:
UV Care
Langerhans, keratinosit 337
dan fibroblast
kerutan kulit
yang dalam
penurunan
jumlah serat
collagen
Figure 1 Number of Langerhans cells in UVB-irradiated epidermal specimens.
Repeated irradiation with low-dose UVB. The total energy of each irradiation was
100 mJ/cm2. Langerhans cells in specimens irradiated four times with 25 mJ/cm2 are
markedly fewer than in specimens irradiated once with 100 mJ/cm2. The data are
presented as mean + S.D. (n ¼ 12). !! P , 0.01 vs. no irradiation, Student’s t-test.
such as atopic dermatitis and psoriasis, was suggested (17 –19). Because reactive
oxygen species are highly reactive, they react with various neighboring in vivo
Reactive Oxygen Species (ROS) in UV-
Induced Skin Damage
ROS + Biological substrate Oxidative damage
Protein
Cellular damage
Lipid
accumulated
DNA
! Aging
ROS activate cel surface reseptor to initiate the release of
Tumor Necrosis Alfa
Nuclear transcirption factor: AP-1. AP-1 activates MMP
ROS cause
Lipid peroxidation
UV Care 343
DNA damage
Figure 7 Inhibitory effect of astaxanthin on UVB-induced skin aging. Grading score for
visible changes of mice skin by vehicle (O), astaxanthin (B), and no UVB (V). The data
are expressed as mean + S.D. (n ¼ 6). Asterisk (! ) indicates the significantly different
values (! P , 0.05, !! P , 0.01) from vehicle and UVB.
Iron Chelators
In the production of reactive oxygen species or free radicals, the ferric ion plays
an important role as a catalyst (Fig. 8). The amount of ferric ion in the skin is
increased by UVB irradiation over a long period of time. When the amount of
iron found in sun-exposed skin of the human body and nonexposed skin was com-
UV light Induced Reactive Oxygen
pared, sun-exposed skin such as the neck, forehead, and cheek had two to four
times as much iron as nonexposed skin such as the thigh and buttock. This
Species
finding suggests (ROS)
that ferric Formations
ions serve as a causative agent of skin damage and
Figure 8 Role of ferrous/ferric iron in generation of reactive oxygen species induced by
UVB irradiation.
Body Defense To Reactive Oxygen Species (ROS)
Reactive Oxygen Species in UV-Induced Skin Damage
1 -
Single oxygen ( O2), superoxide anion (O2 ),
.
hydrogen peroxide (H2O2), hydroxyl radical ( OH)
!
1
Fibroblast irradiated with UVB produces O2
Fibroblast treated with
1
catalase inhibitor resulted increase in
H2O2 (a precursor O2) and cellular damage similar with
fibroblast treated UVB.
1
• O2 Effects:
DNA strand breakage
protein fragmentation
Reactive Oxygen Species in UV-Induced
Skin Damage
1
Single Oxygen ( O2)
1
Skin irradiated by UV produces O2
Propionibacterium acnes1on skin surface produces metabolite called
porphyrin that generates O2 when UV irradiated.
• Effects:
skin surface lipid peroxidation
cross linking collagen in dermis
cellular aging in dermis fibroblast
Reactive Oxygen Species in UV-Induced
Skin Damage
Nitric Oxide (NO)
NO is normally produced by the body.
NO is synthesized by NOS from arginin. Function for
signaling & cytotoxicity.
• Effects on skin when NO is produced following skin UV
irradiated:
NO is produced in keratinocytes —> skin erhythema
stimulates melanogenesis by increasing NOS activity
