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Get to know in detail the mechanism of skin aging

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The accumulation of ROS and damage caused by ROS is one of the most important mechanism that leads to cellular aging.

Important oxygen metabolites, which can cause biological damage to the skin or initiate the formation of more reactive metabolites include superoxide radical, hydrogen peroxide, hypochlorous acid, hydroxyl radicals, nitric oxide radicals and singlet oxygen.

There are many potential target molecules in the skin layers that may be candidates for oxidative stress, such as lipids, proteins, carbohydrates and DNA.

Many chemical reactions can occur between ROS and these potential target molecules. The oxidation induced by ROS may result in lipid peroxidation, membrane protein damage and DNA mutations which play an important role in aging and can further initiate or propagate the development of many diseases.

Lipid peroxidation process can lead to the changes in plasma membrane fluidity and molecules leakage, and consequent disruption of their primary roles.

Recently published results indicate that the process of lipid peroxidation is intensified in the skin epidermis with aging, as well as phospholipase activity which results in the violation of integrity of cell membranes.

ROS can also directly inactivate enzymes and cause protein degradation.

Action of ROS on DNA leads to DNA lesions (base loss, base modifications and single and double DNA breakage events), which can all result in various adverse processes and even cancer.

Despite the fact that skin epidermis possesses an extremely efficient natural antioxidant defenses, including different types of antioxidant enzymes in the skin, such as peroxidase, catalase and glutathione, the protective effect that these offer may be limited by a high production of ROS, generating cellular oxidative stress as a result of the imbalance between antioxidant and oxidant species of living organisms, and this reduction may be the cause of skin aging. Therefore, antioxidants with free radical scavenging activities may have great significance in the protection and therapeutics of age-related diseases involving free radicals.

Skin aging involves progressive skin changes. Morphological changes are accelerated with advancing age and the application of oxidative stressors. Histopathologically, there is a loss of epidermal polarity and physiological disorders of keratinocyte maturation.

Cell population of photoaging dermis changes: fibroblasts become elongated, decayed, hyperplastic and infiltrated by inflammation; elastin quantity decreases with age, even more in the skin exposed to radiation, proportionally to the amount of radiation. Photodamage manifests primarily as the disorganization of fibroblast collagen which forms the connective tissue.

One study has demonstrated that old fibroblasts are more vulnerable to the accumulation of ROS following oxidative stress and are unable to remove them as efficiently as young fibroblasts. Changes in the skin that occur due to aging are shown in Table 1.

Table 1: Components of the skin: function and changes with aging

Cell type/component


Change with age


Barrier function, mechanical

protection, cytokine production

↓barrier function,

↓proliferation and differentiation


Synthesis and degradation of


↓in number


ECM component


↑stability and resistance to enzymatic degradation


ECM component

↓microfibril content,

porous, indistinct, and fragmented

ECM (extracellular matrix), UV (ultraviolet)