The Main Social Factors Affecting Retinoids
Chronological aging is the degrading of the skin protected from the sun. It can be identified by clinical techniques, microanatomy, physiological features that decrease in the skin protected from the sun.
It alters the epidermal turnover rate, reducing skin thickness and constituent cells.
It reduces thermoregulation has healing capacity after a wound and acts as a mechanical barrier.
It causes the release of excessive sweat and sebum, a decrease in immune response, a decrease in vitamin D synthesis and vascular reactions.
It is known as atrophic, causing elasticity degradation and increase vascular bundles.
Vitamin D3 is reduced due to a decrease in 7-dehydrocholesterol in the cells of epidermal tissue.
Photoaging leads to the formation of coarse skin epidermal tissue expands initially later becomes thin, unhealthy skin with wrinkles and hyperpigmentation.
Large pores are present on the skin leading to, benign neoplasm, premalignant lesions, and malignant lesions.
Skin surface becomes rough by the change in stratum corneum and glycosaminoglycan (GAG).
It also causes telangiectasia, a condition where blood vessels become twisted and enlarged.
Retinoid
Vitamin A (retinol) was identified in World War I and with the help of further researches, it was concluded that its deficiency might lead to xerosis and hyperkeratosis. New compounds were synthesized similar to the chemical structure of vitamin A as derivatives. This scheme was launched in 1968 as a retinoid group project.
The retinoid contains Vitamin A (retinol), retinaldehyde, retinoic acid, retinyl esters, and other derivatives as a family.
Cytosolic retinol-binding protein (CRBP) and cytosolic retinoic acid-binding protein (CRABP) possess great affinity towards retinol and retinoic acid.
Retinol comprises 20 carbon molecules with a cyclo-hexenyl ring on a side chain with double bonds present with an alcohol end group in trans configuration.
Alcohol at the end of retinol is oxidized to form an aldehyde and oxidizes, forming a carboxylic acid.
The human body does not synthesize vitamin A. Thus, supplements are available with retinyl esters and beta-carotene.
International union of pure and applied chemistry (IUPAC) confirmed that retinoid compounds comprise four isoprene units with a head-to-tail model.
Retinoids are capable of activating nuclear receptors to introduce genes through transcription and after metabolic transformation.
They treat diseases such as acne and rosacea, psoriasis, hair follicles inflammation, cancer.
Mode of Action
Retinoids are lipophilic; they solubilize in small amounts in body fluids. They are transferred with the help of proteins forming a retinol-protein binding known as prealbumin. In addition, the cytoplasm contains cytosolic retinol-binding protein (CRBP) and cytosolic retinoic acid-binding protein (CRABP) that possess great affinity towards retinol and retinoic acid.
Retinoids binding ability with CRABP 1 and 2 determine the intracellular concentration.
The main form of epidermis present in more quantities in the skin is CRABP 2 compared to CRABP 1.
Retinoids act on a few tissues, organs, and cells. Their derivatives and subgroups help to activate the nuclear receptors to facilitate functions.
The thyroid hormone consists of a receptor present in the form of a steroid termed the retinoid nuclear receptor, classified as retinoic acid receptor (RAR) and retinoid X receptors (RXR).
Isotopes of receptors RXR gamma and RAR alpha are abundant in the skin.
Receptors present in the retinoids bind to the RARE element as dimers; it is a zone of deoxyribonucleic acid (DNA) response.
They play a key role in maintaining the eyes, limbs, intestine, heart, kidney, liver, and nervous system.
They possess anti-comedogenic agents that activate the shedding process in sebaceous gland ducts.
They help in reducing discoloration, pigmentation by 60% and contribute a sufficient amount of melanin to the skin.
