Vitamin A (retinoids) has long been known to play a critical role in homeostasis of various epithelia including epidermis and is important for sustaining normal growth and differentiation. When absorbed, retinol may be esterified with fatty acids to form retinyl esters. Retinol may also be oxidized into retinal, which subsequently may be oxidized to retinoic acid. Reinoids constitute a group of natural and synthetic compounds characterized by vitamin A, all transretinol, ROL and other natural retinoids plays critical role in prevention and repair of dermal photoaging. the anti-aging effect of topical retinoids is mainly linked to the receptor-mediated gene activation induced by the ligand retinoic acid modulating epidermal cell proliferation and differentiation, extracellular matrix production, angiogenesis, oxidative stress and melanocyte function.

1. increases synthesis and inhibit degradation of collagen, changes that are associated with improvement in wrinkling.

2. In the epidermis, topical retinoids may cause hyperplasia, compaction of the stratum corneum, thickening of the granular layer and increased intercellular mucin deposition. These changes are associated with increased smoothness of the skin

Major sources of natural retinoids are animal fats, fish liver oil and yellow and green vegetables (carotenoids).The intestine is the primary site of retinoids and its precursor metabolism in the body. Dietary retinoids and its precursor are taken up intact into the enterocyte, where they can undergo conversion to retinoid.

After intestinal absorption, retinoid production occur by two pathways:

1. By oxidative cleavage of the central double bond followed by reduction to ROL by a microsomal retinal reductase.

2. Apo-carotenoids are formed through excentric cleavage followed by transformation of the apo-carotenoid acids into RAs

The retinol, along with other dietary lipids in the intestinal mucosa, is packaged as retinyl ester in nascent chylomicrons. and approximately 75% of chylomicron retinoid is eventually taken up as part of the chylomicron remnants by the liver, where the majority of the body’s retinoid is stored as reservior.In the liver chylomicron-RE complexes are hydrolyzed and free ROL binds to retinol binding protein (RBP),a transport protein for retinoids. Excess ROL get stored inperisinusoidal stellate cells, called vitamin A storage. Approximately 50 to 80% of the total body vitamin A in humans is stored in the stellate cells in the liver in the form of RES (retinal esters). ROL-RBP complexes released from the liver bind to transthyretin, a serum protein named for its ability to bind and transports simultaneously to target tissue. Till now the exact mechanisms of ROL uptake by target cells are not understood completely.

Several possibilities have been proposed: regulated by unknown factors.

• Receptor-mediated uptake,

• Nonspecific transfer of ROL and RA,

• Fluid phase endocytosis.

Similarly, the mechanism of transcutaneous absorption of topically applied retinoids is also not understood. Topically applied RA is isomerized partially to 9-cis-RA, 13-cis-RA, and other metabolites within the epidermis. Approximately 80% of the RA applied remains on the skin surface, whereas its penetration through the stratum corneum and the hair follicle is vehicle-dependent.

The storage of ROL in human skin occurs through esterification of ROL into RE (Kang et al., 1995). Skin cells contain transferases, LRAT and acyl CoA:acyltransferase (ARAT). These two enzymes catalyze RE synthesis (Torma and Vahlquist, 1987; Kurlandskyet al., 1996) (table 1). The hydrolysis of RE to ROL is regulated by a specific RE hydrolase.

Evidently the anti-aging effect of retinoids is mostly connected to the receptor-mediated gene activation prompted by the ligand retinoic acid adjusting epidermal cell multiplication, differentiation,extracellular matrix creation, angiogenesis, oxidative stress and melanocyte capacity.

Retinoic acid is thought to induce extracellular matrix deposition through two mechanisms.

1. Regulating transcription and synthesis of ECM proteins, including hyaluronic acid and collagen. Together they give the skin a more hydrated and firmer appearance

2. RA is known to reduce the synthesis and activity of MMPs by inhibiting induction of the protein kinase, c-Jun thereby decreasing MMP-driven degradation and reduces dermal ECM turnover.

Diminished dermal turnover with synchronous increased synthesis of ECM within the dermis, prompting advantageous impact of retinoid is an expansion in the thickness of the skin. Despite the fact that retinoids actually thin the stratum corneum. The end result is a thicker, more youthful looking skin. Retinoids also stimulate dermal fibroblasts, which are cells that make the structural framework of tissues and replaces disorganized collagen fibers with new, well-organized fibers. RA also Induces angiogenesis which improves blood flow to the skin and is the reason behind the healthy rosy glowing skin, topical retinoids over the time does the following

• Increased skin thickness and firmness
• Increased skin hydration
• Increased skin tolerance to external factors
• Reduced visible signs of sun damage
• Reduced fine wrinkles
• Restoration of even skin tone and reduced hyperpigmentation
• Reduction in dark circles under the eyes
• Reduced skin roughness
• Reduced irritation from shaving
• Less risk of skin cancer
• Reduced stretch marks
• A healthy, 'rosy glow'

Both natural and photo-induced premature aging of skin are associated with the alteration in dermal epithelium and degradation of collagen, that provides skin structure and function. Retinoids are among the few drugs, effective in treating the clinical signs of agingskin, that includes wrinkling, coarsening, dryness and laxity.