INTRODUCTION:

Polyphenols are plant secondary metabolites and are commonly found in almost all plants. The phenolic components of most polyphenols have a common structural feature of an aromatic ring with at least one hydroxyl substituent [1]. Three phenolics compounds important for humans are phenolic acids, flavonoids and polyphenols [2]. Phenolic acid is divided into hydroxycinnamic and hydroxybenzoic acids [3]. Flavonoids are a group of compounds with low molecular weight, and are derivatives of benzo-y-pyrone. Polyphenols are compounds with high molecular weights divided into two groups- first is condensed group made up of polymers of catechins and epicatechins, and second is a hydrolysable group made up of polymers of gallic and egllagic acids [2]. Polyphenols in plants provides chemical defence against predators and ultra-violet radiation [3].

Tea is prepared from leaves and leaf buds of Camellia sinensis from the family Theaceae. Types of tea like white tea, green tea, oolong and black tea and others are all harvested from this species, but are processed differently to attain different levels of oxidation. The infusion of tea leaves is a beverage which is widely consumed second only to water [4]. The brew of one tea bag in one cup of water produces a solution of 0.35% w/w solids [5].

The composition of an infusion of Green tea or Black tea is listed below [5].

*Components*	*%wt/wt Solids*
Catechins	9%-30%,
Theaflavins	4%,
Simple polyphenols	2%- 3%,
Flavonols	1%-2%
Other polyphenols	6% -23%,
Theanine	3%
Amino acids	3%
Peptides and protein	6%
Organic acids	2%,
Sugars	7%
Other carbohydrates	4%
Lipids	3%
Caffeine	3%,
Other methyl xanthines	<1%
Potassium	5%
Other minerals and ash	5%
Trace of aroma	-

On the basis of the extent of enzymatic reactions which occur during the manufacture, tea is classified into the following types: green tea (non-fermented), black tea (fermented) and oolong tea (specially treated and semi fermented). The oxidized polyphenols in black tea are responsible for briskness, strength, colour, taste and astringency of the black tea infusion [6].

The polyphenols found in tea are more commonly known as flavanols or catechins like epicatechin, epicatechin-3-gallate, epigallocatechin, and epigallocatechin-3-gallate (EGCG), with the latter being the highest in concentration [7]. The principal constituents are caffeine, tannins and essential oils. Tannins comprise of a variety of polyphenolic compounds - most important of these are flavonoids called catechins [6]. Green tea contains higher amounts of catechin derivatives, such as (-)-epicatechin (EC), (-)-epigallocatechin (EGC) and their gallates (ECG and EGCG). During the production of black tea, some of the catechins are converted to theaflavins (TF) and thearubigins (TR) by enzymatic oxidation and coupling reactions (Roy; 2001). Catechins and their derivatives are known to contribute towards the flavour of tea while the aroma is dependent on the presence of different volatile compounds. Theaflavins (TF) are responsible for briskness and brightness while thearubigins (TR) for colour and body or strength (mouth feel). Caffeine is responsible for the stimulating effect of tea and the cancer chemopreventive action of tea is mainly due to its polyphenolic content [6].

UV RADIATION AND ITS EFFECTS ON SKIN

The part of electromagnetic spectrum of the wavelength between 200nm to 400nm is ultra-violet (UV) radiation. It is divided into long wave UVA (320nm-400nm), medium wave UVB (280nm-320nm) and short wave UVC (200nm-280nm) [8]. The longer wave is called aging ray which penetrates deep in the epidermis and dermis of skin. UVA is thousand times effective in tanning effect than UVB. Tanning is caused by melanin darkening in epidermis. Long term UVA exposure burns sensitive skin and if last prolonged than can damage inner structure of corium and results in premature photo-aging of the skin. UVA induces endogenous photosensitization responses in cells. Necrosis of endothelial cells is caused by UVA injury and leads to dermal blood vessel damage. UVA injury damage structural DNA. Impair immune system and causes 67% of malignant melanoma [9].

UVB radiation is called burning ray and makes up 4.5% of UV light. UVB is less but most active in solar light, UVB is thousand times stronger than UVA causing sunburn. UVB is more genotoxic than UVA. UVB acts in epidermal basal cell of skin; it’s directly or indirectly induces adverse biological effects, like formation of pyrimidine, photoproducts, isomerisation of trans to cis urocanic acid, induction of ornithine decarboxylase activity, stimulation of DNA synthesis, free radical production in the skin, cell cycle growth arrest, photoaging and photocarcinogenesis.

For showing biological effects UV must be absorbed by cellular chromophore which transforms the energy into biochemical signals. Nucleic acid and proteins are major cellular chromophores absorbing radiation in the UVB wavelength range. A DNA lesion is seen if DNA absorbs UVB. Lesions like cyclobutane-pyrimidine dimers and pyrimidine-pyrimidine photoproducts. DNA photoproduct formation leads to the activation of p53 protein that induces apoptosis of irradiated keratinocytes by blocking RNA transcription. Damage occurring in S-phase of cell cycle might lead to mutagenesis resulting in mainly cytosine to thymine substitution. On the other hand more UV exposure results keratinocytes to lose their ability to undergo the apoptotic process. Amino acids like tryptophan, tyrosine and biomolecules like NADH, quoins, flavins, porphyrins, 7-dehydrocholesterol and urocanic acid absorbs UVB radiations [9, 10].

SKIN DAMAGE BY UV RADIATION

Skin damage can be caused by UV radiation even if exposed for 2 hours. Keratinosomes decrease is an indicator of skin damage which forms dyskeratotic cells, 16 hours to 18 hours exposure results in intracellular edema whereas 30 hours to 48 hours intercellular edema which develops around damaged keratinocytes. Degeneration of keratinocytes cause mitochondrial swelling and rupture, cytoplasm condensation and pyknotic nuclei appears which is caused by 48 hours to 72 hours of total UV range exposure. This also results into Reactive Oxygen Species (ROS) largely seen in keratinocytes and fibroblasts and is taken out by non-enzymatic enzymatic antioxidants. ROS active metabolites like hydroxyl radical, superoxide active anion and peroxyl radicals and most active ones are single oxygen, hydrogen peroxide and ozone. Reactive Nitrogen Species (RNS) are nitric oxide and nitric dioxide. Free radicals modulate progressive deterioration of cellular structure function resulting loss of cellular integrity by DNA modification and abnormal expression of cellular genes [10].

UV radiation cause skin pigmentation on exposure, melanocytes increase the production of intracellular nitric oxide, triggering the signal transduction cascades to initiate melanogenesis by tyrosinase. Melanogenesis is influenced through a paracrine regulation process involving the keratinocytes [11].

POLYPHENOLS PROTECTIVE ACTION AGAINST OXIDATION AND UV RADIATION

Antioxidant activity of herbal phenolic acids and flavonoids such as quercetin, luteolin and catechins are better antioxidants than the nutrients vitamin C, vitamin E and β-carotene [2, 5]. Phenolics may be beneficial in preventing UV-induced oxygen free radical generation and lipid peroxidation, i.e. events involved in pathological states such as photoaging and skin cancer. This review is a summary of the findings of the photoprotective effects of tea polyphenols in studies of the skin damage induced by UV irradiation [12].

Flavonoids are antioxidant molecules. They absorb UV light and modulate signalling pathways which influences cellular function which can be beneficial for skin health. UV radiation shows negative effects on skin like erythema, edema, sunburned cells, hyperplasia, inflammation, immune-suppression, photoaging and photocarcinogenesis. Certain flavonoids can minimize the adverse skin reactions, demonstration on cell culture, animals, and humans have been proved. Green tea polyphenols shows immense effect when used as chemoprevention and it is most potent at suppressing the carcinogenic activity of UV radiation. Green tea polyphenols are photoprotective on cellular, molecular and biochemical mechanisms in both in vitro and in vivo systems [8, 10].

Polyphenols have been extensively studied as potential chemopreventive agents that could act against external inflammatory stimuli including tumour promoting agents and solar ultraviolet (UV) radiation. Catechin, epicatechin, epigallocatechin, epicatechin gallate and epigallocatechin gallate, are effective free radical scavengers, chain-breaking antioxidants and scavengers of reactive nitrogen species. The tea polyphenols have been attributed both antioxidant properties as scavengers of reactive oxygen species and the activation of phase II detoxifying enzymes [12].

Epigallocatechin (EGC) and epigallocatechin gallate (EGCG) are the predominant catechins in tea protect against UVB-induced skin carcinogenesis in mice projected that reactive oxygen species generated by UVB play a fundamental role in the process of carcinogenesis and that tea polyphenols acted by quenching such oxidant species . UVA component of solar radiation exerts its biological effects primarily by oxidative and antioxidants like the water-soluble ascorbic acid, and the lipophilic K-tocopherol and butylated hydroxytoluene are believed to act as photo-protective agents by their ability to scavenge reactive oxygen species generated during UVA irradiation. Tea polyphenols may have a pro-oxidant role leading to the generation of hydrogen peroxide in human cancer cell lines, regulation of UVA-activated stress response genes in human skin cells. EGC can modulate the expression of haem oxygenase-1 (HO-1), cyclooxygenase-2 (Cox-2) and metalloproteinase-1 (MMP-1) in UVA-irradiated dermal and transformed epidermal keratinocytes [12].

Tea polyphenols are powerful antioxidants and anticarcinogenic compounds, specifically the catechins epigallocatechin-3-gallate (EGCG), epigallocatechin (EGC), and epicatechin-3-gallate (ECG), which account for 30-40 percent of the extractable solids of tea leaves, are believed to mediate many of the cancer chemopreventive effects. Mechanisms of action may include antioxidant and free-radical scavenging activity, and stimulation of detoxification systems through selective induction or modification of phase I and phase II metabolic enzymes. Tea inhibits biochemical markers of tumour initiation and promotion, including the rate of cell replication and thus inhibition of the growth and development of neoplasms. Tea may serve to protect against skin cancer. Tea consumption inhibited the formation of tumours associated with the exposure to UVB sunrays. Where UVB tumours already existed, tea drinking slowed their growth and in some cases, actually decreased their size [3, 12].

EGCG reactivated dying skin cells when exposed during growth of the cells. The skin consists of three layers: the epidermis (outer layer), dermis (middle layer) and hypodermis (inner layer). Tea polyphenols are not absorbed beyond the epidermis, so some benefits are restricted to that outer layer of skin. But EGCG may be a fountain of youth for skin cells as when exposed to EGCG; the old cells found in the upper layers of the epidermis appear to start dividing again as they make DNA and produce more energy and the cells reactivated. EGCG accelerates the differentiation process among new cells. These two effects of EGCG on skin cells in different layers of the epidermis could be potential benefits for skin as diverse as aphthous ulcers, psoriasis, rosacea, wrinkles and wounds. Possibly scar tissue could be prevented from forming with EGCG therapy and diabetics patients with slow healing wounds may benefit from EGCG supplementation [12].

Caffeic acid (3,4-dihydroxycinnamic acid) and ferulic acid (4-hydroxy-3-methoxycinnamic acid) have been demonstrated to protect phospholipidic membranes from UV-induced peroxidation by inhibiting propagation of the lipid peroxidative chain reaction and to react with nitrogen oxides and proved effective in protecting human skin from UVB-induced erythema. Ferulic acid, shown to be a strong UV absorber, is employed as a photoprotective agent in a number of skin lotions and sunscreens [3].

Quercetin (3, 5, 7, 3’, 4’-pentahydroxyflavon) a powerful antioxidant and metal ion chelator, is believed capable of preventing the harmful effects of UV light or at least of reducing the damage. Quercetin protected skin antioxidant systems, namely glutathione peroxidase, glutathione reductase, catalase and superoxide dismutase activities, against UVA irradiating damage in rats to a considerable degree. Oral intake of quercetin prevented UVB-induced immune suppression in SKH-1 hairless mice. In vitro, quercetin and its semi-synthetic derivatives (quercetin 3-O-acetate, quercetin 3-O-propionate, and quercetin 3-O-palmitate) were found to inhibit UVC radiation-induced peroxidation in liposomal membranes [3].

TOPICAL APPLICATION ON SKIN

Photoprotective effects of green tea polyphenols, catechins and others have been demonstrated on humans by both oral supplementation and topical application. Plant extracts is dissolved in solvent so that only plant extracts remains on the dermal tissues. Although delivery is an issue as they cannot penetrate and function on human skin as the market commercial product do. Large influence is exerting by flavonoids because of their specific and nonspecific affinity for different types of proteins throughout the cell. Flavonoids physically block UV penetration, influence DNA repair, attenuate the inflammatory response, preserve immune function and induce cytoprotective pathways have been proved. Mechanisms by which flavonoids protect skin from harmful effects of UV radiation are still under investigation. Topical application of EGCG may prevent UV-B induced immune suppression and precancerous cell changes after UVB exposure. Anti-inflammatory and anticancer property of EGCG and green tea polyphenols can be used to control onset and growth of skin tumours [8, 9].

Antioxidant properties of tea show beneficial effect of tea. Green and white tea shows protection against detrimental effects of UV on cutaneous immunity. UV is not absorbed by topical applied tea products or sunscreen as both have presence of sun protection factor of one. Green and white teas are potential photoprotective agent which can be used in conjunction for sun protection methods. Skin carcinogenesis is result of UV irradiation, thus green tea extract can be used. Green tea extract show reduction of UV induced erythema, DNA damage, formation of radical oxygen species and down regulation of numerous factors related to apoptosis, inflammation, differentiation and carcinogenesis. Green tea extract s chemicals stability and staining properties are unstable. High concentration limits the usability of high green tea extracts in cosmetic products. Low concentration green extracts can be photochemopreventive to skin if doses are taken regularly. Topical green tea extracts also reduces UVB mediated epithelial damages [13].

SKIN RESTORATIVE PROPERTIES OF TEA POLYPHENOLS

1. Antioxidant properties

EGCG is at least 100 times more effective than vitamin C and 25 times better than vitamin E at protecting cells and their genetic material DNA from damage, believed to be linked to cancer, heart disease and other fatal illness. EGCG carries twice the antioxidant potential of resveratrol. It induces inhibition of soyabean lipoxygenase, inhibits TPA and induces oxidative DNA base modification in HeLa cells. It also inhibits Cu²⁺ mediated oxidation of low density lipoprotein (LDL) and reduces tertiary butyl hydro peroxide which creates lipid peroxidation and blocks the production of reactive oxygen species derived from NADPH-cytochorme P450-mediated oxidation of the cooked meat carcinogen i.e 2-amino-3- methylimidazole (4-5-f) quinoline. Green tea water soluble therefore excessive amounts of antioxidants are excreted out by body. Antioxidant activity of EGCG helps tremendously to combat post exercise muscle soreness [8].

2. Anti-ageing and anti-wrinkle properties

Free radicals promote oxidation of nucleic acids, proteins, and lipids and can damage intracellular structures including DNA by regulating transcription factors, such as activator protein 1 (AP-1) and nuclear transcription factor-kappa B (NF-kB). Polyphenols inhibit collagenase activity by two mechanisms first by binding of the essential Zn2+ in the enzyme active site and second by conformational changes on the enzyme due the ability of phenolic compounds to interact with proteins. Metalloproteinases are produced by AP-1 which breaks existing collagen, contributing to skin wrinkling. It is the sum of NF-kB transcription of proinflammatory mediators interleukin (IL)-1, IL-6, IL-8, and tumor necrosis factor-alpha acting through the cell surface responsible for skin aging. Tea polyphenols and EGCG in addition are effective free-radical scavengers, down-regulate UV-induced expression of AP-1 and NF-kB and suppress metalloproteinase and age-related collagen cross-linking in mice. Tea polyphenols inhibit the activity of collagenase and increases collagen biosynthesis rate of human fibroblasts. EGCG topical treatments influence HIF-1α induction and VEGF (vascular endothelial growth factor) expression and may serve as a potential agent in the prevention of telangiectasia (spider veins) [11, 14].

3. Anti-acne properties

Acne vulgaris is the most common skin condition resulting from the effects of hormones. Androgens such as dihydrotestosterone (DHT) and testosterone, the adrenal precursor dehydroepiandrosterone sulfate (DHEAS), estrogens such as estradiol, and other hormones, including growth hormone and insulin-like growth factors (IGFs), could be important in acne. It is being studied whether hormones are taken by serum of sebaceous gland or produced locally within the gland or whether a combination of these processes is involved. Hormonal therapy is an option in women with acne not responding to conventional treatment or with signs of endocrine abnormalities. Study depict potential effects of stable formulation (water in oil emulsion), containing 3% tea extract on skin sebum production for a period of 8 weeks. A statistically significant (p < 0.5%) decrease was found in skin sebum production after long term application of the formulation [15]. EGCG inhibits lipogenesis. Epigallocatechin-3-gallate (EGCG) decreases inflammation induced by SEB-1 sebocytes stimulated by heat-inactivated Propionibacterium acnes through the inhibition of NF-jB and activator protein 1 (AP-1) pathways. Biochemical, genetic, and cellular studies indicate that modulation of AMPK–SREBP-1 and NF-kB/ activator protein 1 (AP-1) signalling pathways mediates the sebosuppressive and anti-inflammatory effects of EGCG [16].

4. Skin lightening properties

Natural skin lightening products containing tyrosinase blockers like phenols and polyphenols, and non-tyrosinase blockers like α- MSH, melanosome transferase and cytokine inhibitors. Gallic acid derivatives of hydroxyflavanols had been isolated from tea as they are identified as strong tyrosinase inhibitors. EGCG and hydroxyflavanols are not only tyrosinase inhibitors, but also decreased MITF (Microphthalmia-associated transcription factor) production in cells. Ellagic acids (EA) polyphenol found in tea with strong antioxidative properties and tyrosinase inhibition. Chelating copper at the active site of tyrosinase to reduce its activity and inhibition of proliferation of melanocytes and melanin synthesis results in skin lightening by EA. EA also show antioxidative and ROS-scavenging activities which contribute to its skin lightening effect [9, 11].

5. Anti-viral properties

Microbial agents, viruses or bacteria attack skin and cause local inflammation. Inflammation can be due to internal elements such as autoimmune diseases that are associated with damage to the skin, resulting in skin lesions, rash, and altered appearance. Tea polyphenols have been recognized for prevention of infection by a range of viruses, such as adenovirus, Epstein-Barr virus and influenza virus. Studies shows that EGCG inactivated HSV (Herpes simplex virus) projecting that the antiviral properties of polyphenols are due to their influential protein binding capacity, follow-on tight binding to the viral coat proteins, and their ability to transform the dynamics of the cell plasma membrane, preventing the entry of viral particles into the cells [8, 11].

6. Anti-Inflammatory properties

The conversion of arachidonic acid into various proinflammatory agents, including leukotrienes is catalyzed by the dioxygenase enzyme. Epicatechin inhibits the dioxygenase and LTA 2 synthase activities of 5-LOX. Epicatechin has also been shown to inhibit 15-LOX-1 [17].

SIDE EFFECTS AND TOXICITY

Tea is generally considered a safe, non-toxic beverage and its consumption is usually without side effects. The average cup of tea contains from 10-50 mg of caffeine, and over-consumption may cause irritability, insomnia, nervousness, and tachycardia. Because studies on its possible teratogenic effect are inconclusive, caffeine consumption is contraindicated during pregnancy. Lactating women should also limit caffeine intake to avoid sleep disorders in infants [7].

CONCLUSION:

Human skin is constantly exposed to the UV irradiation present in sunlight which induces a number of pathobiological cellular changes. Tea polyphenol becomes one of the favourite ingredients for cosmetic preparations as although the effects may be small, they are significant and do meaningfully improve skin feel and appearance with continued use. Also the component are beneficial by being stable in production, storage, and use, be nontoxic to the consumer and have activity at the target site once applied. The development of novel defensive and beneficial strategies can be studied by molecular mechanism of UV-damage and plant phenolics effects for prevention of the unpleasant effects of UV radiation on the skin and improving skin penetration of this bioactive cosmetic by enhancing delivery into the skin.

ACKNOWLEDGEMENTS:

The authors would like to thank HUL (Hindustan Unilever) for financial assistance for the collaborated Research Project and the fellowship provided to the first author.

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Received on 22.02.2015 Accepted on 05.03.2015

Research J. Topical and Cosmetic Sci. 6(1):Jan.–June 2015 page 1-6

DOI: 10.5958/2321-5844.2015.00001.1