The green tea polyphenol, epigallocatechin‐3‐gallate, protects against the oxidative cellular and genotoxic damage of UVA radiation

Tobi, Simon; Gilbert, Mileka; Paul, Nigel D.; McMillan, Trevor J.

doi:10.1002/ijc.10730

Cited by 101 publications

(72 citation statements)

References 54 publications

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“…To date only few substances/extracts have been demonstrated to be capable of protecting/suppressing UVA-induced skin cells/ skin injury e.g. carnosic acid 71 , quercetin 72 , epikatechin 74 , epigallokatechin-3-gallate 74,75 or P. leucotomos extract 76 , silymarin 77 and P. vulgaris extract 78 . Considering the latest knowledge about UV radiation it is necessary to look for new substances possessing both UVA and UVB protection.…”

Section: B) Exogenous Photoprotectionmentioning

confidence: 99%

Ultraviolet Light Induced Alteration to the Skin

Svobodová¹,

Walterová²,

Vostalová³

2006

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

308

243

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Section: B) Exogenous Photoprotectionmentioning

confidence: 99%

Ultraviolet Light Induced Alteration to the Skin

Svobodová¹,

Walterová²,

Vostalová³

2006

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

308

243

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“…In addition, because it has recently been reported that DEP or organic DEP extracts induce pro-oxidative and proinflammatory effects in the respiratory tract that can be negated by thiol antioxidants such as N-acetyl cysteine (NAC) (18,19), we also examined whether NAC or another antioxidant, epigallocatechin 3-gallate (EGCG), which is one of the main polyphenolic constituents of green tea (20,21), could neutralize the suppression of IFN-␥ mRNA expression and protein production by DEP. EGCG in addition to NAC significantly recovered the IFN-␥ production by DEP-treated T cells, which suggested the crucial role of oxidative stress in the effects of DEP.…”

mentioning

confidence: 99%

Cellular Basis of the Role of Diesel Exhaust Particles in Inducing Th2-Dominant Response

Ohtani

Nakagawa

Kurosawa

et al. 2005

The Journal of Immunology

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There is growing evidence that diesel exhaust particles (DEP) can induce allergic diseases with increased IgE production and preferential activation of Th2 cells. To clarify the cellular basis of the role of DEP in the induction of Th2-dominant responses, we examined the effects of DEP on the cytokine production by T cells stimulated with anti-CD3/CD28 Ab and on that by monocyte-derived dendritic cells (MoDCs) stimulated with CD40L and/or IFN-γ. We examined IFN-γ, IL-4, IL-5, IL-8, and IL-10 produced by T cells and TNF-α, IL-1β, IL-10, and IL-12 produced by MoDCs using real-time PCR analysis or by ELISA. To highlight the effects of DEP, we compared the effects of DEP with those of dexamethasone (DEX) and cyclosporin A (CyA). DEP significantly suppressed IFN-γ mRNA expression and protein production, while it did not affect IL-4 or IL-5 mRNA expression or protein production. The suppressive effect on IFN-γ mRNA expression was more potent than that of DEX and comparable at 30 μg/ml with 10−7 M CyA. The suppressive effect on IFN-γ production was also more potent than that of either DEX or CyA. DEP suppressed IL-12p40 and IL-12p35 mRNA expression and IL-12p40 and IL-12p70 production by MoDCs, while it augmented IL-1β mRNA expression. Finally, by using a thiol antioxidant, N-acetyl cysteine, we found that the suppression of IFN-γ production by DEP-treated T cells was mediated by oxidative stress. These data revealed a unique characteristic of DEP, namely that they induce a Th2 cytokine milieu in both T cells and dendritic cells.

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“…2). Since aging is thought to involve the accumulation of oxidative stress, 21,22) it is possible that an age-dependent burden of oxidative stress causes degradation of the immune defense system against the tumor cells. In actual fact, the cytotoxicity of NK cells is known to be dependent on oxidative stress and the activity is often reduced by ROS.…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, GT-catechins, especially EGCG, are known to work as potent radical scavengers and show antioxidative effects against various types of oxidative stress. 22,25) Unno et al demonstrated that long-term intake of EGCG water up-regulated the level of antioxidative activity in the serum of aged SAMP10 mice. 26) Thus, we speculated that GT-catechin intake provided protection from the accumulation of oxidative stress and improved the reduced NK activity with age.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effect of Green Tea Catechins on Experimental Tumor Metastasis in Senescence-Accelerated Mice

Shimizu

Hakamata

et al. 2010

Biological & Pharmaceutical Bulletin

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Tumor metastasis is a key step in the development of a tumor and becomes a critical trigger for the death of a patient. Hematogenous metastasis is established by a series of steps, which begin with the dissociation from primary sites and culminate with the formation of metastatic colonization.1) This process is greatly dependent on surrounding host factors such as host resistance to cancerous cells. 2,3) In a previous study, we demonstrated that the early accumulation of metastatic tumor cells in a target organ after intravenous injection of the cells and following tumor metastasis were enhanced by reduction of the host immune surveillance potential, 4,5) suggesting that avoidance of the surveillance associated with immune cells, such as natural killer (NK) cells, was a critical step for the completion of an experimental tumor metastasis.The senescence-accelerated mice prone (SAMP) strain has been established as a mouse model for aging research 6) and exhibits a more accelerated senescence process than normal mice. 7,8) By using this model, we found that the immune surveillance potential of 8-month-old aged SAMP10 mice was lower than that of 2-month-old young mice, and that the experimental lung metastasis was significantly induced in aged mice. These data suggest that the aging process produces an environment susceptible to metastatic tumor cells in the bloodstream to complete metastasis, and that such an environment is produced with age due to the reduced immune surveillance potential. 9)Green tea (GT)-catechins are functional polyphenols, and are known to have various actions, such as antibiotic, antiinflammatory, antioxidative, and anti-cancer effects. It is anticipated they will become useful as a functional food that promotes human health and longevity. Although animal studies have shown that GT-catechin treatment suppressed tumorigenesis, tumor growth, and tumor angiogenesis, 10,11) the crucial mechanism of the action of GT-catechin against cancer has not been fully elucidated. Our previous study demonstrated that (Ϫ)-epigallocatechin gallate (EGCG, a major component of GT-catechins) suppressed tumor angiogenesis through the inhibition of membrane type-1 matrix metalloproteinase (MT-1MMP) activity and subsequent induction of dormancy of solid tumor growth. 12,13) Tachibana et al. also reported that 67-kDa laminin receptors are a receptor for EGCG and that EGCG treatment inhibited the receptor-mediated signaling pathway and subsequent tumor cell growth.14,15) Several reports have described various such approaches to treat and prevent cancer using GT-catechins. In the present study, we hypothesized that GT-catechin intake modulates the immune surveillance potential in aged mice, and enhances the susceptibility to experimental tumor metastasis. To prove this, we exposed SAMP10 mice to GT-catechin in their drinking water for an extended period of time (aged/catechin mice) and examined their NK activity as an indicator of immune surveillance potential. We then also examined the accumulation of K1735M2 melanoma...

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The green tea polyphenol, epigallocatechin‐3‐gallate, protects against the oxidative cellular and genotoxic damage of UVA radiation

Cited by 101 publications

References 54 publications

Ultraviolet Light Induced Alteration to the Skin

Ultraviolet Light Induced Alteration to the Skin

Cellular Basis of the Role of Diesel Exhaust Particles in Inducing Th2-Dominant Response

Preventive Effect of Green Tea Catechins on Experimental Tumor Metastasis in Senescence-Accelerated Mice

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