Tea (Camellia sinensis, Theaceae) is the most popular beverage in the world. Tea preparations are classified into four types: green, black, oolong and pu-erh teas. The cancer-preventive effects of tea extracts and tea polyphenols have been demonstrated in various experimental systems of mutagenesis and carcinogenesis. Anticarcinogenic effects of tea polyphenols have been reported in the tissues/organs of skin, esophagus, stomach, colon, bladder, lung, liver, pancreas, prostate, and mammary glands of various animal models. These effects are believed to be based on green tea catechins and black tea theaflavins. Polyphenols play potential roles in reducing oxidative stress, modifying carcinogen metabolism, enhancing DNA damage repair, inhibiting tumor promotion and metastasis, and/or modulating cell-cycle arrest, apoptotic death of pre-cancerous/cancerous cells, and oncogenic signal transduction. Indeed, much evidence on the cancer preventive effects of tea polyphenols has been reported in in vitro and animal experiments. However there is insufficient and inconsistent evidence for the association between tea consumption and cancer incidence or mortality in humans. This review includes perspective on: 1) antimutagenic and anticarcinogenic effects in in vitro systems; 2) anticarcinogenic effects in animal models; 3) molecular mechanisms of anticarcinogenesis; 4) biotransformation and pharmacokinetics of tea catechin; 5) epidemiological studies; and 6) possibilities of human cancer prevention by tea polyphenols and future problems for clarification.
N-Nitrosoproline was thought to be nonmutagenic and noncarcinogenic because of its stability. However, it has been reported that N-nitrosoproline releases nitric oxide and shows direct mutagenicity by UV light irradiation. In this study, nitrosation and nitration of glutathione and tyrosine by N-nitrosoproline with UV light are tested. When a neutral solution of N-nitrosoproline and glutathione was irradiated with UV light of 365 nm generated from an 8 W mercury lamp, S-nitrosoglutathione was formed. When a neutral solution of N-nitrosoproline and tyrosine was irradiated with the UV light, a small amount of 3-nitrotyrosine was generated. A similar intensity of UV light of 254 nm induced formation of S-nitrosoglutathione and 3-nitrotyrosine with lesser efficiencies. When UV light of 365 nm was irradiated to a neutral mixture of N-nitrosoproline, gluthathione and tyrosine, a similar amount of S-nitrosoglutathione was generated, while the yield of 3-nitrotyrosine greatly decreased. Similar results to the 365 nm UV light irradiation were observed by sunlight. These results suggest that N-nitrosoproline may induce nitrosation and nitration of cellular components in humans with sunlight.
The cells having unrepaired DNA damage after ultraviolet (UV) exposure must go to apoptotic cell death to avoid mutation and transformation leading to cancer, whereas they must be protected against excess apoptotic cell death. The phosphatidylinositol 3-kinase (PI3-kinase)/Akt is a well-known survival pathway which suppresses apoptosis. The p53 tumor suppressor is a universal sensor of genotoxic stress that also regulates apoptosis. Until now, there are many reports of p53 expression after UV irradiation; however, the detailed time-course study has not been performed, especially the relationship with PI3-kinase/Akt pathway. In this study, PI3-kinase/Akt pathway-mediated time-dependent expressions of p53 and its related molecules after UVB irradiation were examined involving induction of apoptosis. Inhibition of PI3-kinase/Akt pathway by wortmannin and siRNA for Akt1 augmented apoptosis induced by UVB irradiation. p53 was time-dependently phosphorylated and stabilized after UVB irradiation, consistent with the expression of p21. Inhibition of PI3-kinase/Akt pathway clearly suppressed the expressions of p53 and p21. On the other hand, the expression levels of p53 in the presence of proteasome inhibitor were same, whether PI3-kinase/Akt pathway was inhibited or not, indicating that the activation of PI3-kinase/Akt pathway after UVB exposure suppressed proteasome-dependent degradation of p53. These results suggested that PI3-kinase/Akt pathway has important roles to mediate p53 expression and induction of apoptosis after UVB irradiation although the p53 revealed no positive correlation with the induction of apoptosis.
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