Tea has long been known for its health benefits, and recent studies have shed light on its inhibitory effects on mutagenicity and genotoxicity. Mutagenicity refers to the ability of a substance to cause changes in the genetic material of an organism, while genotoxicity refers to the ability to cause damage to DNA.
Several studies have reported that components of green and black tea can be mutagenic to bacteria. However, the mutagenicity of tea is strongly inhibited by catalase, indicating that hydrogen peroxide produced in tea solution plays an essential role in its mutagenicity. On the other hand, there is increasing evidence to show the antimutagenic and antigenotoxic activities of tea and its ingredients in bacteria and mammalian cells.
In a study conducted by Jain et al. in 1989, tea extract and catechins such as EC, EGCG, and EGC were found to decrease the mutagenic effect of N-methyl-N’-nitro-Nnitrosoganidine (MNNG) in the stomachs of rats using E.coli WP2 and S.typhimurium TA100. Similarly, water extracts of green tea and their major polyphenol fraction, including EGCG, EGC, ECG, and EC, were investigated for antimutagenicity. The water extracts of green tea showed a strong inhibitory effect on the backward mutation induced by aflatoxin B1 (AFB1) and benzo (a)pyrene (Bap) in S.typhimurium TA100 and TA98.
The green tea epicatechin compounds (GTEC) also showed inhibitory effects on genotoxicity. In a study conducted by Cheng et al. in 1986, GTEC decreased the frequency of sister chromatid exchanges (SCE) and chromosomal aberrations in V79 cells treated with AFB1. In a 6-thioguanine-resistant mutation assay, it was observed that GTEC significantly inhibited gene forward mutation in a dose-dependent manner in V97 cells treated with AFB1 or Bap.
Fried fish extract (FFE) and its related compound 2-amino-3,4-dimethylimidazo(4,5-f)quinoline (MeIQ) showed potent genotoxicity to bacteria and mammalian cells. However, GTEC strongly inhibited the increase of SCE and micronuclei induced by FFE or MeIQ in V79 or IAR20 cells, and MeIQ-induced backward mutation in S.typhimurium. An inhibitory effect of GTEC on unscheduled DNA synthesis induced by MeIQ or FFE was also found in primary rat hepatocytes.
In an in vivo experiment, green tea water extract or GTEC inhibited micronuclei induced by 1,2-dimethylhydrazine (DMH) in the colon crypt cells of mice. Ito et al. reported in 1989 that rats given the hot water extract from green tea 24 hours before they were injected with AFB1 displayed considerably suppressed AFB1-induced chromosomal aberrations in their bone marrow cells.
In conclusion, tea and its ingredients have been shown to exhibit inhibitory effects on mutagenicity and genotoxicity in various studies. These findings highlight the potential benefits of tea in preventing DNA damage and mutations, which can lead to serious health problems such as cancer. Further research is needed to fully understand the mechanisms behind the inhibitory effects of tea and its ingredients on mutagenicity and genotoxicity. Nonetheless, these studies provide promising evidence for the potential use of tea in cancer prevention and treatment.