Sarunashi Tea Reduced Colon Lesions and Mutagenicity in Mice

A tea brewed from the leaves and twigs of Actinidia arguta, a hardy kiwi relative known in Japan as sarunashi, has shown antimutagenic activity in laboratory tests and reduced the formation of early precancerous lesions in the colons of mice, according to a brief report published in the journal Genes and Environment.

The researchers had previously demonstrated that the juice of A. arguta fruit exhibited antimutagenic activity in the Ames test, a widely used bacterial assay that measures the ability of a substance to reverse mutations in strains of Salmonella typhimurium. They had also observed anticarcinogenic effects of the juice in mouse models of lung and skin tumorigenesis. Because traditional Japanese medicine makes use of decoctions prepared from the leaves, bark and other parts of plants, the team hypothesized that a tea made from sarunashi leaves and twigs might carry similar protective properties.

To prepare the tea, leaves and twigs harvested in June from Shin-jo village in Okayama Prefecture were processed, with the material consisting of 85 percent leaves and 15 percent twigs, at a commercial facility in Niimi City. Two grams of the dried tea material were steeped in 200 milliliters of hot water at 98 degrees Celsius for two minutes, and the resulting infusion was filtered and stored frozen until use.

In the Ames test, the team examined whether sarunashi-tea could suppress the mutagenicity of six distinct compounds: aflatoxin B1, benzo(a)pyrene, 7,12-dimethylbenz(a)anthracene, and three heterocyclic amines known as MeIQx, Trp-P-2 and PhIP. The assays were performed with bacterial strain TA100 for aflatoxin B1, benzo(a)pyrene and DMBA, and with strain TA98 for the heterocyclic amines, in both cases in the presence of a rat liver homogenate fraction for metabolic activation.

The results showed that the mutagenicity of aflatoxin B1 and benzo(a)pyrene, detected with TA100, and that of MeIQx, Trp-P-2 and PhIP, detected with TA98, was significantly reduced in the presence of sarunashi-tea. The amount of tea needed to achieve 50 percent inhibition, a standard benchmark the researchers call the ID50 value, was approximately 100 microliters per plate for benzo(a)pyrene, 25 microliters per plate for MeIQx and 50 microliters per plate for Trp-P-2. For aflatoxin B1 and PhIP, mutagenicity did not fall to 50 percent or below even at the highest tea concentrations tested. Importantly, the tea itself showed no mutagenic activity against either bacterial strain, and microscopic examination confirmed that the bacterial background lawn was intact, ruling out cytotoxicity as an explanation for the reduced colony counts.

Comparing the new results with the team’s earlier data on sarunashi-juice revealed a consistent pattern. The ID50 values for the tea toward benzo(a)pyrene, MeIQx and Trp-P-2 were 2.9, 2.5 and 6.3 times higher, respectively, than the corresponding values for the juice. The researchers interpret this to mean that similar antimutagenic components are likely present in both preparations, but at concentrations roughly 2.5 to 6.3 times lower in the tea than in the juice. In their previous work, the juice required approximately 15, 35, 20, 10, 8.0 and 8.0 microliters per plate to reach the 50 percent inhibition threshold against aflatoxin B1, benzo(a)pyrene, DMBA, MeIQx, Trp-P-2 and PhIP, respectively.

The second arm of the study tested whether drinking sarunashi-tea could prevent the formation of aberrant crypt foci, microscopic lesions in the colon that are considered the earliest identifiable neoplastic changes in rodent models of colon carcinogenesis and are widely used as preneoplastic biomarkers. Forty-eight male CD1 mice, four weeks old at purchase, were divided into four groups. Two groups received weekly subcutaneous injections of 1,2-dimethylhydrazine, a colon-specific carcinogen, at 20 milligrams per kilogram of body weight for two weeks, while the other two groups received phosphate buffered saline instead. One week after the second injection, one carcinogen-treated group and one control group had their drinking water replaced with sarunashi-tea for the remainder of the experiment, which lasted 20 weeks from the start.

All 48 mice survived to the end of the experiment, and none developed colon tumors. Body weights at the end of the study showed no significant differences among the four groups. When the colons were examined under a light microscope after staining with methylene blue, the total number of aberrant crypt foci in the tea-drinking, carcinogen-treated group was significantly reduced to 60.5 percent of the number observed in the carcinogen-treated group that drank plain water. The number of foci containing one to three crypts was also significantly decreased, to 64.1 percent of the control value. No aberrant crypt foci were observed in either of the two groups that had not received the carcinogen.

The findings place sarunashi alongside other plant-derived compounds that have shown chemopreventive potential in colon carcinogenesis models. The authors note that crude alpha-mangostin, a xanthone derivative from mangosteen pericarp, significantly inhibited the induction of aberrant crypt foci in rats treated with 1,2-dimethylhydrazine, and that treatment with a COX-2 inhibitor also significantly reduced the appearance of these lesions. Non-steroidal anti-inflammatory drugs, which inhibit COX enzymes and modulate cell proliferation, have been reported to reduce the risk of colorectal cancer in humans. Colorectal cancer is the second most common fatal malignancy in Japan, giving the research a clear public health context.

As for the active ingredients, the researchers point to polyphenolic components as likely candidates. In earlier work, the major polyphenolic component of sarunashi-juice was identified as isoquercetin, a flavonoid glycoside, and isoquercetin was previously shown to reduce NNK-induced lung tumorigenesis in mice and to decrease phosphorylation of the Akt signaling protein in cultured A549 lung cells. The authors suggest that isoquercetin present in sarunashi-tea might contribute to both the antimutagenic effects observed in the Ames test and the inhibitory effects on aberrant crypt foci formation. They also note that antimutagenic activity does not appear to be distributed throughout the genus Actinidia, since an extract of matatabi, Actinidia polygama, a close relative of sarunashi, did not show antimutagenicity against Trp-P-2 or benzo(a)pyrene in earlier research, suggesting the protective components may be specific to A. arguta. The team emphasizes that further investigation is needed to determine the mechanisms behind the antimutagenicity and the suppression of aberrant crypt foci, and to identify the active components in the tea. As a brief report based on animal and bacterial models, the study does not establish effects in humans, but it adds sarunashi-tea to the growing list of plant-derived infusions under evaluation for chemopreventive properties.

Subject of Research: Antimutagenic and chemopreventive effects of tea prepared from Actinidia arguta leaves and twigs in bacterial and mouse models

Article Title: Antimutagenic effects of a tea made from Actinidia arguta, sarunashi in Japanese, and its inhibitory effects on the formation of aberrant crypt foci induced by 1,2-dimethylhydrazine in mice

Article References: Saiki, Y., Miyake, N., & Arimoto-Kobayashi, S. (2025). Antimutagenic effects of a tea made from Actinidia arguta, sarunashi in Japanese, and its inhibitory effects on the formation of aberrant crypt foci induced by 1,2-dimethylhydrazine in mice. Genes and Environment, 47(1), Article 25. https://doi.org/10.1186/s41021-025-00348-6

Image Credits: AI Generated

DOI: 10.1186/s41021-025-00348-6

Keywords: Actinidia arguta, sarunashi, antimutagenicity, Ames test, aberrant crypt foci, 1,2-dimethylhydrazine, colon carcinogenesis, chemoprevention, isoquercetin, polyphenols, mice, heterocyclic amines