https://ntp.niehs.nih.gov/go/tr585abs

Abstract for TR-585

Toxicology Studies of Green Tea Extract in F344/NTac Rats and B6C3F1/N Mice and Toxicology and Carcinogenesis Studies of Green Tea Extract in Wistar Han [Crl:WI(Han)] Rats and B6C3F1/N Mice (Gavage Studies)

CASRN: GREENTEAEXTR
Synonyms/Common Names: Green tea catechin polyphenols; green tea; green tea polyphenols; camellia sinensis
Report Date: April 2016

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Abstract

Dried concentrated extracts from Camellia sinensis contain high amounts of catechins and are a popular source for green tea extract nutraceutical supplements and medicinal uses. Supplements containing green tea extract are commonly consumed for weight loss and green tea extracts are popular ingredients in sunblocks, cream rinses, and other cosmetics. Numerous studies in both experimental animals and clinical settings have examined the possible anticancer, anti-inflammatory, antimicrobial, and cardio- and neuroprotective properties of green tea extract. The presumed active ingredient of green tea extract, epigallocatechin gallate (EGCG), was originally nominated by the National Cancer Institute for toxicity and carcinogenicity studies because it is the most abundant catechin in green tea extract, it was being investigated as a potential chemotherapeutic agent, and there was a lack of adequate information with regard to its toxicity. However, the NTP selected green tea extract [containing EGCG (48.4% by weight) and other green tea catechins] for study because human exposure is to green tea extract products that contain concentrated mixtures of various green tea catechins. The NTP analyzed four lots of green tea extract and selected a source based on quantities of EGCG, consistency with other products on the market, and availability in bulk quantity. Oral gavage was chosen as the route of administration because it was considered most relevant to human exposure. Male and female F344/NTac rats and B6C3F1/N mice were administered green tea extract in water by gavage for 3 months and male and female Wistar Han [Crl:WI(Han)] rats (referred to as Wistar Han rats) and B6C3F1/N mice were administered green tea extract in water by gavage for 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, Escherichia coli, and mouse peripheral blood erythrocytes.

Three-month study in F344/NTac rats

Groups of 10 male and 10 female core study rats were administered 0, 62.5, 125, 250, 500, or 1,000 mg green tea extract/kg body weight in deionized water by gavage, 5 days per week for 14 weeks. Groups of 10 male and 10 female clinical pathology study rats were administered the same doses for 23 days. One 125 mg/kg female died during week 7. Mean body weights of males and females administered 250 mg/kg or greater were significantly less than those of the vehicle controls.

The cauda epididymis, epididymis, and testes weights of 1,000 mg/kg males were significantly less than those of the vehicle controls. Females administered 1,000 mg/kg had longer estrous cycles and spent significantly more time in extended diestrus than did the vehicle controls. These data indicate that green tea extract exhibited the potential to be a reproductive toxicant in male and female F344/NTac rats.

Several nonneoplastic liver lesions were observed in three of ten 1,000 mg/kg females. Lesions included hepatocyte necrosis, bile duct hyperplasia, oval cell hyperplasia, and mitosis. There were significant increases in the incidences of several nonneoplastic lesions in the nose of 1,000 mg/kg males and females including inflammation (females); hyperplasia in the Bowman’s gland of the olfactory epithelium; nerve atrophy; and atrophy, metaplasia, and pigmentation in the olfactory epithelium; the increased incidences of inflammation (females), nerve atrophy, and olfactory epithelium metaplasia and pigmentation (males) were also significant in the 500 mg/kg groups. The incidences of histiocyte cellular infiltration in the mesenteric lymph node in 125 mg/kg or greater males were significantly increased compared to that in the vehicle control group.

Three-month study in mice

Groups of 10 male and 10 female mice were administered 0, 62.5, 125, 250, 500, or 1,000 mg green tea extract/kg body weight in deionized water by gavage, 5 days per week for 14 weeks. Six males and four females administered 1,000 mg/kg died before the end of the study; early deaths were due to liver necrosis. Mean body weights of males administered 250 mg/kg or greater and females administered 125 mg/kg or greater were significantly less than those of the vehicle controls. Clinical findings included lethargy, abnormal breathing, and ataxia in females that died early.

A significantly decreased spermatid per testis count was observed in 500 mg/kg males. Females administered 500 mg/kg spent significantly more time in extended diestrus than did the vehicle controls. These data indicate that green tea extract exhibited the potential to be a reproductive toxicant in male and female mice.

In the liver, the incidences of glycogen depletion were significantly increased in 250 and 500 mg/kg males and 500 and 1,000 mg/kg females. In addition, the incidences of centrilobular necrosis were significantly increased in 1,000 mg/kg males and females, and the incidence of karyomegaly was significantly increased in 1,000 mg/kg females. The incidences of nerve atrophy, olfactory epithelium atrophy, and olfactory epithelium metaplasia of the nose were significantly increased in males administered 250 mg/kg or greater and in 500 and 1,000 mg/kg females; the incidence of olfactory epithelium necrosis was significantly increased in 1,000 mg/kg females. The incidences of lymphoid atrophy in the spleen were significantly increased in 500 and 1,000 mg/kg females. The incidences of atrophy of the mandibular lymph node and thymus were significantly increased in 1,000 mg/kg males and females.

Two-year study in Wistar Han rats

Groups of 60 male and 60 female rats were administered 0 or 1,000 mg green tea extract/kg body weight and groups of 50 male and 50 female rats were administered 100 or 300 mg/kg in deionized water by gavage, 5 days per week for up to 105 weeks. Ten male and 10 female rats randomly selected from the vehicle control and 1,000 mg/kg groups were evaluated at 3 months; no significant increases in mortality or nonneoplastic lesion incidences were observed at 3 months. In the 2-year study, there were significant decreases in survival in 1,000 mg/kg males and females compared to the vehicle control groups. Mean body weights of 300 and 1,000 mg/kg males were at least 10% less than those of the vehicle control groups after weeks 41 and 9 of the study, respectively; mean body weights of dosed groups of female rats were at least 10% less after weeks 65 (100 mg/kg), 61 (300 mg/kg), and 57 (1,000 mg/kg).

No increases in the incidences of neoplasms in male or female rats were attributed to the administration of green tea extract.

At 2 years, the incidences of hepatic necrosis were significantly increased in 1,000 mg/kg males and females, and the incidence of oval cell hyperplasia was significantly increased in 1,000 mg/kg females.

In the glandular stomach of 1,000 mg/kg males and 300 and 1,000 mg/kg females at 2 years, the incidences of mucosa necrosis were significantly greater than the vehicle control incidences. At 2 years, the incidences of mucosa necrosis in all segments of the small intestine were significantly increased in 1,000 mg/kg males and females.

At 3 months, the incidences of nerve and olfactory epithelium atrophy in the nose in 1,000 mg/kg males and the incidence of pigmentation in the olfactory epithelium of 1,000 mg/kg females were significantly increased. At 2 years, the incidences of numerous nonneoplastic lesions of the nose were generally significantly increased in all dosed groups of males and females. These lesions included mineralization and pigmentation of the lamina propria; suppurative inflammation of the nasopharyngeal duct; nerve atrophy; atrophy, respiratory metaplasia, and pigmentation of the olfactory epithelium; respiratory epithelium atrophy; and deformity and hyperostosis of the turbinate. The incidences of suppurative inflammation were significantly increased in 1,000 mg/kg males and in 300 and 1,000 mg/kg females, and the incidences of basal cell hyperplasia of the olfactory epithelium were significantly increased in males and females administered 300 or 1,000 mg/kg. Incidences of additional nonneoplastic nasal lesions were significantly increased in one or more dosed groups of males and/or females.

The incidences of suppurative inflammation in the lung and inflammation of the heart (epicardium) were significantly increased in 1,000 mg/kg males and females at 2 years.

The incidences of bone marrow hyperplasia in all dosed groups of females were significantly greater than the vehicle control incidence.

The incidences of lymphoid depletion were significantly increased in the spleen of 1,000 mg/kg males and all dosed groups of females.

Two-year study in mice

Groups of 50 male and 50 female mice were administered 0, 30, 100, or 300 mg green tea extract/kg body weight in deionized water by gavage, 5 days per week for 105 weeks. Survival of dosed groups was similar to that of the vehicle control groups. Mean body weights of 100 and 300 mg/kg males were at least 10% less than those of the vehicle control group after weeks 89 and 65, respectively, and mean body weights of 100 and 300 mg/kg females were at least 10% less after weeks 25 and 17, respectively.

The incidences of hematopoietic cell proliferation and inflammation in the liver were significantly increased in 300 mg/kg males. The incidences of numerous nonneoplastic lesions of the nose were generally significantly increased in all dosed groups of males and females. These lesions included foreign body, suppurative inflammation, nerve atrophy, atrophy and respiratory metaplasia of the olfactory epithelium, and squamous metaplasia and necrosis of the respiratory epithelium. The incidences of hyperostosis, olfactory epithelium fibrosis, septum perforation, and turbinate atrophy were significantly increased in 100 and 300 mg/kg males and females, and the incidences of respiratory epithelium hyperplasia were significantly increased in 30 and 300 mg/kg males and 100 and 300 mg/kg females. The incidence of nasopharyngeal duct degeneration was significantly increased in 300 mg/kg males.

The incidences of lymphoid hyperplasia and plasma cell infiltration of the mandibular lymph node were significantly increased in 100 and 300 mg/kg males and females.

The incidences of bone marrow hyperplasia were significantly increased in all dosed groups except 30 mg/kg females.

Genetic toxicology

Green tea extract was mutagenic in S. typhimurium strains TA98 and TA100 in the presence of induced rat liver S9; no mutagenicity was observed in these strains without S9 or in the E. coli strain WP2 uvrA/pKM101, with or without S9. In vivo, no increases in the frequencies of micronucleated erythrocytes were seen in peripheral blood of male or female B6C3F1/N mice in the 3-month study.

Conclusions

Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity (see a summary of the Peer Review Panel comments and the public discussion on this Technical Report in Appendix L) of green tea extract in male or female Wistar Han rats administered 100, 300, or 1,000 mg/kg. There was no evidence of carcinogenic activity of green tea extract in male or female B6C3F1/N mice administered 30, 100, or 300 mg/kg.

Administration of green tea extract resulted in increased incidences of nonneoplastic lesions of the liver, glandular stomach, small intestine (duodenum, ileum, and jejunum), nose, lung, heart, and spleen in male and female rats; bone marrow of female rats; the nose, mandibular lymph node, and bone marrow of male and female mice; and the liver of male mice.

National Toxicology Program (NTP). 2016. NTP technical report on the toxicology studies of green tea extract in F344/NTac rats and B6C3F1/N mice and toxicology and carcinogenesis studies of green tea extract in Wistar Han [Crl:WI(Han)] rats and B6C3F1/N mice (gavage studies). Research Triangle Park, NC: National Toxicology Program. Technical Report 585. https://doi.org/10.22427/NTP-TR-585

Studies

Summary of the Two-year Carcinogenesis and Genetic Toxicology Studies of Green Tea Extract
  Male
Wistar Han Rats
Female
Wistar Han Rats
Male
B6C3F1/N Mice
Female
B6C3F1/N Mice
Doses in water by gavage 0, 100, 300, or 1,000 mg/kg 0, 100, 300, or 1,000 mg/kg 0, 30, 100, or 300 mg/kg 0, 30, 100, or 300 mg/kg
Survival rates 35/50, 37/50, 43/50, 24/50 26/50, 28/50, 23/50, 4/50 33/50, 36/50, 33/50, 37/50 34/50, 33/50, 44/50, 39/50
Body weights 300 and 1,000 mg/kg groups at least 10% less than vehicle control group after weeks 41 and 9, respectively 100, 300, and 1,000 mg/kg groups at least 10% less than vehicle control group after weeks 65, 61, and 57, respectively 100 and 300 mg/kg groups at least 10% less than vehicle control group after weeks 89 and 65, respectively 100 and 300 mg/kg groups at least 10% less than vehicle control group after weeks 25 and 17, respectively
Nonneoplastic effects Liver: necrosis (1/50, 2/50, 2/50, 13/50)

Stomach, glandular: mucosa necrosis (0/49, 3/50, 3/50, 21/50)

Small intestine, duodenum: mucosa, necrosis (0/50, 1/47, 1/49, 10/48)

Small intestine, ileum: mucosa necrosis (0/50, 1/48, 2/49, 6/45)

Small intestine, jejunum: mucosa necrosis (0/49, 0/47, 2/48, 9/46)

Small intestine, (duodenum, ileum, jejunum): Necrosis (0/49, 2/46, 4/48, 14/45)

Nose: suppurative inflammation (11/50, 12/50, 20/50, 42/50); lamina propria, mineralization (0/50, 33/50, 34/50, 44/50); lamina propria, pigmentation (0/50, 4/50, 11/50, 25/50); nasopharyngeal duct, suppurative inflammation (0/50, 6/50, 8/50, 20/50); nerve, atrophy (0/50, 33/50, 44/50, 44/50); olfactory epithelium, atrophy (1/50, 38/50, 41/50, 41/50); olfactory epithelium, hyperplasia, basal cell (0/50, 1/50, 9/50, 28/50); olfactory epithelium, metaplasia, respiratory (4/50, 40/50, 43/50, 47/50); olfactory epithelium, necrosis (1/50, 3/50, 0/50, 12/50); olfactory epithelium, pigmentation (6/50, 18/50, 12/50, 21/50); respiratory epithelium, atrophy (0/50, 2/50, 5/50, 6/50) respiratory epithelium, metaplasia, squamous (0/50, 1/50, 3/50, 7/50); turbinate, deformity (0/50, 16/50, 22/50, 35/50); turbinate, hyperostosis (0/50, 18/50, 27/50, 40/50)

Lung: suppurative inflammation (0/50, 1/50, 3/50, 10/50)

Heart (epicardium)
: inflammation (0/50, 0/50, 1/50, 5/50)

Spleen: lymphoid depletion (1/50, 2/50, 1/50, 13/50)
Liver: necrosis (3/50, 2/48, 5/49, 24/46); oval cell hyperplasia (1/50, 2/48, 3/49, 16/46)

Stomach, glandular
: mucosa necrosis (0/50, 1/49, 7/49, 20/44)

Small intestine, duodenum
: mucosa, necrosis (0/47, 0/48, 1/48, 5/39)

Small intestine, ileum
: mucosa necrosis (0/45, 0/46, 0/47, 5/36)

Small intestine, jejunum
: mucosa necrosis (0/45, 0/43, 1/45, 6/40)

Small intestine, (duodenum, ileum, jejunum)
: Necrosis (0/44, 0/42, 2/44, 10/33)

Nose
: foreign body (3/49, 2/49, 4/50, 8/49); suppurative inflammation (5/49, 3/49, 17/50, 35/49); epithelium, nasopharyngeal duct, necrosis (0/49, 1/49, 2/50, 7/49); epithelium, nasopharyngeal duct, regeneration (0/49, 0/49, 0/50, 8/49); lamina propria, mineralization (3/49, 23/49, 30/50, 22/49); lamina propria, pigmentation (1/49, 0/49, 6/50, 14/49); nasopharyngeal duct, suppurative inflammation (0/49, 2/49, 5/50, 15/49); nerve, atrophy (0/49, 38/49, 41/50, 38/49); olfactory epithelium, atrophy (2/49, 35/49, 42/50, 34/49); olfactory epithelium, hyperplasia, basal cell (0/49, 0/49, 8/50, 20/49); olfactory epithelium, metaplasia, respiratory (1/49, 42/49, 43/50, 36/49); olfactory epithelium, necrosis (0/49, 3/49, 1/50, 18/49) olfactory epithelium, pigmentation (0/49, 11/49, 7/50, 5/49); respiratory epithelium, atrophy (0/49, 8/49, 9/50, 3/49); respiratory epithelium, necrosis (0/49, 1/49, 2/50, 17/49); respiratory epithelium, pigmentation (0/49, 1/49, 5/50, 5/49); turbinate, deformity (0/49, 6/49, 20/50, 15/49); turbinate, hyperostosis (0/49, 18/49, 32/50, 36/49)

Lung
: suppurative inflammation (1/50, 3/49, 2/50, 9/48)

Heart (epicardium)
: inflammation (0/50, 2/48, 2/50, 4/48)

Bone marrow: hyperplasia (6/50, 14/50, 16/50, 13/50)

Spleen: lymphoid depletion (0/50, 7/49, 5/48, 17/43)
 
Liver: hematopoietic cell proliferation (2/50, 2/50, 6/50, 10/50); inflammation (4/50, 1/50, 5/50, 12/50)

Nose: foreign body (1/50, 10/49, 16/50, 25/50); hyperostosis (0/50, 0/49, 28/50, 46/50); suppurative inflammation (14/50, 40/49, 49/50, 48/50); nasopharyngeal duct, degeneration (0/50, 0/49, 4/50, 9/50); nerve, atrophy (0/50, 26/49, 49/50, 50/50); olfactory epithelium, atrophy (4/50, 24/49, 28/50, 3/50); olfactory epithelium, fibrosis (0/50, 4/49, 37/50, 43/50); olfactory epithelium, metaplasia, respiratory (11/50, 45/49, 49/50, 49/50); respiratory epithelium, metaplasia, squamous (0/50, 14/49, 39/50, 46/50); respiratory epithelium, hyperplasia (5/50, 20/49, 10/50, 19/50); respiratory epithelium, necrosis (0/50, 7/49, 16/50, 27/50); septum, perforation (1/50, 0/49, 26/50, 37/50); turbínate, atrophy (0/50, 0/49, 41/50, 50/50)

Mandibular lymph node: lymphoid hyperplasia (0/50, 1/50, 31/50, 37/50); plasma cell infiltration (1/50, 1/50, 24/50, 41/50)

Bone marrow: hyperplasia (5/50, 42/50, 38/50, 46/50)
Nose: foreign body (4/48, 8/48, 13/50, 17/50); hyperostosis (0/48, 0/48, 21/50, 48/50); suppurative inflammation (4/48, 24/48, 44/50, 47/50); nerve, atrophy (0/48, 13/48, 47/50, 48/50); olfactory epithelium atrophy (0/48, 18/48, 26/50, 17/50); olfactory epithelium, fibrosis (0/48, 1/48, 39/50, 43/50); olfactory epithelium, metaplasia, respiratory (2/48, 36/48, 49/50, 48/50); respiratory epithelium, hyperplasia (1/48, 1/48, 22/50, 15/50); respiratory epithelium, metaplasia, squamous (0/48, 8/48, 42/50, 42/50); respiratory epithelium, necrosis (0/48, 4/48, 28/50, 32/50); septum, perforation (0/48, 0/48, 38/50, 42/50); turbinate, atrophy (0/48, 0/48, 40/50, 48/50)

Mandibular lymph node
: lymphoid hyperplasia (0/50, 1/48, 8/49, 12/48); plasma cell infiltration (0/50, 0/48, 31/49, 18/48)

Bone marrow
: hyperplasia (6/50, 11/50, 41/50, 34/50)
Neoplastic effects None None None None
Level of evidence of carcinogenic activity No evidence No evidence No evidence No evidence
Genetic Toxicology
Assay Results
Bacterial gene mutations:
 
Positive in S. typhimurium strains TA98 and TA100 with S9, negative in TA98 and TA100 without S9, and negative in E. coli with or without S9
Micronucleated erythrocytes
Mouse peripheral blood in vivo:
Negative