Stimulation by caffeine of spontaneous mammary tumorigenesis in mice

Nagasawa, Hiroshi; Konishi, Reiko

doi:10.1016/0277-5379(88)90322-7

Cited by 10 publications

(8 citation statements)

References 8 publications

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“…Previous reports also indicated that caffeine enhances the formation of pancreatic tumors (Nishikawa et al, 1992) and mammary gland tumors (Welsch and Aylsworth, 1983;Nagasawa and Konishi, 1988). Inspite of the several studies that have been reported on different extracts of kolanut, there has not been any extensive analysis and characterization of the active compounds in the seed.…”

Section: Introductionmentioning

confidence: 99%

Gas chromatography mass spectrometry (GC-MS) analysis of ethanolic extracts of kolanut (Cola nitida) (vent) and its toxicity studies in rats

Omoaghe¹,

Isehunwa²

2015

J. Med. Plants Res.

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In this study, gas chromatography-mass spectrometry (GC/MS) was used to analyse the isolated caffeine from kolanut and deternine the acute and chronic toxicity of the extract and the isolated caffeine. In chronic toxicity test, rats were divided into five groups (10 rats per group). Each rat was administered with normal saline (control group), crude kolanut extract (11.9 mg/kg), isolated caffeine (7.5 mg/kg), synthetic caffeine (6 mg/kg) or (6 mg/kg) decaffeinated kolanut extract orally for 90 days. Biochemical assessment and body weight of the rats were determined. In acute test, the limit test dose of 2000 mg/kg was administered to the rat and observed for 48 h post treatment. This dose caused behavioural changes but did not cause mortality in the rats tested. The results of the chronic administration showed that caffeine significantly (P < 0.05) decreased body weight. Liver enzymes were significantly (P < 0.05) increase, total plasma protein levels, creatinine, bilirubin, very low density lipoprotein (VLDL), low density lipoprotein (LDL) and total serum cholesterol levels were also significantly (P < 0.05) higher. However, urea was significantly (P < 0.05) lower in the caffeine treated groups. The results of the GC-MS analysis showed that the isolated caffeine from kolanut extract contains 82.69% pure caffeine with 96% in quality. Our results showed that the kolanut extract is rich in high quality caffeine and chronic consumption of it is associated with significant toxic effects as shown by elevated biochemical parameters, and reduction in body weight.

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Section: Introductionmentioning

confidence: 99%

Gas chromatography mass spectrometry (GC-MS) analysis of ethanolic extracts of kolanut (Cola nitida) (vent) and its toxicity studies in rats

Omoaghe¹,

Isehunwa²

2015

J. Med. Plants Res.

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“…The stimulatory effect of tea, caffeine, or EGCG on apoptosis in tumors of tumor-bearing mice suggests that enhanced apoptosis may be a unifying mechanism by which tea, caffeine, or EGCG inhibit carcinogenesis and tumor growth. Although administration of caffeine inhibits carcinogenesis in several animal models (21)(22)(23)(24)(25)(26)(27)(28)(29), carcinogenesis is stimulated in some animal models (30)(31)(32)(33)(34). The reasons caffeine inhibits carcinogenesis in some animal models and enhances carcinogenesis in other models are not known.…”

Section: Treatment Of Skh-1 Hairless Mice With Uvb (30 Mj͞cmmentioning

confidence: 99%

Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis and selectively increase apoptosis in UVB-induced skin tumors in mice

Lü

Lou

Xie

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

275

216

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SKH-1 hairless mice were irradiated with ultraviolet B (UVB) twice weekly for 20 weeks. These tumor-free mice, which had a high risk of developing skin tumors during the next several months, were then treated topically with caffeine (6.2 mol) or (؊)-epigallocatechin gallate (EGCG; 6.5 mol) once a day 5 days a week for 18 weeks in the absence of further treatment with UVB. Topical applications of caffeine to these mice decreased the number of nonmalignant and malignant skin tumors per mouse by 44% and 72%, respectively. Topical applications of EGCG decreased the number of nonmalignant and malignant tumors per mouse by 55% and 66%, respectively. Immunohistochemical analysis showed that topical applications of caffeine or EGCG increased apoptosis as measured by the number of caspase 3-positive cells in nonmalignant skin tumors by 87% or 72%, respectively, and in squamous cell carcinomas by 92% or 56%, respectively, but there was no effect on apoptosis in nontumor areas of the epidermis. Topical applications of caffeine or EGCG had a small inhibitory effect on proliferation in nonmalignant tumors as measured by BrdUrd labeling (16 -22%), and there was also a similar, but nonsignificant, inhibitory effect on proliferation in malignant tumors. The results suggest a need for further studies to determine whether topical applications of caffeine or EGCG can inhibit sunlight-induced skin cancer in humans.tea constituents ͉ programmed cell death ͉ caspase 3 S kin cancer is a major cancer in the United States, and its incidence is expected to increase substantially because of increased recreational exposure to sunlight and depletion of the ozone layer (1, 2). The identification and use of protective agents should have an important impact on the formation of these cancers. Although the use of sunscreens is an approach that has decreased the risk of skin cancers (3, 4), there is also a need to identify additional approaches for skin cancer prevention in individuals previously exposed to high-dose levels of sunlight (high-risk individuals). Treatment of SKH-1 hairless mice with ultraviolet B (UVB) (30 mJ͞cm 2 ) twice a week for 20 weeks resulted in mice without tumors but with epidermal hyperplasia and a high risk of developing skin tumors during the next several months in the absence of further UVB treatment (initiated high-risk mice) (5). This animal model resembles humans who are heavily exposed to sunlight early in life and then have reduced exposure later in life. We have used UVB-pretreated high-risk mice for evaluating the effects of potential chemopreventive agents on skin tumor formation in the absence of further exposure to UVB. Oral administration of green tea, black tea, or caffeine to UVBpretreated high-risk mice inhibited tumorigenesis, but the decaffeinated teas had little or no activity, and reconstitution of the decaffeinated teas with caffeine restored biological activity (5). These observations indicate that caffeine is a major cancer chemopreventive constituent in tea. Potential antitumor mechanisms include...

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“…The total number of HAN were increased in the caffeine-treated groups compared with controls in each species, but was statistically significant in C3H mice only. The same authors (53) found that caffeine significantly (P < 0.01) stimulated spontaneous mammary tumorigenesis in both breeder and virgin C3H mice. The stimulation was found to be more marked in virgins than breeders.…”

Section: Caffeine and Mammary Gland Developmentmentioning

confidence: 81%

Caffeine and the Development of the Normal and Neoplastic Mammary Gland

Welsch

1994

Experimental Biology and Medicine

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There has been much interest in the role of dietary factors in the etiology and progression of breast disease. Due to its wide consumption and the many biochemical and physiological effects it exerts, caffeine has been extensively examined in both clinical and experimental animal studies. To date, clinical studies investigating a possible relationship between caffeine consumption and breast disease in humans have yielded inconsistent and inconclusive results. In experimental animal studies utilizing laboratory mice and rats, caffeine has been shown to stimulate mammary gland lobulo-alveolar development and secretion. The development of mammary gland tumors can be either stimulated or suppressed depending upon the animal species and strain, and the stage of tumorigenesis (initiation/promotion) at which caffeine is administered. Many laboratories have proposed that antagonism of the adenosine receptor is the most plausible mechanism to account for the many biological activities of caffeine. However, other mechanisms by which caffeine act cannot be discounted. The significant modifying role of caffeine on normal and neoplastic mammary gland development in experimental animals provides a biological foundation from which to implicate caffeine as a potential modulator of developmental growth of normal, benign, and carcinomatous human breast tissues.

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Stimulation by caffeine of spontaneous mammary tumorigenesis in mice

Cited by 10 publications

References 8 publications

Gas chromatography mass spectrometry (GC-MS) analysis of ethanolic extracts of kolanut (Cola nitida) (vent) and its toxicity studies in rats

Gas chromatography mass spectrometry (GC-MS) analysis of ethanolic extracts of kolanut (Cola nitida) (vent) and its toxicity studies in rats

Topical applications of caffeine or (−)-epigallocatechin gallate (EGCG) inhibit carcinogenesis and selectively increase apoptosis in UVB-induced skin tumors in mice

Caffeine and the Development of the Normal and Neoplastic Mammary Gland

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