The influence of caffeine on tunour indicidence in Sprague-Dawley rats

Möhr, U.; Althoff, J.; Ketkar, M.B.; Conradt, Peter; Morgareidge, Kenneth

doi:10.1016/0278-6915(84)90367-3

Cited by 25 publications

(13 citation statements)

References 9 publications

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“…In the present study, it was clearly shown that caffeine intake interacts with ID but neither SDM nor PB to promote thyroid carcinogenesis. In previous studies, administration of 0.2% caffeine for 2 years in Sprague-Dawley rats (Mohr et al, 1984) and for 78 weeks in Wistar rats (Takayama and Kuwabara, 1982) failed to induce neoplasia when given continuously in their drinking water. It was also suggested that coffee consumption plays a protective role against development of benign or malignant thyroid neoplasms (Linos et al, 1989).…”

Section: Histopathologymentioning

confidence: 92%

Specificity of Co-Promoting Effects of Caffeine on Thyroid Carcinogenesis in Rats Pretreated with N-Bis(2-hydroxypropyl)nitrosamine

et al. 2004

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The specificity of copromotion effects of caffeine with known goitrogenic factors on thyroid carcinogenesis was examined in rats pretreated with Nbis(2-hydroxypropyl)nitrosamine (DHPN). Male F344 rats were divided into 8 groups, each consisting of 10 animals, and received a single sc injection of 2,800 mg/kg DHPN. From one week after the DHPN initiation, they were given basal diet, iodine deficiency (ID) diet, 500 ppm phenobarbital (PB) solution or 1,000 ppm sulfadimethoxine (SDM) solution with or without 1,500 ppm caffeine feeding for 12 weeks. The caffeine, PB, SDM, and ID treatments significantly ( p < 0.05 or 0.01) increased the relative thyroid weights, and the increases with PB or ID were further ( p < 0.05 or 0.01) enhanced in combination with caffeine. SDM drastically promoted thyroid carcinogenesis in association with increased serum TSH levels regardless of the caffeine treatment. Thyroid follicular carcinomas and adenomas were more frequently observed in the additional caffeine groups than in the ID alone groups. The incidence and multiplicity of focal thyroid follicular hyperplasias in the ID-treated groups were significantly ( p < 0.05 and 0.01) elevated in the case of combination with caffeine. Increases in serum TSH levels with PB or ID were also further enhanced in combination with caffeine. Serum thyroid hormone levels were significantly ( p < 0.01) decreased by SDM but significantly ( p < 0.05 or 0.01) increased by caffeine, PB or ID. Our results clearly indicate that dietary caffeine at a high dose of 1,500 ppm interacts with ID, but neither SDM nor PB, to promote rat thyroid carcinogenesis although the combined caffeine + PB treatment somewhat affected thyroid weights as well as thyroid hormone levels.

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Section: Histopathologymentioning

confidence: 92%

Specificity of Co-Promoting Effects of Caffeine on Thyroid Carcinogenesis in Rats Pretreated with N-Bis(2-hydroxypropyl)nitrosamine

et al. 2004

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“…As it was previously reported that caffeine did not influence the incidence of spontaneously occurring mammary tumors in rodents, 31,32) it presumably exerts its effects via an impact on PhIP metabolism. In fact, caffeine at the higher doses in the present experiment clearly inhibited the metabolic activation of PhIP into proximal or ultimate carcinogenic species in vitro, as also observed for the novel lipophilic phenolic antioxidant HTHQ, 29) which similarly inhibits PhIP-induced mammary tumor development.…”

Section: Discussionmentioning

confidence: 70%

“…34) To our knowledge, however, no toxicological or morphological effects on the colon have so far been found in other experimental animals exposed to caffeine. 19,31,32) Furthermore, coffee consumption appears to have a protective influence against colon and rectal cancer in man, with reduction in bile acid and neutral sterol concentration in the bowel due to interference with bile secretion proposed as a possible underlying mechanism. 35) As PhIP and caffeine intakes (11.9 and 86.9 mg/ kg/day, respectively) in the present study were extremely high when compared to estimated actual PhIP (mean 72, range 0-865 ng/day) 36) and caffeine (3-5 mg/kg/day) 19) ingestion levels, risk to humans might be negligible.…”

Section: Discussionmentioning

confidence: 99%

Organ‐dependent Modifying Effects of Caffeine, and Two Naturally Occurring Antioxidants α‐Tocopherol and n‐Tritriacontane‐16,18‐dione, on 2‐Amino‐1‐methyl‐6‐phenylimidazo [4,5‐b] pyridine (PhIP)‐induced Mammary and Colonic Carcinogenesis in Female F344 Rats

Hagiwara¹,

Boonyaphiphat

Tanaka³

et al. 1999

Japanese Journal of Cancer Research

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or TTAD groups tended to be decreased while their multiplicities were significantly lowered. With regard to colon tumor development, on the other hand, rats given PhIP plus caffeine exhibited an elevated incidence (75% versus 15% in the control), whereas α α α α-tocopherol and TTAD had no effect. Surprisingly, metabolic activation of PhIP was inhibited by addition of caffeine in an in vitro assay. The results indicate that caffeine exerts a potent chemopreventive action against PhIPinduced mammary carcinogenesis, but acts as a co-carcinogen for PhIP-induced colonic carcinogenesis.

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“…Caffeine is reported to exhibit a clastogenic potential in almost all of the mammalian cell lines, although it is non-carcinogen (Ishidate et al, 1988;Mohr et al, 1984;Takayama and Kuwabara, 1982). The result of MLA using the agar plate method is also positive (Clive et al, 1990).…”

Section: Discussionmentioning

confidence: 99%

Multi-endpoint genotoxic assay using L5178Y (Tk+/- -3.7.2c) cells

et al. 2009

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-When the mouse lymphoma Tk assay (MLA) provides a positive result, its cause can be roughly estimated by examining colony sizes. An increase in the number of large colonies means that the compound tested has point mutational potential, while an increase in small colonies indicates the poten--ly increased the thymidine kinase (Tk) mutation frequencies derived from large colonies as well as those from small colonies in the standard protocol, although the frequencies derived from a small colony were higher than those from large colonies at higher doses. Therefore, we prolonged the expression period from 2 days, a standard period, to 6 days after treatment and then examined the Tk and Hprt mutations simultaneously. The result showed that caffeine gave a completely negative result on a mutation test for both Tk and Hprt. On the other hand, ethyl methanesulfonate (EMS), a genotoxic carcinogen, showed a positive cells. In conclusion, when MLA gives a positive result and the cause is ambiguous, in order to identify the of Tk and Hprt gene mutation simultaneously after 6-day expression and to perform an in vitro micronucleus assay during the expression period.

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The influence of caffeine on tunour indicidence in Sprague-Dawley rats

Cited by 25 publications

References 9 publications

Specificity of Co-Promoting Effects of Caffeine on Thyroid Carcinogenesis in Rats Pretreated with N-Bis(2-hydroxypropyl)nitrosamine

Specificity of Co-Promoting Effects of Caffeine on Thyroid Carcinogenesis in Rats Pretreated with N-Bis(2-hydroxypropyl)nitrosamine

Organ‐dependent Modifying Effects of Caffeine, and Two Naturally Occurring Antioxidants α‐Tocopherol and n‐Tritriacontane‐16,18‐dione, on 2‐Amino‐1‐methyl‐6‐phenylimidazo [4,5‐b] pyridine (PhIP)‐induced Mammary and Colonic Carcinogenesis in Female F344 Rats

Multi-endpoint genotoxic assay using L5178Y (Tk+/- -3.7.2c) cells

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