On the promoting action of tamoxifen in a model of hepatocarcinogenesis induced by p-dimethylaminoazobenzene in CF1 mice

Caballero, Fabiana; Gerez, Esther Noemí; Oliveri, Leda; Falcoff, Nora; Batlle, Alcira; Vázquez, Elba S.

doi:10.1016/s1357-2725(01)00056-5

Cited by 18 publications

(17 citation statements)

References 23 publications

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“…In this study, CIM did not modify catalase activity in either controls or in DAB Experimental Therapeutics Cimetidine and P450 in hepatocarcinogenesis F Caballero et al treated animals. Instead, as previously reported (Caballero et al, 2001) a significant inhibition has been observed in animals receiving only the carcinogen (A S : 50%; B S : 74%) (Figure 4a).…”

Section: Experimental Therapeuticssupporting

confidence: 80%

“…It is noteworthy, that increased GST, diminished catalase, and enhanced LP reflecting initiation of carcinogenesis (Gerez et al, 1998a,b;Caballero et al, 2001), were not modified by CIM, in spite of its partial reversal in the increased P450 levels.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulation of damage alters gene function and clonal expansion of mutated cells (Cerutti, 1994). During drug metabolism, generated reactive oxygen species (ROS) play a key role in several stages of carcinogenesis (Halliwell, 1999;Caballero et al, 2001).…”

mentioning

confidence: 99%

“…Considering that in our experimental model, the sustained P450 induction provoked as a consequence of the carcinogen metabolism, is responsible for the liver injury and the peroxidative damage, our aim was to investigate if diminution of P450 caused by CIM could avoid the biochemical aberrations associated with the initiation stage of hepatocarcinogenesis (Gerez et al, 1998a,b;Caballero et al, 2001).…”

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confidence: 99%

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Interaction of cimetidine with P450 in a mouse model of hepatocarcinogenesis initiation

et al. 2002

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Many drugs and xenobiotics are lipophilic and they should be transformed into more polar water soluble compounds to be excreted. Cimetidine inhibits cytochrome P450. The aim of this study was to investigate the preventive and/or reversal action of cimetidine on cytochrome P450 induction and other metabolic alterations provoked by the carcinogen pdimethylaminoazobenzene. A group of male CF1 mice received a standard laboratory diet and another group was placed on dietary p-dimethylaminoazobenzene (0.5% w w 71 ). After 40 days of treatment, animals of both groups received pdimethylaminoazobenzene and two weekly doses of cimetidine (120 mg kg 71 , i.p.) during a following period of 35 days. Cimetidine prevented and reversed d-aminolevulinate synthetase induction and cytochrome P450 enhancement provoked by p-dimethylaminoazobenzene. However, cimetidine did not restore haem oxygenase activity decreased by p-dimethylaminoazobenzene. Enhancement in glutathione S-transferase activity provoked by p-dimethylaminoazobenzene, persisted in those animals then treated with cimetidine. This drug did not modify either increased lipid peroxidation or diminution of the natural antioxidant defence system (inferred by catalase activity) induced by p-dimethylaminoazobenzene. In conclusion, although cimetidine treatment partially prevented and reversed cytochrome P450 induction, and alteration on haem metabolism provoked by p-dimethylaminoazobenzene AB, it did not reverse liver damage or lipid peroxidation. These results further support our hypothesis on the necessary existence of a multiple biochemical pathway disturbance for the onset of hepatocarcinogenesis initiation.

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Section: Experimental Therapeuticssupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Interaction of cimetidine with P450 in a mouse model of hepatocarcinogenesis initiation

et al. 2002

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“…It reduces the level of estrogen and estrogen receptor with no change in progesterone contents (Liu et al, 2004). It was revealed that TAM in high dose is a known liver carcinogen in rats (Ahotupa et al, 1994;Caballero et al, 2001) which is due to oxygen radical overproduction that occurs during TAM metabolism. This strong hepatocarcinogenic effect of TAM in rats raises issues bearing on the prophylactic chronic administration to healthy women.…”

Section: Introductionmentioning

confidence: 99%

Allicin enhances chemotherapeutic response and ameliorates tamoxifen-induced liver injury in experimental animals

Suddеk

2014

Pharmaceutical Biology

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Context: Tamoxifen (TAM) is widely used for treatment of hormone-dependent breast cancer; however, it may be accompanied with hepatic injury. Allicin is the most abundant thiosulfinate molecule from garlic with the potential to provide beneficial effects on various diseases. Objective: To elucidate the effect of commercially available allicin on both antitumor activity and liver injury of TAM. Materials and methods: The cytotoxicity of TAM and/or allicin was evaluated in vitro using cultured Ehrlich ascites carcinoma (EAC) cells and in vivo against murine tumor (solid) model of EAC. TAM induced liver injury in rats by intraperitoneally (i.p.) injection at a dose of 45 mg/kg, for 7 successive days.Results: TAM at a dose of 3 mM (IC 50 ) significantly decreased percent survival of EAC to 52%. TAM combination with allicin (5 or 10 mM) showed a significant cytotoxic effect compared with the TAM-treated group as manifested by a decrease in percent survival of EAC to 35% and 29%, respectively. Allicin (10 mg/kg, orally) enhanced the efficacy of TAM (1 mg/kg, i.p.) in mice as manifested by a significant increase in solid tumor growth inhibition by 82% compared with 70% in the TAM group. In rats, TAM intoxication resulted in a significant decline in SOD, GSH, and total protein with significant elevation in TBARS, ALT and AST, ALP, LDH, total bilirubin, gGT, and TNF-a levels. These changes are abrogated by allicin treatment. Discussion and conclusion: The results suggest the beneficial role of allicin as an adjuvant to TAM in cancer treatment by alleviating liver injury.

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On the Promoting Action of Tamoxifen in the P-Dimethylaminoazobenzene Induced Hepatocarcinogenesis CF1 Mice Model and the Cytoprotective Role of Heme Oxygenase

Vázquez

Gerez

Caballero

et al. 2002

Heme Oxygenase in Biology and Medicine

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On the promoting action of tamoxifen in a model of hepatocarcinogenesis induced by p-dimethylaminoazobenzene in CF1 mice

Cited by 18 publications

References 23 publications

Interaction of cimetidine with P450 in a mouse model of hepatocarcinogenesis initiation

Interaction of cimetidine with P450 in a mouse model of hepatocarcinogenesis initiation

Allicin enhances chemotherapeutic response and ameliorates tamoxifen-induced liver injury in experimental animals

On the Promoting Action of Tamoxifen in the P-Dimethylaminoazobenzene Induced Hepatocarcinogenesis CF1 Mice Model and the Cytoprotective Role of Heme Oxygenase

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