Antioxidants and multistage carcinogenesis in mouse skin

Perchellet, Jean‐Pierre; Perchellet, Elisabeth M.

doi:10.1016/0891-5849(89)90124-x

Cited by 209 publications

(111 citation statements)

References 201 publications

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“…Alternatively, chemopreventive agents acts as antioxidant and counteracts the increased amount of oxidants generated by toxicants (Wattenberg 1985). Reactive oxygen species are widely generated in biological systems either by normal metabolic pathways or as a consequence of exposure of chemical carcinogen is extensively studied and may result in membrane dysfunction, protein inactivation, DNA damage and ultimately contribute to the multisteps process of carcinogenesis (Perchellet & Perchellet 1989;Sun 1990). The collective action of both antioxidants and phase II enzymes such as glutathione S-transferase and quinone reductase, besides small non-enzymatic water soluble biomolecules, is to protect against the adverse effects of oxidants or reactive metabolites of precarcinogens (Perchellet & Perchellet 1989;Sun 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Reactive oxygen species are widely generated in biological systems either by normal metabolic pathways or as a consequence of exposure of chemical carcinogen is extensively studied and may result in membrane dysfunction, protein inactivation, DNA damage and ultimately contribute to the multisteps process of carcinogenesis (Perchellet & Perchellet 1989;Sun 1990). The collective action of both antioxidants and phase II enzymes such as glutathione S-transferase and quinone reductase, besides small non-enzymatic water soluble biomolecules, is to protect against the adverse effects of oxidants or reactive metabolites of precarcinogens (Perchellet & Perchellet 1989;Sun 1990). Reiners et al (1991) have shown depleted levels of antioxidant enzymes in 7,12-dimethylbenz(a)anthracene-12-O-tetradecanoylphorbol-13-acetate-treated skin and in skin tumours induced chemically.…”

Section: Discussionmentioning

confidence: 99%

“…Reiners et al (1991) have shown depleted levels of antioxidant enzymes in 7,12-dimethylbenz(a)anthracene-12-O-tetradecanoylphorbol-13-acetate-treated skin and in skin tumours induced chemically. Depletion of these enzymes following exposure to carcinogens and/or tumour promoter has also been observed (Perchellet & Perchellet 1989;Sun 1990). Adversely cancer chemoprevention studies have shown that following the administration of chemopreventive agents, the levels of antioxidant enzymes are elevated in various organs of test animals (Wattenberg 1990).…”

Section: Discussionmentioning

confidence: 99%

“…Several reports suggest pronounced effects of peroxides as compared to O 2 in producing cytotoxicity/genotoxicity in the cellular systems (Perchellet & Perchellet 1989;Sun 1990). Besides, the highly reactive OH, generated from H 2 O 2 via the HaberWeiss-like-Fenton reaction (Perchellet & Perchellet 1989) is known to damage macromolecules, specifically DNA to produce pathological alterations (Sun 1990;Perchellet & Perchellet 1989). In view of these facts, the enhancement in the activity of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, and catalase in liver and kidney of curcumin fed animals suggests that such a treatment could protect the cells/tissues against the cytotoxic/genotoxic effects of peroxides and OH.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, curcumin inhibits the expression of c-fos, c-myc and c-jun (Kakar & Roy 1994;Limtrakul et al 2001) and induces apoptosis (Piwocka et al 2001). Despite the fact that 1) curcumin and its derivatives have shown a significant protection against tumourigenesis in several animal tumour bioassay systems (Sharma 1976;Satoskar et al 1986;Huang et al 1992;Goel et al 2001;Mori et al 2001Surh et al 2001 2) depletion in the activities of antioxidant and phase II enzymes occur during tumourigenesis (Perchellet & Perchellet 1989;Sun 1990) 3) cancer chemopreventive agents enhances the activity of these enzymes in target tissues (Wattenberg & Loccia 1990). Since it is capable of inhibiting various kinds of injuries and neoplasm particularly those, which are mediated through the generation of reactive oxygen species.…”

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confidence: 99%

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Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

272

147

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Dietary antioxidants protect laboratory animals against the induction of tumours by a variety of chemical carcinogens. Among possible mechanism of protection against chemical carcinogenesis could be mediated via-antioxidantdependent induction of detoxifying enzymes. Curcumin, a yellow pigment from Curcuma longa, is a major component of turmeric and is commonly used as a spice and food colouring material and exhibits antiinflammatory, antitumour, and antioxidant properties. In this study we therefore investigated the effect of dietary supplementation of curcumin on the activities of antioxidant and phase II-metabolizing enzymes involved in detoxification, and production of reactive oxygen species were quantified in ddY male mice. Dietary supplementation of curcumin (2%, w/v) to male ddY mice for 30 days significantly increased the activities of glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase and catalase to 189%, 179%, 189%, and 181% in liver and 143%, 134%, 167% and 115% in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.001). Parallel to these changes, curcumin feeding to mice also resulted in a considerable enhancement in the activity of phase II-metabolizing enzymes viz. glutathione S-transferase and quinone reductase to 1.7 and 1.8 times in liver and 1.1 and 1.3 times in kidney respectively as compared with corresponding normal diet fed control (PϽ0.05-0.01). In general, the increase in activities of antioxidant and phase II-metabolizing enzymes was more pronounced in liver as compared to kidney. The induction of such detoxifying enzymes by curcumin suggest the potential value of this compound as protective agent against chemical carcinogenesis and other forms of electrophilic toxicity. The significance of these results can be implicated in relation to cancer chemopreventive effects of curcumin against the induction of tumours in various target organs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Iqbal

Sharma

Okazaki

et al. 2003

Pharmacology & Toxicology

272

147

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Camptothecin post-treatments inhibit the biochemical events linked to the tumor-promoting component of carcinogenesis in mouse epidermisin vivo

et al. 1996

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USA. 2O(S)-Camptothecin (CPT), a topoisomerase I inhibitor specifically toxic toward S-phase cells, was tested topically for i t s ability to inhibit the biochemical markers of skin tumor promotion. CPT has no or very little inhibitory effect on the covalent binding of an initiating dose of 7, I2-dimethylbenz-[a]anthracene (DMBA) to DNA at 24 hr, but CPT post-treatments remarkably inhibit stimulations of DNA synthesis caused by the tumor promoter 12-0-tetradecanoylphorbol-I 3-acetate (TPA)at 16 hr and a carcinogenic dose of DMBA at 7 days. CPT is a much more potent inhibitor if it is applied 10-14 hr after TPA or 4-6 days after DMBA, when DNA synthesis starts being stimulated after the periods of early inhibition caused by TPA and DMBA. When applied I 2 hr after the tumor promoter, the ability of 3-3,000 nmol of CPT to inhibit TPA-stimulated DNA synthesis at 16 hr is dose-dependent. A single dose of 500 nmol of CPT inhibits the entire time course for the stimulation of DNA synthesis observed 16-64 hr after TPA. CPT also reduces the various DNA responses to chronic TPA treatments and structurally different non-TPA-type tumor promoters. CPT may indirectly decrease the ornithine decarboxylase-inducing activity of multiple TPA treatments because it can inhibit the stimulation of RNA synthesis by this compound. However, CPT fails to alter TPA-stimulated hydroperoxide production in relation t o i t s inability to inhibit TPA-stimulated protein synthesis. On an equal dose basis, topotecan and 10-hydroxycamptothecin are more and less effective than CPT, respectively, whereas 10, I I -methylenedioxycamptothecin is much more potent than its parent compound at inhibiting the DNA response to TPA. A single dose of 400 nmol of CPT has no effect on tumor initiation when applied 4 hr before or I hr after a single subcarcinogenic dose of DMBA. In contrast, 400 nmol of CPT chronically applied I hr before or 24 hr after each treatment with TPA remarkably inhibits the complete tumor-promoting activity of this agent. CPT post-treatments also inhibit the respective activities of TPA and mezerein in the 1st and 2nd stages of skin tumor promotion.o 1996 Wiley-Liss, Inc. 20(S)-Camptothecin (CPT), a cytotoxic plant alkaloid isolated from Camptotheca acuminata, exhibits a broad spectrum of anti-tumor activity (Wall and Wani, 1995;Potmesil, 1994).CPT targets type I DNA topoisomerase (Topo I), a nuclear enzyme that relaxes supercoiled DNA by creating transient single-strand breaks (SSBs). Top0 I is covalently attached to the broken strand of DNA and the SSBs are normally resealed by this enzyme. CPT stabilizes the reversible covalent Top0 I-DNA intermediate and forms a covalent ternary complex, Top0 I-CPT-DNA, which prevents the religation of the SSB. CPT is a cell cycle-specific anti-cancer drug because the collision between the advancing replication fork and the cleavable ternary complex creates highly toxic and long-lived DNA double-strand breaks (DSBs) (Hsiang et al., 1989; Tsao et ab, 1993; Ryan et al., 1994;Pantazis et al

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Tea antioxidants in cancer chemoprevention

Katiyar¹,

Mukhtar²

1997

J. Cell. Biochem.

177

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In recent years, the concept of cancer chemoprevention has matured greatly. Significant reversal or suppression of premalignancy in several sites by chemopreventive agents appears achievable. This article summarizes experimental data on chemopreventive effects of tea polyphenols in different tumor bioassay systems. Tea (Camellia sinensis) is cultivated in about 30 countries, and is the most widely consumed beverage in the world. Three main commercial tea varieties-green, black, and oolong-are usually consumed, but most experimental studies demonstrating the antimutagenic and anticarcinogenic effects of tea have been conducted with water extract of green tea, or a polyphenolic fraction isolated from green tea (GTP). The majority of these studies have been conducted in a mouse skin tumor model system where tea is fed either as water extract through drinking water, or as purified GTP. GTP has been shown to exhibit antimutagenic activity in vitro, and inhibit carcinogen-as well as UV-induced skin carcinogenesis in vivo. Tea consumption has also been shown to afford protection against chemical carcinogen-induced stomach, lung, esophagus, duodenum, pancreas, liver, breast, and colon carcinogenesis in specific bioassay models. Several epicatechin derivatives (polyphenols) present in green tea have been shown to possess anticarcinogenic activity; the most active is (Ϫ)-epigallocatechin-3-gallate, which is also the major constituent of GTP. The mechanisms of tea's broad cancer chemopreventive effects are not completely understood. Several theories have been put forward, including inhibition of UV-and tumor promoter-induced ornithine decarboxylase, cyclo-oxygenase, and lipoxygenase activities, antioxidant and free radical scavenging activity; enhancement of antioxidant (glutathione peroxidase, catalase, and quinone reductase) and phase II (glutathione-S-transferase) enzyme activities; inhibition of lipid peroxidation, and anti-inflammatory activity. These properties of tea polyphenols make them effective chemopreventive agents against the initiation, promotion, and progression stages of multistage carcinogenesis.

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Antioxidants and multistage carcinogenesis in mouse skin

Cited by 209 publications

References 201 publications

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Dietary Supplementation of Curcumin Enhances Antioxidant and Phase II Metabolizing Enzymes in ddY Male Mice: Possible Role in Protection against Chemical Carcinogenesis and Toxicity

Camptothecin post-treatments inhibit the biochemical events linked to the tumor-promoting component of carcinogenesis in mouse epidermisin vivo

Tea antioxidants in cancer chemoprevention

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