Four anticarcinogens (oltipraz, alpha-tocopherol, beta-carotene and phenethylisothiocyanate [PEITC]) were studied with respect to their effects on oesophageal, gastric, colonic and hepatic (i) glutathione (GSH) content, (ii) glutathione S-transferase (GST) enzyme activity, (iii) GST isoenzyme levels, and (iv) glutathione peroxidase (GPx) enzyme activity in male Wistar rats. GST enzyme activity was significantly increased in oesophagus (1.9X) and colon (1.2X) by PEITC and in liver (1.4X) by oltipraz. GST Alpha was doubled in the liver by oltipraz, alpha-tocopherol and PEITC. GST Mu levels were increased by beta-carotene and PEITC in stomach and liver, by oltipraz in liver and by alpha-tocopherol in stomach. PEITC induced colonic GST Pi levels (1.3X). GSH content was induced in liver by oltipraz (1.4X) and alpha-tocopherol (1.2X) and in colon by PEITC (1.6X). Each of the anticarcinogens tested increased GPx activity at one or more sites: Se-dependent and total GPx activities were induced in 31.3% and 37.5% of all possibilities, respectively. Major induction in total GPx was found in stomach by alpha-tocopherol (1.8X). In conclusion our data demonstrate that dietary administration of oltipraz, PEITC, alpha-tocopherol and beta-carotene, may exert chemopreventive effects in the digestive tract of the rat by enhancing GST, GPx, and, to a lesser extent, GSH levels.
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http://dx.doi.org/10.1093/carcin/17.7.1439 | DOI Listing |
Mutat Res
December 2005
Department of Health Sciences, University of Genoa, via A. Pastore 1, I-16132 Genoa, Italy.
A review of almost 2000 studies showed that the large majority of 39 putative cancer chemopreventive agents induced "spontaneous" apoptosis. Inhibition of the programmed cell death triggered by a variety of stimuli was consistently reported only with ascorbic acid, alpha-tocopherol, and N-acetylcysteine (NAC). We performed experimental studies in rodents exposed to cigarette smoke, either mainstream (MCS) or environmental (ECS), and UV-A/B-containing light.
View Article and Find Full Text PDFAnticancer Res
July 2004
Department of Gastroenterology, University Medical Centre St Radboud, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.
Background: Dietary compounds or nonsteroidal anti-inflammatory drugs (NSAIDs) may reduce cancer rates. Elevation of phase II detoxification enzymes might be one of the mechanisms leading to cancer prevention. We investigated the effects of dietary anticarcinogens and NSAIDs on rat gastrointestinal UDP-glucuronosyltransferases (UGT).
View Article and Find Full Text PDFEur Urol
July 1999
Experimental Toxicology and Carcinogenesis Division, IIT Research Institute, Chicago, Ill. 60616, USA.
The high incidence and long latent period of prostate cancer make it an ideal target for chemoprevention. We have evaluated a series of agents for chemopreventive efficacy using a model in which hormone-dependent prostate cancers are induced in the Wistar-Unilever (WU) rat by sequential treatment with antiandrogen (cyproterone acetate), androgen (testosterone propionate), and direct-acting chemical carcinogen (N-methyl-N-nitrosourea), followed by chronic androgen stimulation (testosterone). This regimen reproducibly induces prostate cancers in high incidence, with no gross toxicity and a low incidence of neoplasia in the seminal vesicle and other non-target tissues.
View Article and Find Full Text PDFCarcinogenesis
November 1998
Department of Gastroenterology, St Radboud University Hospital, Nijmegen, The Netherlands.
Several naturally occurring food components or non-steroidal anti-inflammatory drugs (NSAIDs) may reduce gastrointestinal cancer rates. Recently we have shown that dietary administration of such compounds enhanced the glutathione S-transferase (GST) enzyme activity and class alpha, mu and pi isoenzyme levels in the rat gastrointestinal tract. Elevation of the levels of GSTs, a family of biotransformation enzymes with many functions such as detoxification of carcinogens, might be one of the mechanisms that lead to cancer prevention.
View Article and Find Full Text PDFOncol Rep
July 1998
Department of Gastroenterology, St. Radboud University Hospital, 6500 HB Nijmegen, The Netherlands.
Several naturally occurring and synthetic food components reduce gastrointestinal cancer. Many of these compounds are scavengers of free radicals, formed during oxidative stress. Glutathione peroxidases (GPxs) protect against free radicals by catalysing their inactivation, thereby consuming glutathione (GSH).
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