Journal Article

MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION: Effect of oltipraz, α-tocopherol, β-carotene and phenethylisothiocyanate on rat oesophageal, gastric, colonic and hepatic glutathione, glutathione S-transferase and peroxidase

Esther M.M. van Lieshout, Wilbert H.M. Peters and Jan B.M.J. Jansen

in Carcinogenesis

Volume 17, issue 7, pages 1439-1445
Published in print July 1996 | ISSN: 0143-3334
e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.7.1439
MOLECULAR EPIDEMIOLOGY AND CANCER PREVENTION: Effect of oltipraz, α-tocopherol, β-carotene and phenethylisothiocyanate on rat oesophageal, gastric, colonic and hepatic glutathione, glutathione S-transferase and peroxidase

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Four anticarcinogens (oltipraz, α-tocopherol, β-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 (1.9 ×) and colon (1.2×) by PEITC and in liver (1.4×) by oltipraz. GST Alpha was doubled in the liver by oltipraz, α-tocopherol and PEITC. GST Mu levels were increased by β-carotene and PEITC in stomach and liver, by oltipraz in liver and by α-tocopherol in stomach. PEITC induced colonic GST Pi levels (13×). GSH content was induced in liver by oltipraz (1.4×) and α-tocopherol (1.2×) and in colon by PEITC (1.6×). 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 α-tocopherol (1.8×). In conclusion our data demonstrate that dietary administration of oltipraz, PEITC, α-tocopherol and β-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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Subjects: Clinical Cytogenetics and Molecular Genetics

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