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      Decreased Levels of 2‐Amino‐3‐methylimidazo[4,5‐ f]quinoline‐DNA Adducts in Rats Treated with β‐Carotene, α‐Tocopherol and Freeze‐dried Aloe

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          Abstract

          To assess mechanisms of chemoprevention of hepatocarcinogenesis by trans‐β‐carotene (β‐C), DL‐α‐tocopherol (α‐T), and freeze‐dried whole leaves of Kidachi aloe (Aloe), formation of 2‐amino‐3‐methylimidazo[4,5‐ f]quinoline (IQ)‐DNA adducts was measured by 32P‐post‐labeling analysis, and CYP1A1 and CYP1A2 protein levels were analyzed by ELISA. Group 1 rats were fed diet containing 0.02%β‐C, 1.5%α‐T or 30% Aloe over an 8‐day period, while group 2 was given basal diet alone. On day 7, all animals were subjected to two‐thirds partial hepatectomy (PH). Twelve hours after PH, they received a single dose of the carcinogenic food pyrolysate IQ (100 mg/kg) intragastrically, to initiate hepatocarcinogenesis. Rats were killed 6, 12, 24 and 48 h after IQ administration. The levels of adducts, expressed as relative adduct labeling values in rats treated with β‐C, α‐T and Aloe, were decreased as compared with the control group at hour 24 (36 h after PH), with a significant difference in the case of the β‐C group (46.4% of the control value). Similarly, all showed a tendency for decrease at hour 48. Furthermore, the levels of CYP1A2, known to be responsible for activation of IQ, showed a significant reduction at hour 24. It is concluded that β‐C, and possibly also α‐T and Aloe, have the potential to reduce IQ‐DNA adduct formation, presumably as a result of decreased formation of active metabolites. The results may explain, at least in part, the previously observed inhibitory effects of these compounds on induction of preneoplastic hepatocellular lesions.

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          Most cited references46

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          Dietary carcinogens and anticarcinogens. Oxygen radicals and degenerative diseases.

          B N Ames (1983)
          The human diet contains a great variety of natural mutagens and carcinogens, as well as many natural antimutagens and anticarcinogens. Many of these mutagens and carcinogens may act through the generation of oxygen radicals. Oxygen radicals may also play a major role as endogenous initiators of degenerative processes, such as DNA damage and mutation (and promotion), that may be related to cancer, heart disease, and aging. Dietary intake of natural antioxidants could be an important aspect of the body's defense mechanism against these agents. Many antioxidants are being identified as anticarcinogens. Characterizing and optimizing such defense systems may be an important part of a strategy of minimizing cancer and other age-related diseases.
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            Enhancing effect of various hepatocarcinogens on induction of preneoplastic glutathione S-transferase placental form positive foci in rats--an approach for a new medium-term bioassay system.

            A large series of assays of the hepatocarcinogenic potential of 112 different compounds were carried out using a rapid bioassay system developed in this laboratory based on the two-step concept of hepatocarcinogenesis. Rats were initially given a single dose (200 mg/kg) of diethylnitrosamine (DEN) i.p. and starting 2 weeks later were treated with test compounds for 6 weeks and then killed, all rats being subjected to two-thirds partial hepatectomy (PH) at week 3. Carcinogenic potential was scored by comparing the number and area per cm2 of induced glutathione S-transferase placental form-positive (GST-P+) foci in the liver with those of the corresponding control group given DEN alone. Positive was scored for a significant increase in the value of GST-P+ foci, negative for no change or a decrease. Results were compared to reported Salmonella/microsome and long-term carcinogenicity test findings. Of the liver carcinogens, 10 out of 11 (90.9%) mutagenic, and 11 out of 13 (84.6%) non-mutagenic compounds gave positive results (mean, 87.5%). Carcinogens other than the hepatocarcinogens gave less positive results (two out of 17, 11.8%). None of the compounds reported as non-carcinogenic demonstrated positivity suggesting that the assay system does not suffer from the disadvantage of false-positive results. The protocol system also provided information concerning the inhibitory potential of compounds such as anti-oxidants. It is concluded that the present experimental protocol which requires far fewer animals and shorter duration than a long-term carcinogenicity test has practical applications for the rapid and economical screening of environmental hepatocarcinogens and their inhibitory agents.
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              Inhibition of 4-nitroquinoline-1-oxide-induced rat tongue carcinogenesis by the naturally occurring plant phenolics caffeic, ellagic, chlorogenic and ferulic acids.

              The modifying effects of dietary administration of the plant phenolic antioxidants caffeic acid (CA), ellagic acid (EA), chlorogenic acid (CGA) and ferulic acid (FA) during the initiation phase on 4-nitroquinoline-1-oxide (4-NQO)-induced tongue carcinogenesis and on the number and area of silver-stained nucleolar organizer region proteins (AgNORs), a new cell proliferation marker, of the tongue squamous epithelium were investigated in male F344 rats. Rats were fed the diet containing 500 p.p.m. CA, 400 p.p.m. EA, 250 p.p.m. CGA or 500 p.p.m. FA for 7 weeks. One week after the commencement of the diets, 4-NQO (20 p.p.m.) was administered in the drinking water for 5 weeks. Feeding of four phenolic compounds significantly reduced the incidences of tongue neoplasms (squamous cell papilloma and carcinoma) and preneoplastic lesions (hyperplasia and dysplasia) by 32 weeks, and rats fed CA or EA had no tongue neoplasms. The number and area of AgNORs per nucleus were decreased significantly by dietary treatment with these four phenolics. Thus, CA, EA, CGA and FA inhibited the tongue carcinogenesis induced by 4-NQO when they were administered concurrently with the carcinogen. These results might suggest possible application of these natural substances for cancer chemoprevention in tongue in addition to other tissues (skin, lung, liver and esophagus).
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                Author and article information

                Journal
                Jpn J Cancer Res
                Jpn. J. Cancer Res
                10.1111/(ISSN)1349-7006a
                CAS
                Japanese Journal of Cancer Research : Gann
                Blackwell Publishing Ltd (Oxford, UK )
                0910-5050
                1876-4673
                April 1996
                : 87
                : 4 ( doiID: 10.1111/cas.1996.87.issue-4 )
                : 342-348
                Affiliations
                [ 1 ]Chemotherapy, National Cancer Center Research Institute, 5‐1‐1 Tsukiji, Chuo‐ku, Tokyo, 104
                [ 2 ]Carcinogenesis Division, National Cancer Center Research Institute, 5‐1‐1 Tsukiji, Chuo‐ku, Tokyo, 104
                [ 3 ]Department of Hygienic Chemistry, Pharmaceutical Institute, Tohoku University, Aobayama, Sendai 980
                [ 4 ]Second Department of Pathology, Fujita Health University, School of Medicine, Kutsukakecho, Toyoake, Aichi 470‐11
                [ 5 ]Institute of Pharmacognosy, Fujita Health University, Ohtoricho, Hisai, Mie 514‐12
                Author notes
                [*] [* ]To whom correspondence should be addressed.
                Article
                CAE342
                10.1111/j.1349-7006.1996.tb00228.x
                5921102
                8641964
                5932ed9b-99a0-4a60-876b-a2362d48561e
                History
                Page count
                References: 52, Pages: 7
                Categories
                Article
                Custom metadata
                2.0
                April 1996
                Converter:WILEY_ML3GV2_TO_NLMPMC version:4.6.9 mode:remove_FC converted:04.11.2015

                chemoprevention,hepatocarcinogenesis,initiation,β‐carotene,iq‐dna adduct

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