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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compares the toxic effects of the carotenoids, beta-carotene and canthaxanthin, and alpha-tocopherol (vitamin E) on human tumor cells and their normal counterparts in vitro. Seven different malignant cell lines were examined: oral carcinoma (two cell lines), breast (two cell lines), lung carcinoma (two cell lines), and malignant melanoma. The in vitro cell culture assays showed a consistent morphologic change in the affected tumor cells following treatment with carotenoid or vitamin E. A rounding of the tumor cells and eventual lifting off the tissue culture plate were observed. These changes were apparent after 1 to 5 hours of treatment depending on the tumor cell line. Associated with these observable cellular changes were quantitative reductions in proliferation (3H-thymidine proliferation) and succinic dehydrogenase activity (MTT assay). In addition, there was a noticeable change in protein expression, with an increased expression of a 70-kD protein following treatment with beta-carotene. This protein was associated with tumor cells showing a decrease in proliferation (oral carcinoma, malignant melanoma) but not with normal keratinocytes or melanocytes. These studies substantiate a selective cytotoxic effect on human tumor cell growth by carotenoids and alpha-tocopherol in vitro, and may provide an explanation of the therapeutic activity of these agents and their possible use in the treatment of premalignancy or early oral carcinoma.
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PMID:The selective cytotoxic effect of carotenoids and alpha-tocopherol on human cancer cell lines in vitro. 154 92

Male Sprague-Dawley rats were fed from weaning low (1-5 ppm) and normal (26-50 ppm) vitamin E diets for 30-34 weeks. Dietary fat was also varied from 5% (Experiment 1) to 20% (Experiments 2 and 3). Intestinal tumors were induced by 1,2-dimethylhydrazine given subcutaneously as 10 weekly doses at 20 mg/kg body wt. Tumor incidence was lower by 30% and burden was 25%-50% lower for low vitamin E rats than for vitamin E-replete rats. This result was independent of the fat content of the diet. In Experiment 3, vitamin E and calcium were assessed for their influence on intestinal tumors at two levels, with dietary vitamin E at 5 and 50 ppm and calcium at 0.2% and 1.0% in a 2 x 2 factorial experiment. The high calcium-low vitamin E diet produced the greatest fall in tumor incidence and burden relative to the other treatments. In this experiment, vitamin E deficiency reduced tumor incidence and calcium supplementation reduced tumor burden, with a significant interaction of the two. However, this group also showed evidence of reduced food intake and kidney change (calcification), which may have confounded the result. This points to a risk associated with this combination of nutrients at these levels in long-term experiments.
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PMID:The influence of dietary vitamin E and calcium status on intestinal tumors in rats. 157 44

The effects of combined dietary vitamin E supplementation and a relatively low increase in selenium levels on 7,12-dimethylbenz[a]anthracene (DMBA) induction of lipid peroxidation in the short term and development of mammary tumors in the long term were investigated in female Sprague-Dawley rats. Control animals were fed the basal diet (20 mg/kg vitamin E and 0.6 mg/kg selenium) throughout the experiment. Three other groups received a high vitamin E diet (235 mg/kg vitamin E and 0.6 mg/kg selenium) at different times, the first two from three weeks after DMBA treatment and the other throughout the experiment. When the vitamin E diet with selenium supplementation was applied until three weeks after DMBA or until the termination of the experiment, tumor yields (tumors per rat) were significantly inhibited compared with the control group. On the other hand, delaying the supplementation of vitamin E until three weeks postcarcinogen produced no prophylactic effect. The elevation of lipid peroxidation levels observed immediately after DMBA administration was also significantly inhibited in both mammary fat pads and livers of animals in the high vitamin E group. It was therefore concluded that the inhibitory effect of vitamin E in combination with selenium on tumorigenesis might be causally related to reduction of carcinogen treatment associated with lipid peroxidation, the latter presumably playing an important role in DMBA-induced mammary carcinogenesis.
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PMID:Inhibition of 7,12-dimethylbenz[a]anthracene-induced lipid peroxidation and mammary tumor development in rats by vitamin E in conjunction with selenium. 158 6

Two forms of vitamin E, tocopherol and tocotrienol, were tested for chemopreventive activity in two chemically induced rat mammary-tumor models. When mammary tumors were induced by 7,12-dimethylbenz(a)anthracene (DMBA, 50 mg/kg), only the tocotrienol group had a statistically significant increase in tumor latency. There was no effect of either compound on tumor multiplicity. When tumors were induced by N-nitrosomethylurea (NMU, 30 mg/kg), neither analogue of vitamin E modified latency, whereas tocotrienol increased tumor multiplicity. In summary, neither vitamin analog had a major impact on mammary-tumor development after tumor induction with either DMBA or NMU.
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PMID:A comparison of tocopherol and tocotrienol for the chemoprevention of chemically induced rat mammary tumors. 184 66

Low oxygen tension, a high content of reducing equivalents and endogenous vitamin E are responsible for the resistance of cancer cells to oxidative stress-based therapy. N,N'-bis(2-hydroperoxy-2-methoxyethyl)-1,4,5,8-naphthalene-tetra- carboxylic-diimide (NP-III), capable to release radicals both in the absence and in the presence of oxygen upon UV-illumination, is a new potential anticancer agent. UV-induced reactions of NP-III in rat liver microsomes were studied under aerobic and anaerobic conditions with (i) vitamin E homologue, chromanol-alpha-C-6 having a shorter (6-carbon) hydrocarbon side chain and higher antioxidant activity, and (ii) the spin-trap 5,5-dimethyl-1-pyrroline-1-oxide, DMPO. UV-induced generation of chromanoxyl radicals was observed in the presence of NP-III under aerobic conditions, which was SOD+catalase sensitive. Hydroxyl-, superoxide- and alkoxyl-radical DMPO adducts were found upon UV-illumination of NP-III under aerobic conditions and only hydroxyl-radical adducts under anaerobic conditions. The light-dependent generation of oxy- and chromanoxyl free radicals and depletion of endogenous antioxidants suggests to be a promising strategy to overcome the inherent resistance of tumor cells to oxidative stress.
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PMID:UV induces oxy- and chromanoxyl free radicals in microsomes by a new photosensitive organic hydroperoxide, N,N'-bis(2-hydroperoxy-2-methoxyethyl)- 1,4,5,8-naphtalene-tetra-carboxylic-diimide. 184 1

Cis-unsaturated fatty acids (c-UFAs) such as gamma-linolenic acid (GLA), arachidonic acid (AA) and eicosapentaenoic acid (EPA) can kill tumor cells selectively in vitro. As c-UFAs have the ability to augment free radical generation, the effect of antioxidants, free radical quenchers and augmentors of free radical generation such as iron and copper salts on fatty acid-induced tumor cell death was studied. In addition, the role of lipid peroxidation in the tumoricidal action of c-UFAs was also examined. Results indicate that vitamin E, uric acid, glutathione peroxidase, superoxide dismutase and ATP can block, whereas iron, copper and catalase enhance the tumoricidal action of GLA. The ability of GLA, AA and EPA to kill tumor cells correlated with the amount of lipid peroxidation these fatty acids can induce as measured by thiobarbituric acid test. It was also observed that 14C-labelled linoleic acid uptake was almost the same whereas that of 14C-labelled arachidonic acid and eicosapentaenoic acid were substantially less in tumor cells compared to normal cells. Tumor cells incorporated major portions of the fatty acids in the ether lipid and phospholipid fractions, whereas normal cells incorporated the fatty acids primarily in the phospholipid fraction. These results suggest that c-UFA-induced tumoricidal action is a free radical dependent process and that there are significant differences between normal and tumor cells in fatty acid uptake and distribution.
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PMID:Tumoricidal action of cis-unsaturated fatty acids and their relationship to free radicals and lipid peroxidation. 185 Jun 58

Natural vitamin E and synthetic vitamin E (dl-alpha-tocopheryl acetate) were tested for their tumorigenicity in rodents. Transplantable tumors, at the site of injection, were induced by repeated injections of these compounds in two strains of mice, NFS/N and C57BL/6N x C3H/He F1, and in a strain of rats, Fischer 344. Natural vitamin E was tumorigenic in both strains of female mice only when injected with soya oil. In contrast, dl-alpha-tocopheryl acetate alone was capable of inducing tumors in Fischer 344 rats. Only one out of 5 male NFS/N mice given dl-alpha-tocopheryl acetate developed a tumor. Therefore, Fischer 344 rats were more susceptible to tumor formation by dl-alpha-tocopheryl acetate than NFS/N mice. dl-alpha-Tocopheryl acetate with soya oil or with palm oil also resulted in the formation of transplantable tumors in NFS/N mice and Fischer 344 rats. There was no difference in the tumor incidence between mice treated with dl-alpha-tocopheryl acetate alone and dl-alpha-tocopheryl acetate plus soya oil or palm oil. However, in rats, the incidence was lower for a group treated with dl-alpha-tocopheryl acetate plus palm oil than for those with dl-alpha-tocopheryl acetate alone and with dl-alpha-tocopheryl acetate plus soya oil.
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PMID:Induction of transplantable tumors by repeated subcutaneous injections of natural and synthetic vitamin E in mice and rats. 190 98

Twigs-dry leaves smoke condensate (TDS), as a source of clastogenic ROS and carcinogenic PAH, was investigated for its in vitro DNA-damaging effect in calf thymus DNA and human peripheral lymphocytes. An aqueous turmeric component--Aq.T--with an established antioxidant activity, was tested as a DNA protectant. TDS induced 13-fold damage to calf thymus DNA as judged by the emergence of a DNA damage specific, fluorescent product (em: 405 nm). Aq.T at 800 ng/microL extended 69% protection to calf thymus DNA and was comparable to the other protectants such as curcumin, BHA, vitamin E, SOD, and CAT. In human peripheral lymphocytes, TDS induced extensive DNA damage in comparison with the tumor promoter TPA, as judged by FADU. Aq.T at 300 ng/microL extended 90% protection to human lymphocyte DNA against TDS-induced damage, and was more effective than the other protectants--DABCO, D-mannitol, sodium benzoate, vitamin E (ROS quenchers), SOD, CAT (antioxidant enzymes), tannic acid, flufenamic acid, BHA, BHT, n-PG, curcumin and quercetin (antioxidants). Aq.T offered 65% protection to human lymphocyte DNA against TPA-induced damage and was comparable to SOD. The above results indicate that TDS induces substantial DNA damage in calf thymus DNA and human lymphocytes and Aq.T is an efficient protectant.
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PMID:DNA damage by smoke: protection by turmeric and other inhibitors of ROS. 193 45

The aim of the experiment was to study the effect of three specialized food rations on activity of superoxide dismutase (SOD) in tissues of rats with transplanted Walker's carcinosarcoma 256 exposed to carminomycin. It was shown that the three specialized rations were able to significantly modify the SOD activity in the tissues of the rats with Walker's carcinosarcoma 256 at the background of treatment with carminomycin. Thus, the ration enriched with copper and zinc salts and folic acid activated SOD in the animals of all the groups. Still, the effect was higher in the tumor-bearing animals and the rats treated with carminomycin i.e. under conditions of oxidative stress. The use of the ration enriched with sulfur-containing amino acids, sodium selenide and vitamin E led to decreasing of the efficiency of the fermentative dismutation of O2 in the healthy rats and marked activating of SOD in the tumor-bearing animals. The ration containing lyophilized vegetables and vitamin E provided a significant increase in the SOD activity in the healthy rats. However, its potential was not sufficient for overcoming the SOD inhibiting effect of the tumor growth.
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PMID:[Alimentary methods of maintaining the superoxide dismutase activity in the tissues of rats during growth of a transplanted tumor and administration of carminomycin]. 195 87

To investigate the effects of both diol esterification and coadministration with antioxidant on the tumorigenicity of fecapentaene-12 (FP-12) preparations, diacetylfecapentaene-12 (DAFP-12) in dimethylsulfoxide (DMSO) was applied to SENCAR mouse skin with or without the stabilizer, vitamin E, twice/week for 5 weeks, following which all animals were promoted for up to 25 weeks by weekly applications of 12-O-tetradecanoylphorbol-13-acetate (TPA). While positive controls receiving 7,12-dimethylbenz[a]anthracene (DMBA) instead of DAFP-12 in a similar protocol all developed papillomas (average of 23/animal), papilloma incidence in mice given DAFP-12 did not differ significantly from that of the vehicle control. We conclude that DAFP-12 shows little or no tumor initiating activity for mouse skin even when coadministered with vitamin E.
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PMID:Carcinogenicity study of fecapentaene-12 diacetate on skin painting in SENCAR mice. 200 49


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