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 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of vitamin E as a protective agent against adriamycin-induced toxicity in CDF1 and BDF1 mice resulted in potentiation of the chemotherapeutic index of adriamycin. A single dose of 15 mg of adriamycin per kg body weight produced a significantly reduced mean survival time. A dosage of adriamycin of 15 mg per kg body weight was employed in the following experiments. In P388 ascites tumor-bearing mice, four consecutive injections of several doses of vitamin E before injection of adriamycin produced a significant prolongation of the mean survival. In concomitant studies of serum tocopherol content, 7 to 10 micrograms/ml appeared to be an appropriate serum concentration, in accordance with the result of our previous report on its immunopotentiation effect. alpha-tocopherol seemed to have a two- to three-fold greater physiological activity than alpha-tocopheryl acetate. Dietary vitamin E treatments offered no protection against adriamycin toxicity, because the serum tocopherol content reached only 4.39 micrograms/ml in mice given the vitamin E-sufficient feed in this study. The results suggested that an increase of the serum tocopherol level to about two to three times the untreated control would be required before the adriamycin treatment to reduce its toxicity.
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PMID:Effect of vitamin E on toxicity and antitumor activity of adriamycin in mice. 310 29

The chemopreventive efficacies of selenate, selenite, selenium dioxide, selenomethionine and selenocystine were examined during the promotion phase of carcinogenesis in the 7,12-dimethylbenz[a]anthracene-induced mammary tumor model in rats. Each agent was added to the diet at a final concentration of 3 p.p.m. selenium. In general there was no significant difference in the potency of these five selenium compounds in inhibiting the development of mammary tumors. The interaction of vitamin E (500 p.p.m.) with either selenite or selenomethionine was further characterized in a second carcinogenesis study. Results of this experiment suggested that vitamin E enhanced the protective effect of selenite but not that of selenomethionine. In an attempt to explore the synergistic mechanism of selenium and vitamin E, the effects of these two agents on mitogen-induced blastogenesis and natural killer cytotoxic activity were also investigated. No consistent changes in these in vitro immune functions were detected resulting from supranutritional feeding of either selenite or vitamin E or both. The metabolism of inorganic versus organic selenium was discussed in relation to their role in the control of neoplastic growth as well as to their selective modulation by vitamin E.
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PMID:Mammary cancer chemoprevention by inorganic and organic selenium: single agent treatment or in combination with vitamin E and their effects on in vitro immune functions. 311 43

Oxidative stress has been suggested to play an integral role in the cancer process. It may be particularly significant during tumor progression, where there is likely to be a large amount of free radicals generated by infiltrating inflammatory cells and dying tumor cells. In order to test this hypothesis, a variety of free radical scavengers and antioxidants were assessed for their ability to inhibit tumor progression. The murine skin multistage carcinogenesis model was used to generate papillomas, which are a population of putative precancerous lesions. Various test agents were applied topically to papillomas in order to determine if they would decrease the incidence of the malignant lesion, squamous cell carcinoma. The agents tested included: reduced glutathione (GSH), butylated hydroxyanisole, vitamin E, copper(II) (3,5-diisopropylsalicylate)2, sodium benzoate, N-acetyl cysteine and disulfiram. Under the conditions of our experiments, only GSH and disulfiram inhibited tumor progression to a significant degree. Additional studies indicated that GSH prevented cancer development in a dose-dependent manner. Another experiment demonstrated that when papillomas received repeated topical applications of diethylmaleate, a GSH-depleting agent, tumor progression was enhanced. Collectively these data suggest that sufficient glutathione levels may be important in preventing cancer formation.
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PMID:Effect of exogenous glutathione on tumor progression in the murine skin multistage carcinogenesis model. 313 44

Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of two murine neuroblastomas (C1300, NS-20) was investigated in vivo. Five groups of mice were prepared; group 1 were fed the control diet, group 2 were fed a vitamin E-deficient diet, group 3 were fed a vitamin E-supplemented diet, group 4 were fed the control diet and plus vitamin E solution given intraperitoneally during the treatment (solvent i.p. group), and group 5 were given vitamin E in the same manner (20 mg/kg/day; vitamin E i.p. group). Cisplatin (6 mg/kg) was injected intraperitoneally into the mice of each group during the treatment. In case of the C1300 neuroblastoma, the antitumor activity of cisplatin was most enhanced in the mice receiving vitamin E i.p., and the intra-tumor vitamin E and platinum levels were significantly higher in this group than in the other groups (P less than 0.01, and P less than 0.05 respectively). In contrast, in animals transplanted with the NS-20 murine neuroblastoma, which proved to be a cisplatin-tolerant tumor in separate experiments, no combined effect of those drugs was observed, although the intra-tumor level of platinum was elevated. The possibility was that vitamin E increases the influx of cisplatin into the tumor cells and acts after incorporation of cisplatin through the plasma membrane. Vitamin E did not accentuate the cisplatin-induced renal impairment in vitamin E-loaded groups. Those results suggested that vitamin E should be considered as a co-agent of cisplatin for the treatment of neuroblastoma.
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PMID:Combined effects of vitamin E (alpha-tocopherol) and cisplatin on the growth of murine neuroblastoma in vivo. 320 17

Chemoprevention of various epithelial cancers with vitamins or minerals has been the subject of multiple intervention trials to assess the impact of supplementation. These include several trials in patients with adenomatous polyps of the colon, a precursor lesion for colon cancer. The authors interviewed 255 women who underwent colonoscopy at Columbia Presbyterian Medical Center between 1983 and 1985 with a telephone-administered structured questionnaire. Eleven interviews were excluded for various reasons. Overall, 57.7 percent of the 244 interviewees used vitamin pills on a regular basis (at least once a week for a year); 6.6 percent of the interviewees used vitamin A, 20.7 percent used vitamin C, and 16.2 percent used vitamin E. There were no statistically significant differences in vitamin usage among women with adenomatous polyps of the colon (105 cases), women with colon cancer (56 cases), and women without colonic neoplasia (83 cases). Despite widespread use of supplementary vitamins, this study failed to demonstrate major benefits in preventing colon polyps or cancer.
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PMID:Vitamin supplements among women with adenomatous polyps and cancer of the colon. Preliminary findings. 337 66

Adriamycin used in combination with vitamin E (Tocopherol) was evaluated in the treatment of Nb rat prostate adenocarcinoma. Vitamin E has been shown to enhance the growth-inhibitory effects of adriamycin on human prostatic carcinoma cells in vitro. The adriamycin-vitamin E treatment groups had the lowest average final tumor volume, but the mortality rate was 57% (17/30). These results suggest that vitamin E may play a role in enhancing the cytotoxic effects of adriamycin, but may not have any protective effect on normal cells as previously suggested through in vitro methods.
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PMID:Adriamycin-vitamin E combination therapy for treatment of prostate adenocarcinoma in the Nb rat model. 341 71

Vitamin E was shown to regress established epidermoid carcinomas of Syrian hamster buccal pouch in 20 experimental animals following tumor induction by applications three times a week of 0.5% 7,12-dimethylbenz[a]anthracene (CAS: 57-97-6) in mineral oil for 13 weeks. The vitamin E was injected into the tumor-bearing buccal pouch twice weekly for 4 weeks in a dose of 250 micrograms in minimum essential medium. Twenty animals were maintained as untreated controls, and another 20 animals were sham-inoculated vehicle controls. Microscopic examination of buccal pouches with regressed tumor showed small epidermoid carcinomas with degeneration of tumor cells and a dense infiltrate of leukocytes, lymphocytes, and histiocytes. Buccal pouches of control animals showed large well-differentiated or moderately differentiated epidermoid carcinomas. The hamster buccal pouch cancer model presents many similarities to human oral cancer, including expression of the same oncogene, and these results offer hope for the chemotherapy of human oral cancer with the use of a relatively nontoxic agent injected locally.
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PMID:Regression by vitamin E of experimental oral cancer. 347 5

The effects of cabbage and vitamin E on colon carcinogenesis were investigated in Swiss mice treated with 1,2-dimethylhydrazine. Throughout the experiment the mice were fed a laboratory chow diet (46 mg vitamin E per kg) or chow containing 13 g cabbage per 100 g or 180 mg vitamin E per kg. Starting after 31 days of diet treatment the mice received 7 weekly s.c. injections of DMH. They were sacrificed 17 weeks after the first dose of DMH. While diet did not significantly alter colon tumor response, some trends were observed. Female mice given cabbage had a higher incidence (percent of mice with a tumor) and multiplicity (tumors per tumor bearing mouse) of colon tumors. Males were little affected by cabbage apart from a lower incidence of adenocarcinomas. Compared with mice fed the control diet those given vitamin E had a higher colon tumor incidence. This effect, which was stronger in females, was due to an increased incidence of adenomas. Vitamin E had little apparent affect on tumor multiplicity apart from a reduction in adenocarcinomas in females and adenomas in males. The data do not support the view that cabbage and vitamin E are protective against colon cancer.
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PMID:Cabbage and vitamin E: their effect on colon tumor formation in mice. 356 89

The effect of both a vitamin E-deficient and a high polyunsaturated fat (PUFA) diet was tested on rats injected with the colon carcinogen 1,2-dimethylhydrazine (DMH). In vivo lipid peroxidation was monitored by measuring exhaled ethane from the animals. Higher mean weights were found in animals fed high PUFA and vitamin E-sufficient diets. There was no difference in ethane exhalation between DMH-treated and control animals regardless of diet. Mean ethane exhalation was highest in animals fed either vitamin E-deficient or high PUFA diets. There was no difference in tumor formation between the vitamin E-deficient and the vitamin E-sufficient groups. The high PUFA groups had more tumors than the low PUFA groups. Diet was shown to be the major factor affecting ethane exhalation. There was no evidence that vitamin E-deficiency promoted DMH-induced tumors or that DMH caused increased lipid peroxidation.
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PMID:In vivo ethane production in vitamin E-deficient rats with DMH-induced colon cancer. 365 79

High intakes of some fat-soluble vitamin or trace metals have been associated with a decreased risk of cancer. A mechanism to help explain their anticancer action might be immunosuppression during deficiency or immuno-enhancement with high intakes. In vitro, retinol suppressed T-lymphocyte functions, whereas high dietary vitamin A enhanced macrophage functions. High intakes of vitamin E can enhance some anticancer, immune defenses. Selenium excess was not very suppressive of immune functions in vitro, but did retard tumor cell growth. Selenium and zinc deficiencies are associated with immunosuppression. Enhanced immune functions by high intakes of trace elements and vitamins provide a mechanism to explain in part the concomitant decreased cancer incidence.
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PMID:Immunological enhancement by fat-soluble vitamins, minerals, and trace metals: a factor in cancer prevention. 373 Nov 96


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