Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0240066 (iron deficiency)
 7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Natural killer (NK) cell activity is impaired in iron-deficient rats. Natural killer cells destroy tumor cells; therefore, iron-deficient rats may be less able to combat cancer growth. Natural killer cell cytotoxicity, both basal and interferon gamma (IFN gamma)-stimulated, was studied in moderately and severely iron-deficient rats challenged with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed ad libitum semipurified diets containing 8, 13 or 42 mg Fe/kg. A pair-fed group was fed the 42 mg Fe/kg diet at the level consumed by the 8 mg Fe/kg group. Following 6 wk of dietary treatment, DMBA-treated rats received a single intragastric dose of DMBA. Dietary treatment was continued. Rats were killed at 1, 4, 8, 14 and 20 wk post-DMBA treatment. Natural killer cell cytotoxicity (both basal and IFN gamma-stimulated) was analyzed. Feeding the 13 mg Fe/kg diet resulted in lower NK cell activity (P = 0.006) and greater tumor burden (P = 0.045) and tumor incidence. Interferon gamma treatment relieved the lower NK cell cytotoxicity observed in moderate iron deficiency. Feeding the 8 mg Fe/kg diet impaired NK cell activity (P = 0.006), but tumor burden and incidence were less than in moderate iron deficiency. In this model, iron deficiency, particularly moderate iron deficiency, contributed to cancer development and compromised NK cell cytotoxicity.
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PMID:Iron deficiency alters DMBA-induced tumor burden and natural killer cell cytotoxicity in rats. 172 72

Mammary tumor incidence, natural killer (NK) cell activity, and tumor necrosis factor-alpha (TNF-alpha) activity were measured in iron (Fe)-deficient and iron-replete rats treated with the carcinogen 7,12-dimethylbenz[a]anthracene (DMBA). Female weanling rats were fed AIN-76 diets: the iron-deficient group was fed 5 mg Fe/kg diet; the control group was fed 50 mg Fe/kg diet; the food-restricted group was fed 50 mg Fe/kg diet in the amount consumed by the iron-deficient group; and the replete group was fed 5 mg Fe/kg diet for 45 days and then 50 mg Fe/kg diet. After six weeks of feeding, the rats were given a single intragastric dose of DMBA. Feeding the iron-deficient diet for 20 weeks reduced hematocrit, hemoglobin, liver iron, and tumor iron values and increased spleen weight. Dietary iron repletion for 14 weeks reversed these effects of iron deficiency. Splenic NK cell cytotoxicity against YAC-1 cells was highest in the control group. Repleting rats with 50 mg Fe/kg diet corrected iron deficiency but did not restore NK cell cytotoxicity. No significant differences in macrophage TNF-alpha bioactivity were found among groups. Cumulative tumor incidence over all weeks was lowest in the iron-deficient rats. Iron repletion during the promotion phase of tumorigenesis attenuates the protective effects of iron deficiency. Food restriction to the extent present in the iron-deficient group did not protect against tumorigenesis. The iron-deficient group had the lowest tumor burden and delayed onset of tumors. Iron deficiency significantly reduces tumor incidence in DMBA-treated rats by mechanisms other than NK cell cytotoxicity, TNF-alpha activity, and food restriction.
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PMID:Iron repletion attenuates the protective effects of iron deficiency in DMBA-induced mammary tumors in rats. 858 49