Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum cortisol and antigen-specific and polyclonal immunoglobulin G (IgG) concentrations were measured to investigate the relationship between vitamin A status and immune function in lambs. Twenty-four 3-mo-old crossbred ewe lambs weighing approximately 10 kg were each fed 900 g/d of a carotene-deficient diet. The 12 control lambs also received a 100,000 IU oral dose of vitamin A palmitate every 2 wk. All lambs were given primary and secondary antigenic challenges. Lambs were slaughtered at the end of the secondary challenge period. Liver vitamin A concentrations were greater (P less than .001) in the control animals (69.5 vs 1.3 micrograms/g wet tissue). Both groups of lambs exhibited a similar growth response until d 105, after which daily gain of the control lambs exceeded (P less than .03) that of the A-deficient lambs. Polyclonal serum IgG concentrations were greater (P less than .05) in the A-deficient lambs on d 49 to 124 and on d 151 (P less than .10). Ovalbumin-specific serum IgG concentrations tended to be greater in the control lambs throughout the primary and secondary challenge periods. Control lambs had greater titers on d 164 (P less than .07) and d 190 (P less than .03). Vitamin A status appeared to have no consistent effects on serum cortisol concentrations. Spleen weights were greater (P less than .002) in the A-deficient lambs. Lungs from 11 of 12 A-deficient lambs contained abscesses, as opposed to 1 of 12 for the control lambs. Both polyclonal and antigen-specific IgG concentrations were affected by vitamin A status. Serum cortisol concentrations did not appear to mediate this effect.
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PMID:Vitamin A deficiency: serum cortisol and humoral immunity in lambs. 231 33

The 100,000 x g supernatant (cytosolic) fraction of rat tissue homogenates catalyzes the oxidation of all-trans retinal to retinoic acid. Kidney, testis, and lung were the most active of the tissues examined. The presence of enzyme activity in liver and intestine could be detected only when a substrate concentration beyond the saturation point for retinal reductase was used. Spleen, brain, and plasma had no activity. Boiled supernatants did not catalyze the reaction. The enzymatic product was chemically and physically identified as retinoic acid. The cytosol of kidney tissue also catalyzed the conversion of retinol to retinoic acid. These data indicate that kidney tissue has the highest retinal oxidase activity and suggest that it may play a major role in the oxidative metabolism of retinol in the body.
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PMID:Enzymatic oxidation of all-trans retinal to retinoic acid in rat tissues. 317 18

Although the anticarcinogenic and antiproliferative effects of vitamin A (retinol) have been extensively studied in vitro, there are few data regarding the response of human tumor cells to this agent in vivo. We have studied the effects of retinol on the human breast carcinoma cell line, MDA-MB-231. Initial in vitro studies on monolayer cultures demonstrated a retinol-induced growth inhibition that was reversible as well as time and dose dependent. A similar dose-dependent decrease in tumor cell growth was shown in vivo when BALB/c-nu/nu (athymic) mice were inoculated s.c. with MDA-MB-231 cells and given graded nontoxic doses of retinol intragastrically for 3 weeks. Tumor cells were also inhibited from lung colonization as "artificial" metastatic lesions when injected i.v. into athymic mice following retinol treatment. Spleen cells from these mice were assayed for natural killer cells as determined by their cytotoxic activity on 51Cr-labeled target cells. There was no change in natural killer activity with any dose of retinol. We conclude that retinol has a dose-dependent antiproliferative effect on human breast carcinoma in vivo as well as in vitro. Further, the retinol-induced tumor inhibition seen in T-cell-deficient mice does not appear to be due to enhancement of host immunity and thus may be solely a direct effect of retinol on the tumor.
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PMID:Growth inhibition by retinol of a human breast carcinoma cell line in vitro and in athymic mice. 649 37