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GARCIA-SOLIS
Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion.Garcia-Solis
P, Alfaro Y, Anguiano B, Delgado G, Guzman RC, Nandi S, Diaz-Munoz M,
Vazquez-Martinez O, Aceves C.
“We analyzed the effect of molecular iodine
(I2), potassium iodide (KI) and a subclinical concentration of thyroxine
(T4) on the induction and promotion of mammary cancer induced by
N-methyl-N-nitrosourea. Virgin Sprague-Dawley rats received short or
continuous treatment. Continuous I2 treated rats exhibited a strong and
persistent reduction in mammary cancer incidence (30%) compared to
controls (72.7%). Interruption of short or long term treatments resulted
in a higher incidence in mammary cancer compared to the control groups.
The protective effect of I2 was correlated with the highest expression of
the I-/Cl- transporter pendrin and with the lowest levels of
lipoperoxidation expression in mammary glands. Triiodothyronine serum
levels and Na+/I- symporter, lactoperoxidase, or p53 expression did not
show any changes. In conclusion continuous I2 treatment has a potent
antineoplastic effect on the progression of mammary cancer and its effect
may be related to a decrease in the oxidative cell
environment.”
Differential uptake and signaling or molecular iodine (I2) in lactating, virgin, or neoplastic mammary glandsGarcia-Solis P, Delgado G, Anguiano B, Aceves C 13th International Thyroid Meeting, Buenos Aires, Arg. (Abstract) Thyroid 15 (Suppl 1) S-128. [abstract only]
Conclusion: 1) I2 is differentially taken up by lactating, virgin and neoplastic MG [mammary gland], suggesting the existence of mammary iodine uptake pathways in addition to NIS and PEN. 2) Gene expression of thyroid and MG is differentially regulated by I2.
5'Deiodinase in two breast cancer cell lines: effect of triiodothyronine, isoproterenol and retinoids.Garcia-Solis P, Aceves C. Mol Cell Endocrinol. 2003 Mar 28;201(1-2):25-31. Abstract only
"Thyroid hormones participate in the regulation of growth, development and energy expenditure of vertebrates. Type I (D1) and type II 5'deiodinases catalyze the peripheral conversion of the thyroid prohormone thyroxine to the active form triiodothyronine (T3). D1 is expressed in organs like liver, thyroid, and lactating mammary gland. This enzyme is regulated in an organ-specific manner by a wide number of factors like carbohydrates, T3, thyrotropin, and catecholamines. However, it has been shown that in several types of cancer the expression of D1 is reduced, lost, or regulated by different components. In the present work we describe the expression and regulation of 5'deiodinases in two breast cancer cell lines: MCF-7 (ovarian hormone-dependent) and MDA-MB-231 (ovarian hormone-independent). Our results showed that MCF-7 cells expressed D1 activity ( approximately 10 pmol I(-)/mg protein per h), which was stimulated only by retinoic acid treatments, but not by T3 or the beta-adrenergic agonist isoproterenol. In MDA-MB-231 cells, deiodinase activity was not detected in control conditions nor under any of these treatments. These results support the notion that D1 expression could represent a sensitive differentiation marker."
See also articles by Aceves.
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