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Prenatal Exposure to Sodium Arsenite Alters Placental Glucose 1, 3, and 4 Transporters in Balb/c Mice.

Gutiérrez-Torres DS, González-Horta C, Del Razo LM, Infante-Ramírez R, Ramos-Martínez E, Levario-Carrillo M, Sánchez-Ramírez B - Biomed Res Int (2015)

Bottom Line: Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased.In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm.The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

View Article: PubMed Central - PubMed

Affiliation: Programa de Maestría en Ciencias en Biotecnología, Facultad de Ciencias Químicas, Universidad Autónoma de Chihuahua, Circuito No. 1 Nuevo Campus Universitario, 31125 Chihuahua, CHIH, Mexico.

ABSTRACT
Inorganic arsenic (iAs) exposure induces a decrease in glucose type 4 transporter (GLUT4) expression on the adipocyte membrane, which may be related to premature births and low birth weight infants in women exposed to iAs at reproductive age. The aim of this study was to analyze the effect of sodium arsenite (NaAsO2) exposure on GLUT1, GLUT3, and GLUT4 protein expression and on placental morphology. Female Balb/c mice (n = 15) were exposed to 0, 12, and 20 ppm of NaAsO2 in drinking water from 8th to 18th day of gestation. Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy. NaAsO2 exposure induced a significant decrease in fetal and placental weight (P < 0.01) and increases in infarctions and vascular congestion. Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased. In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm. The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

No MeSH data available.


Related in: MedlinePlus

Immunelocalization of glucose transporters in placenta of female mice. The photomicrographs represent immunelocalization of GLUT transporters in placenta from nonexposed females. Samples were counterstained with hematoxylin after an immunohistochemical procedure. (a), (c), and (e) show a positive signal for GLUT1, 3, and 4, respectively, (arrows) in mouse placenta. GLUT1 was identified on both sides of the maternal-fetal interface while GLUT3 was localized mainly in the fetal endothelium. GLUT4 was detected in both syncytiotrophoblast and stromal cells. Positive controls were mounted in rat tissues: (b) heart for GLUT1; (d) testis for GLUT3; and (f) heart for GLUT4. The signal for GLUT1 and GLUT4 was localized on myocytes sarcoplasm and GLUT3 in cytosol of Sertoli cells. ME: maternal erythrocyte; FE: fetal erythrocyte. Magnification 60x.
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fig2: Immunelocalization of glucose transporters in placenta of female mice. The photomicrographs represent immunelocalization of GLUT transporters in placenta from nonexposed females. Samples were counterstained with hematoxylin after an immunohistochemical procedure. (a), (c), and (e) show a positive signal for GLUT1, 3, and 4, respectively, (arrows) in mouse placenta. GLUT1 was identified on both sides of the maternal-fetal interface while GLUT3 was localized mainly in the fetal endothelium. GLUT4 was detected in both syncytiotrophoblast and stromal cells. Positive controls were mounted in rat tissues: (b) heart for GLUT1; (d) testis for GLUT3; and (f) heart for GLUT4. The signal for GLUT1 and GLUT4 was localized on myocytes sarcoplasm and GLUT3 in cytosol of Sertoli cells. ME: maternal erythrocyte; FE: fetal erythrocyte. Magnification 60x.

Mentions: GLUT1, GLUT3, and GLUT4 were expressed in the labyrinth (Figure 2); in the case of GLUT1, protein expression was identified on both sides of the maternal-fetal interface, mainly in the brush border of the syncytiotrophoblast layer (Figure 2(a)) and weakly in the fetal endothelium. In the case of GLUT3, protein expression was localized mainly in syncytiotrophoblast layer (Figure 2(c)). Finally, GLUT4 expression showed the same pattern as that observed for GLUT1; the protein was expressed on both sides of the maternal-fetal interface (Figure 2(e)). No changes in the localization of GLUT transporters were detected in placentas from females exposed to NaAsO2 (data not shown). The controls for antibody heterologous recognition using rat heart (GLUT1; Figure 2(b) and GLUT4; Figure 2(f)) and rat testis (GLUT3; Figure 2(d)) showed strong signal for each protein.


Prenatal Exposure to Sodium Arsenite Alters Placental Glucose 1, 3, and 4 Transporters in Balb/c Mice.

Gutiérrez-Torres DS, González-Horta C, Del Razo LM, Infante-Ramírez R, Ramos-Martínez E, Levario-Carrillo M, Sánchez-Ramírez B - Biomed Res Int (2015)

Immunelocalization of glucose transporters in placenta of female mice. The photomicrographs represent immunelocalization of GLUT transporters in placenta from nonexposed females. Samples were counterstained with hematoxylin after an immunohistochemical procedure. (a), (c), and (e) show a positive signal for GLUT1, 3, and 4, respectively, (arrows) in mouse placenta. GLUT1 was identified on both sides of the maternal-fetal interface while GLUT3 was localized mainly in the fetal endothelium. GLUT4 was detected in both syncytiotrophoblast and stromal cells. Positive controls were mounted in rat tissues: (b) heart for GLUT1; (d) testis for GLUT3; and (f) heart for GLUT4. The signal for GLUT1 and GLUT4 was localized on myocytes sarcoplasm and GLUT3 in cytosol of Sertoli cells. ME: maternal erythrocyte; FE: fetal erythrocyte. Magnification 60x.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4538324&req=5

fig2: Immunelocalization of glucose transporters in placenta of female mice. The photomicrographs represent immunelocalization of GLUT transporters in placenta from nonexposed females. Samples were counterstained with hematoxylin after an immunohistochemical procedure. (a), (c), and (e) show a positive signal for GLUT1, 3, and 4, respectively, (arrows) in mouse placenta. GLUT1 was identified on both sides of the maternal-fetal interface while GLUT3 was localized mainly in the fetal endothelium. GLUT4 was detected in both syncytiotrophoblast and stromal cells. Positive controls were mounted in rat tissues: (b) heart for GLUT1; (d) testis for GLUT3; and (f) heart for GLUT4. The signal for GLUT1 and GLUT4 was localized on myocytes sarcoplasm and GLUT3 in cytosol of Sertoli cells. ME: maternal erythrocyte; FE: fetal erythrocyte. Magnification 60x.
Mentions: GLUT1, GLUT3, and GLUT4 were expressed in the labyrinth (Figure 2); in the case of GLUT1, protein expression was identified on both sides of the maternal-fetal interface, mainly in the brush border of the syncytiotrophoblast layer (Figure 2(a)) and weakly in the fetal endothelium. In the case of GLUT3, protein expression was localized mainly in syncytiotrophoblast layer (Figure 2(c)). Finally, GLUT4 expression showed the same pattern as that observed for GLUT1; the protein was expressed on both sides of the maternal-fetal interface (Figure 2(e)). No changes in the localization of GLUT transporters were detected in placentas from females exposed to NaAsO2 (data not shown). The controls for antibody heterologous recognition using rat heart (GLUT1; Figure 2(b) and GLUT4; Figure 2(f)) and rat testis (GLUT3; Figure 2(d)) showed strong signal for each protein.

Bottom Line: Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased.In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm.The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

View Article: PubMed Central - PubMed

Affiliation: Programa de Maestría en Ciencias en Biotecnología, Facultad de Ciencias Químicas, Universidad Autónoma de Chihuahua, Circuito No. 1 Nuevo Campus Universitario, 31125 Chihuahua, CHIH, Mexico.

ABSTRACT
Inorganic arsenic (iAs) exposure induces a decrease in glucose type 4 transporter (GLUT4) expression on the adipocyte membrane, which may be related to premature births and low birth weight infants in women exposed to iAs at reproductive age. The aim of this study was to analyze the effect of sodium arsenite (NaAsO2) exposure on GLUT1, GLUT3, and GLUT4 protein expression and on placental morphology. Female Balb/c mice (n = 15) were exposed to 0, 12, and 20 ppm of NaAsO2 in drinking water from 8th to 18th day of gestation. Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy. NaAsO2 exposure induced a significant decrease in fetal and placental weight (P < 0.01) and increases in infarctions and vascular congestion. Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased. In contrast, GLUT4 expression was significantly lower (P < 0.05) in placentas from females exposed to 12 ppm. The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

No MeSH data available.


Related in: MedlinePlus