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You searched for +publisher:"Texas A&M University" +contributor:("Villalobos, Alice R.A."). Showing records 1 – 3 of 3 total matches.

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Texas A&M University

1. Francis Stuart, Samantha D. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.

Degree: MS, Toxicology, 2014, Texas A&M University

Cadmium (Cd) is a toxic heavy metal with no known physiological function in higher order animals. Previous studies in primary cultures of neonatal rat choroid plexus (CP) epithelial cells indicated Cd induced oxidative stress and stimulated apical choline transport, and suggested zinc (Zn) supplementation might abate both oxidative stress and modulation of transport. The objective of this thesis was to elucidate how Zn, a nutritive mineral normally accumulated by CP, attenuated oxidative stress. I hypothesize that Zn, which can function as a pro-antioxidant, abates Cd-induced oxidative stress either by induction of metallothionein-1 (MT-1) or enhancement of glutathione (GSH) biochemistry. Thus, in primary cultures of neonatal rat CP epithelial cells, I characterized the effects of sub-micromolar Cd and efficacy of Zn supplementation to attenuate Cd-induced cellular and oxidative stress without or with manipulation of GSH synthesis. To characterize the Cd-induced stress response, CP epithelial cells were treated with 0 or 500 nM CdCl_(2) in serum-free medium (SFM) for 12 h; samples were collected at 3, 6, 9, and 12 h. Induction of heme oxygenase-1 (HO-1), heat-shock protein 70 (HSP70), and metallothionein-1 (MT-1) in Cd-treated cells was compared to time-matched controls by immunoblot and qRT-PCR analyses. Cd induced the catalytic and modifier subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. To elucidate the effects Zn supplementation in Cd-treated cells depleted of GSH, cells were supplemented for 48 h with 0 or 25 μM ZnCl_(2) alone or with 100 μM buthionine sulfoximine (BSO), an inhibitor of GCL, before treatment with 0 or 500 nM CdCl_(2) ± 100 μM BSO ± 10μM ZnCl_(2) in SFM for 12 h. By luminescence assay, intracellular GSH and oxidized glutathione (GSSG) concentrations were measured. Cd increased intracellular GSH and GSSG, but markedly decreased GSH:GSSG ratio. Inhibition of GSH synthesis exacerbated Cd-induced stress. However, Zn supplementation attenuated the stress response irrespective of BSO treatment, as per decreased induction of HSP70. These data indicate that CP adapts to low-dose Cd by up-regulation of stress proteins and GSH synthesis. Zinc supplementation also may attenuate Cd-induced cellular and oxidative stress, but cytoprotection is independent of GSH status. Advisors/Committee Members: Villalobos, Alice R.A. (advisor), Abbott, Louise (committee member), Tian, Yanan (committee member).

Subjects/Keywords: choroid plexus; cadmium; zinc; oxidative stress; glutathione; metallothionein; heat-shock protein 70; hemeoxygenase

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Francis Stuart, S. D. (2014). The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/152822

Chicago Manual of Style (16th Edition):

Francis Stuart, Samantha D. “The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.” 2014. Masters Thesis, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/152822.

MLA Handbook (7th Edition):

Francis Stuart, Samantha D. “The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus.” 2014. Web. 01 Mar 2021.

Vancouver:

Francis Stuart SD. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/152822.

Council of Science Editors:

Francis Stuart SD. The Pro-Antioxidant Role of Zinc Supplementation in Cadmium-Treated Choroid Plexus. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/152822


Texas A&M University

2. Elmore, Sarah Elizabeth. Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans.

Degree: PhD, Toxicology, 2016, Texas A&M University

Aflatoxins (AFs) are toxic metabolites produced by Aspergillus flavus and A. parasiticus. Fumonisins (FBs) are also toxic products of fungi, specifically Fusarium verticilloides and F. proliferatum. Both toxins commonly contaminate staple grains and cereals such as maize and groundnuts. Aflatoxin B1 (AFB1) is the most toxic and prevalent of the AFs. Chronic dietary exposure to AFs is a known risk factor for hepatocellular carcinoma and may also affect protein metabolism and the immune system. Fumonisin B1 (FB1) is the most abundant and toxicologically significant of the congeners. In populations where AFs and FBs are inextricable contaminants, a multi-faceted approach must be implemented to reduce exposure to these toxins, especially in the young who are more susceptible. Alternative methods such as calcium montmorillonite clay (UPSN or ACCS100) as an enterosorbent therapy that focus on reducing biological exposure to AFs and FBs in foods already contaminated are desirable as a secondary defense to the harmful effects of these toxins. Therefore, I propose to test the efficacy of UPSN in food matrices, identify populations at high risk for AFs and FBs with urinary biomarkers, and finally, combine clay technology and biomarker analysis to intervene with UPSN or ACCS100 in frequently exposed human populations. In these studies UPSN was able to significantly reduce AFB1 under common cooking conditions in a corn meal matrix suggesting a potential delivery of the clay directly in the contaminated food. A high prevalence of exposure to variable AFB1 and FB1 levels in participants from Monterrey, Mexico was observed. After a two week crossover trial in a high risk area of Kenya with 3.0g ACCS100/day mixed in water, urinary aflatoxin M1 (an AFB1 metabolite) was significantly reduced compared to the placebo group. ACCS100 was found to be safe and well tolerated suggesting potential for reducing exposure to AF in this particular population during outbreak situations. In a 3-month intervention with 3.0g or 1.5g ACCS100/day (encapsulated) in San Antonio, Texas, AFB1-lysine (an AFB1 protein adduct) was significantly reduced in the Low Dose group (1.5g) compared to Placebo. ACCS100 was well tolerated in the majority of participants and no significant changes in serum biochemistry or hematology were detected in any treatment group. Thus, use of calcium montmorillonite clay at doses as low as 1.5g/day and delivered in capsules, food, drink, or water may provide a viable strategy to reduce dietary AFB1 bioavailability in populations exposed to this toxin for up to 3 months. Moreover, AF and FB exposure is a global and unavoidable public health concern and biomarkers are important tools for monitoring exposure. Advisors/Committee Members: Phillips, Timothy D. (advisor), Harvey, Roger B. (committee member), Safe, Stephen H. (committee member), Villalobos, Alice R.A. (committee member).

Subjects/Keywords: Aflatoxin; Fumonisin; Calcium Montmorillonite Clay; ACCS100; UPSN; Enterosorption; Clay Mitigation Therapy; Biomarkers Of Exposure

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Elmore, S. E. (2016). Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/157053

Chicago Manual of Style (16th Edition):

Elmore, Sarah Elizabeth. “Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans.” 2016. Doctoral Dissertation, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/157053.

MLA Handbook (7th Edition):

Elmore, Sarah Elizabeth. “Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans.” 2016. Web. 01 Mar 2021.

Vancouver:

Elmore SE. Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans. [Internet] [Doctoral dissertation]. Texas A&M University; 2016. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/157053.

Council of Science Editors:

Elmore SE. Aflatoxin and Fumonisin Exposure: International Survey and Enterosorption Mitigation Strategy in Humans. [Doctoral Dissertation]. Texas A&M University; 2016. Available from: http://hdl.handle.net/1969.1/157053

3. Aquino, Mayra. Regulation of Zinc Transport in the Choroid Plexus.

Degree: MS, Food Science and Technology, 2014, Texas A&M University

The choroid plexus epithelium forms the blood-cerebrospinal fluid barrier, but also accumulates and transports nutritive minerals, such as zinc, into and out of the cerebrospinal fluid. The goal of this thesis was to analyze interdependent regulation of zinc transporters with metallothionein as the choroid plexus epithelium adapts to increases or decreases in extracellular zinc. My first objective was to characterize time-dependent changes in zinc transporter and MT-1 expression as extracellular zinc was pharmacologically depleted or supplemented. My second objective was to characterize changes in zinc transporter and MT-1 expression in response to exposure to prolactin. My experimental approach was to analyze gene expression of ZnT1, Zip1, Zip6, MT-1 and carbonic anhydrase (CA-2) in primary cell cultures of neonatal rat choroid plexus and isolated tissues in which extracellular zinc was depleted with 10 μM diethylene triamine pentaacetic acid or supplemented with 25 μM ZnCl_(2) for 48 h. Gene expression was analyzed by fluorescence quantitative real-time polymerase chain reaction. Zinc accumulation studies indicate choroid plexus cells maintain capacity to accumulate zinc, even when zinc is chelated. In cells, zinc depletion decreased expression of MT-1 and ZnT1 at 3 h and increased Zip1 expression; Zip6 expression fluctuated. In isolated tissues, zinc depletion down-regulated MT-1 and ZnT1 expression, while up-regulating Zip1 and Zip6 expression. In cells, zinc supplementation induced MT-1, ZnT1 and Zip6 expression at 3 h. Zip1 expression decreased at 3 h. In isolated tissues zinc supplementation up-regulated MT-1 and ZnT1 expression, but did not alter Zip1 and Zip6 expression. These data indicate there is coordinated regulation of MT-1 and zinc transporters as extracellular zinc altered. Prolactin up-regulated gene expression of CA-2, MT-1, ZnT-1 and Zip6 in choroid plexus cells. The JAK/STAT inhibitor AG-490 increased CA-2 and MT-1 expression, but decreased ZnT1 and Zip6 expression. AG-490 further increased expression of CA-2 and MT-1 in prolactin treated cells. This suggests the JAK/STAT signaling pathway might tonically suppress basal expression of MT-1 and CA-2. AG-490 partially reversed up-regulation of ZnT-1 and Zip6 expression by prolactin. These data indicate there is a coordinated regulation of MT-1 and zinc transporters during extracellular zinc depletion or supplementation. Advisors/Committee Members: Harris, Kerri B. (advisor), Villalobos, Alice R.A. (advisor), Gomes, Carmen L. (committee member).

Subjects/Keywords: Zinc; Choroid Plexus

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Aquino, M. (2014). Regulation of Zinc Transport in the Choroid Plexus. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/153201

Chicago Manual of Style (16th Edition):

Aquino, Mayra. “Regulation of Zinc Transport in the Choroid Plexus.” 2014. Masters Thesis, Texas A&M University. Accessed March 01, 2021. http://hdl.handle.net/1969.1/153201.

MLA Handbook (7th Edition):

Aquino, Mayra. “Regulation of Zinc Transport in the Choroid Plexus.” 2014. Web. 01 Mar 2021.

Vancouver:

Aquino M. Regulation of Zinc Transport in the Choroid Plexus. [Internet] [Masters thesis]. Texas A&M University; 2014. [cited 2021 Mar 01]. Available from: http://hdl.handle.net/1969.1/153201.

Council of Science Editors:

Aquino M. Regulation of Zinc Transport in the Choroid Plexus. [Masters Thesis]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/153201

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