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Observations on dietary aluminum level, time duration exposure to dietary aluminum, and the influence of specific dietary blocking agents on tissue aluminum accumulation in the rat
dc.contributor.advisor | Landmann, W. A. | |
dc.creator | Kettleson, Kenneth Carl Angus | |
dc.date.accessioned | 2020-09-02T21:04:56Z | |
dc.date.available | 2020-09-02T21:04:56Z | |
dc.date.issued | 1986 | |
dc.identifier.uri | https://hdl.handle.net/1969.1/DISSERTATIONS-23812 | |
dc.description | Typescript (photocopy). | en |
dc.description.abstract | Two experiments were conducted to observe the association of dietary aluminum (Al) with tissue Al accumulation. Other objectives included: to determine if alginic acid (AA) and pectin (P) in the diet could inhibit Al accumulation in tissues, and to relate time of exposure of dietary Al to Al tissue accumulation. The first experiment was conducted with a test diet feeding period of 35 days in a factorial arrangement of treatments with 24 rats, six rats per treatment. The dietary treatments were: groups 0 and 1, no added dietary Al (Al < 20 ppm) with or without 5% AA; groups 2 and 3, 400 ppm additional dietary Al with or without 5% AA. Kidney tissue analyzed by neutron activation showed no significant Al accumulation, or influence of the blocking agent. The second experiment was conducted over two time intervals (phase I with 24 rats for 28 days, and phase II with 26 rats for 56 days) and was done with 7 different diets. The diets included a control (basal with no added Al or blocking agent), the basal with 425 or 640 ppm Al added, with 5% AA or 5% P added to each Al test level. The Al source for both experiments was aluminum dibasic acetate. Tissues collected and pooled for analyses by inductively coupled plasma atomic emission spectroscopy included bone, brain, and kidney. The addition of 425 ppm Al to the diets stimulated body weight gain by about 10% relative to the controls. The blocking agents suppressed Al-induced weight gain, although AA stimulated feed intake (P < 0.05). Trends in Al accumulation appeared to occur in bone and brain tissues associated with dietary Al; but independent of blocking agents and independent of time exposure to the dietary Al. However, no statistical analyses were possible on the pooled tissue analytical means, and therefore, no conclusions can be drawn. We may speculate that in the rat the tissue residency half-life of Al is low, or that the tissues have a saturation limit. | en |
dc.format.extent | xi, 98 leaves | en |
dc.format.medium | electronic | en |
dc.format.mimetype | application/pdf | |
dc.language.iso | eng | |
dc.rights | This thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use. | en |
dc.rights.uri | http://rightsstatements.org/vocab/InC/1.0/ | |
dc.subject | Major nutrition | en |
dc.subject.classification | 1986 Dissertation K44 | |
dc.subject.lcsh | Aluminum | en |
dc.subject.lcsh | Toxicology | en |
dc.subject.lcsh | Aluminum | en |
dc.subject.lcsh | Physiological effect | en |
dc.subject.lcsh | Rats | en |
dc.subject.lcsh | Physiology | en |
dc.title | Observations on dietary aluminum level, time duration exposure to dietary aluminum, and the influence of specific dietary blocking agents on tissue aluminum accumulation in the rat | en |
dc.type | Thesis | en |
thesis.degree.grantor | Texas A&M University | en |
thesis.degree.name | Doctor of Philosophy | en |
thesis.degree.name | Ph. D | en |
dc.contributor.committeeMember | Ellis, William C. | |
dc.contributor.committeeMember | Greene, L. Wayne | |
dc.contributor.committeeMember | Nation, Jack R. | |
dc.type.genre | dissertations | en |
dc.type.material | text | en |
dc.format.digitalOrigin | reformatted digital | en |
dc.publisher.digital | Texas A&M University. Libraries | |
dc.identifier.oclc | 18055035 |
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