Calcium regulation and physiological function in animals exposed to lead Public Deposited

http://ir.library.oregonstate.edu/concern/graduate_thesis_or_dissertations/cf95jg12b

Descriptions

Attribute NameValues
Creator
Abstract or Summary
  • Tissue distribution studies of calcium and lead in brain tissue of rats were increased subsequent to a single intravenous injection of lead, 10 mg/kg, in the form of lead acetate. Time-course studies demonstrated that brain concentrations of calcium and lead (in terms of wet tissue weight) were found to be increased at days 1, 3 and 7 post treatment. At 24 hours brain levels of calcium and lead were elevated 70 and 350% respectively. Over the subsequent 48 hours, brain levels of calcium reached maximal values and brain lead decreased slightly from day 1 values. At the end of 7 days, brain concentrations of calcium and lead were still elevated significantly above controls. The effect of lead on calcium in liver, heart, kidney, skeletal muscle, smooth muscle, hair, bone and serum of lead-exposed rats were not significantly altered. Studies were undertaken to determine if the effect was mediated by the thyroid-parathyroid complex. Calcium concentrations in the brain of lead-treated thyroparathyroidectomized (TX-PTX) rats were 30, 47 and 70% lower at days 1, 3 and 7, respectively, when compared to levels of intact lead-injected rats at 10 mg/kg. Brain levels of lead in lead-treated TX-PTX rats were comparable to levels in treated intact animals. This implies that the thyroparathyroid system was necessary for complete expression of increased levels of brain calcium, but not essential for lead distribution in brain tissue of rats. Concentrations of brain lead were dose related, but the effect of lead on brain calcium was not. At 5 mg/kg of lead, brain calcium was increased maximally after 24 hours when compared to the effects produced by other doses of lead, e.g. , 10, 25 and 50 mg/kg. At 72 hours, brain calcium was elevated about two-fold in lead-treated rats regardless of the dose of lead administered; these levels of calcium were found unchanged or slightly lower at 7 days. Doses of lead at 25 and 50 mg/kg were not associated with altered calcium levels in the other tissues. In comparison, levels of brain lead associated with the various doses of lead changed little over the same time-course except for the 50 mg/kg dose of lead; at this dose brain lead continued to increase over 7 days. Employment of dry tissue weight established that increased hydration of brain tissue was another effect of lead on brain tissue in lead-treated rats. This additional effect of lead was associated only with the 25 and 50 mg/kg doses and was prominent at days 3 and 7. Elevated brain concentrations of calcium and lead with increased brain water suggested that lead's actions were on the permeability of brain tissue. Alterations of biological parameters were determined in male rats chronically exposed to dietary lead, 300 parts per million for 8 weeks in the form of lead acetate. Equal concentrations of lead in water and in food differed in influencing various biological parameters. Whole-blood concentrations of lead were significantly elevated in all animals exposed to dietary lead. Lead-food and the combined effect of lead-water and lead-food significantly increased whole-blood levels of lead (10.5 and 17.9 μg/ 100 ml), respectively, above the levels in the lead-water group. Muscle concentrations of lead in the tibialis anterior of lead-food groups were increased significantly above the muscle levels in control, reconstituted food and lead-water groups. Absorption and distribution of lead depended on whether lead was administered in food or water. Calcium concentrations in brain, blood and muscle (tibialis anterior) and lead levels in brain tissues of rats fed lead in their chow were increased, although not statistically significant. These elevated levels were associated with altered neuromuscular parameters that were determined in situ. The ratio of muscle twitch amplitude/tetanus amplitude of the tibialis anterior was reduced significantly in the lead-food groups. Prolongation of the active state of contraction in tetanus due to increased intracellular calcium and/or lead's influence on the duration of the active state of muscle contraction mediated by the motor axons were suggested to account for the results. The tibialis anterior of lead-food groups tetanized at significantly lower frequencies than the other groups. Increased neuromuscular transmission and/or responsiveness at the junctional sites were suggested to explain these observations. It was not ascertained if elevated levels of calcium in blood, brain and muscle and/or the body burden of lead produced the alterations of the examined neuromuscular system. Infusion of calcium (120 mg/kg/hr) to intact and conscious rabbits caused progressive increases in the serum concentration of thyrocalcitonin as determined by radioimmunologic methods. The hormone was detected in the blood of six normal rabbits at a mean concentration of 0. 80 ng/ml ± S. E. 0. 25; an increased level of thyrocalcitonin was detected within 15 minutes after infusion of calcium, and peak concentrations were found during maximal hypercalcemia. Peak levels of thyrocalcitonin declined to pre-infusion levels within 30 minutes after cessation of calcium infusion in the normal rabbit. Also, the infusion of lead, 6 mg/kg/hr, tended to increase concomitantly serum calcium and thyrocalcitonin levels in rabbits, although the elevations were not statistically significant.
Resource Type
Date Available
Date Copyright
Date Issued
Degree Level
Degree Name
Degree Field
Degree Grantor
Commencement Year
Advisor
Academic Affiliation
Non-Academic Affiliation
Subject
Rights Statement
Peer Reviewed
Language
Digitization Specifications
  • File scanned at 300 ppi (Monochrome) using ScandAll PRO 1.8.1 on a Fi-6770A in PDF format. CVista PdfCompressor 5.0 was used for pdf compression and textual OCR.
Replaces
Additional Information
  • description.provenance : Approved for entry into archive by Patricia Black(patricia.black@oregonstate.edu) on 2013-11-22T21:24:25Z (GMT) No. of bitstreams: 1 HoffmanNorbertE1974.pdf: 811435 bytes, checksum: 26a9dead37afb1dc9a6f9755c08d4447 (MD5)
  • description.provenance : Approved for entry into archive by Kirsten Clark(kcscannerosu@gmail.com) on 2013-11-26T21:19:18Z (GMT) No. of bitstreams: 1 HoffmanNorbertE1974.pdf: 811435 bytes, checksum: 26a9dead37afb1dc9a6f9755c08d4447 (MD5)
  • description.provenance : Made available in DSpace on 2013-11-26T21:19:18Z (GMT). No. of bitstreams: 1 HoffmanNorbertE1974.pdf: 811435 bytes, checksum: 26a9dead37afb1dc9a6f9755c08d4447 (MD5) Previous issue date: 1973-08-31
  • description.provenance : Submitted by Madison Medley (mmscannerosu@gmail.com) on 2013-11-22T21:08:39Z No. of bitstreams: 1 HoffmanNorbertE1974.pdf: 811435 bytes, checksum: 26a9dead37afb1dc9a6f9755c08d4447 (MD5)

Relationships

Parents:

This work has no parents.

Last modified

Downloadable Content

Download PDF

Items