The Effect of Lead (Pb) on Mice’s Parathyroid Gland’s Regulation of Calcium Level

Authors

  • Ruotong Zhang

DOI:

https://doi.org/10.61173/594yat07

Keywords:

Lead (Pb) Exposure, Parathyroid Hormone (PTH), Calcium-Sensing Receptor (CaSR), Vitamin D, Glutathione (GSH) Activity, Oxidative Stress, Flint Water Crisis, Calcium Homeostasis

Abstract

This study will use biochemical markers that include parathyroid hormone (PTH) levels, calcium-sensing receptor (CaSR) expression, Vitamin D levels, and glutathione (GSH) activity to study the effects of lead (Pb) exposure on mice. We can understand how Pb affects calcium regulation, oxidative stress response, and calcium homeostasis using these biomarkers. The experiment is conducted using ELISA, flow cytometry (FACS), and GSH assays with mice exposed to Pb. Our results suggest that lead exposure can lead to several outcomes: biomarkers are affected significantly, biomarkers are partially affected with some unchanged, and biomarkers are completely unaffected. These results are relevant to real world environmental health crises like the Flint water crisis because Pb contamination led to health problems. The goal of understanding the mechanisms of Pb toxicity is to help inform people to mitigate the negative effects of Pb exposure.

References

[1] Pauli, Benjamin J. “The Flint water crisis.” Wiley Interdisciplinary Reviews: Water 7.3 (2020): e1420.

[2] Hanna-Attisha, Mona, et al. “Elevated blood lead levels in children associated with the Flint drinking water crisis: a spatial analysis of risk and public health response.” American journal of public health 106.2 (2016): 283-290

[3] Wani, Ab Latif et al. “Lead toxicity: a review.” Interdisciplinary toxicology vol. 8,2 (2015): 55-64. doi:10.1515/ intox-2015-0009

[4] Needleman, H. L. (2004). Lead Poisoning. Annual Review of Medicine, 55(1), 209–222. doi:10.1146/annurev. med.55.091902.103653.

[5] Khalil, N., Morrow, L. A., Needleman, H., & Talbott, E. O. (2009). Lead exposure and endocrine function in boys at the age of pubertal onset. Environmental Research, 109(4), 418–424. doi:10.1016/j.envres.2009.02.010.

[6] Zhao, W., et al. (2006). “Lead exposure and calcium metabolism: a review.” Environmental Health Perspectives, 114(2), 224-229.

[7] Monir, A U et al. “The effect of lead on bone mineral properties from female adult C57/BL6 mice.” Bone vol. 47,5 (2010): 888-94. doi:10.1016/j.bone.2010.07.013

[8] Elisa Technical Guide, assets.thermofisher.com/TFS-Assets/ LSG/manuals/ELISA_guide_man.pdf. Accessed 31 Aug. 2024.

[9] McKinnon, Katherine M. “Flow Cytometry: An Overview.” Current protocols in immunology vol. 120 5.1.1-5.1.11. 21 Feb. 2018, doi:10.1002/cpim.40

[10] Glutathione Assay Kit, cdn.caymanchem.com/cdn/ Dean&Francis Ruotong Zhang insert/703002.pdf. Accessed 31 Aug. 2024.

[11] Duan, Yifei et al. “The Blood Lead Levels of Children and the Loss of Ca2+ from Neurons Owing to Lead.” International journal of environmental research and public health vol. 18,22 12051. 17 Nov. 2021, doi:10.3390/ijerph182212051

[12] Khan M, Jose A, Sharma S. Physiology, Parathyroid Hormone. [Updated 2022 Oct 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK499940/

[13] White, Elissa et al. “Pharmacochaperone-mediated rescue of calcium-sensing receptor loss-of-function mutants.” Molecular endocrinology (Baltimore, Md.) vol. 23,7 (2009): 1115-23. doi:10.1210/me.2009-0041

[14] Rahman, Abdur et al. “Lead Affects Vitamin D Metabolism in Rats.” Nutrients vol. 10,3 264. 26 Feb. 2018, doi:10.3390/ nu10030264

[15] Diamond, G L et al. “Gastrointestinal absorption of metals.” Drug and chemical toxicology vol. 20,4 (1997): 345-68. doi:10.3109/01480549709003892

[16] Lopes, Ana Carolina B Almeida et al. “Lead Exposure and Oxidative Stress: A Systematic Review.” Reviews of environmental contamination and toxicology vol. 236 (2016): 193-238. doi:10.1007/978-3-319-20013-2_3

[17] Janowiak, Blythe E et al. “Gamma-glutamylcysteine synthetase-glutathione synthetase: domain structure and identification of residues important in substrate and glutathione binding.” Biochemistry vol. 45,35 (2006): 10461-73. doi:10.1021/bi052483v

[18] Fleet, James C. “The role of vitamin D in the endocrinology controlling calcium homeostasis.” Molecular and cellular endocrinology vol. 453 (2017): 36-45. doi:10.1016/ j.mce.2017.04.008

[19] Mastali, Vahid Parvizi et al. “The effect of short-term vitamin D on the antioxidant capacity following exhaustive aerobic exercise.” African health sciences vol. 23,1 (2023): 584- 591. doi:10.4314/ahs.v23i1.61

[20] Xue, Yingben, and James C Fleet. “Intestinal vitamin D receptor is required for normal calcium and bone metabolism in mice.” Gastroenterology vol. 136,4 (2009): 1317-27, e1-2. doi:10.1053/j.gastro.2008.12.051Iamartino, Luca, and Maria Luisa Brandi. “The calcium-sensing receptor in inflammation: Recent updates.” Frontiers in physiology vol. 13 1059369. 18 Nov. 2022, doi:10.3389/fphys.2022.1059369

[21] Iamartino, Luca, and Maria Luisa Brandi. “The calciumsensing receptor in inflammation: Recent updates.” Frontiers in physiology vol. 13 1059369. 18 Nov. 2022, doi:10.3389/ fphys.2022.1059369

[22] Hewison, M et al. “1alpha-Hydroxylase and the action of vitamin D.” Journal of molecular endocrinology vol. 25,2 (2000): 141-8. doi:10.1677/jme.0.0250141

[23] Jones, Glenville et al. “25-Hydroxyvitamin D-24- hydroxylase (CYP24A1): its important role in the degradation of vitamin D.” Archives of biochemistry and biophysics vol. 523,1 (2012): 9-18. doi:10.1016/j.abb.2011.11.003

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Published

2024-12-31