Increased bone calcium dissociation in lead-exposed rats

Main Article Content

Eko Suhartono
Yeni Wahyu Ulfarini
Triawanti Triawanti
Warih Anggoro Mustaqim
Rizky Taufan Firdaus
Muhammad Hafidz Maulana Setiawan


BACKGROUND Lead is still a major environmental and occupational health hazard, since it is extensively used in the production of paints, gasoline and cosmetics. This causes the metal to be ubiquitous in the environment, being found in the air, soil, and water, from which it can enter the human body by inhalation or ingestion. Absorbed lead is capable of altering the calcium levels in bone. The aim of this study was to demonstrate the effect of lead on bone calcium levels by measuring the reaction constant, Gibbs free energy, and enthalpy. METHODS This study was of pure experimental design using 100 male albino rats (Rattus norvegicus). The experimental animals were assigned by simple randomization to two groups, one group receiving lead acetate orally at a dosage of 100 mg/ kgBW, while the other group did not receive lead acetate. The intervention was given for 4 weeks and the rats were observed weekly for measurement of bone calcium levels by the permanganometric method. RESULTS This study found that k1 (hydroxyapatite dissociation rate constant) was 0.90 x 10-3 dt-1, and that k2 (hydroxyapatite association rate constant) was 6.16 x 10-3 dt-1 for the control group, whereas for the intervention group k1 = 26.20 x 10-3 dt-1 and k2 = 16.75 x 10-3 dt-1. Thermodynamically, the overall reaction was endergonic and endothermic (ΔG > 0 and ΔH > 0). CONCLUSIONS Lead exposure results in increased dissociation rate of bone in comparison with its association rate. Overall, the reaction was endergonic and endothermic (ΔG > 0 and ΔH > 0).

Article Details

How to Cite
Suhartono, E., Ulfarini, Y. W., Triawanti, T., Mustaqim, W. A., Firdaus, R. T., & Setiawan, M. H. M. (2012). Increased bone calcium dissociation in lead-exposed rats. Universa Medicina, 31(3), 151–158.
Review Article


Soemirat J, editor. Toksikologi lingkungan. Yogyakarta: Gadjah Mada University Press; 2004.

Drum DA. Are toxic biometals destroying your children’s future? Bio Metals 2009;22:679-700.

Patrick L. Lead toxicity, a review of the literature. Part I: Exposure, evaluation, and treatment. Altern Med Rev 2006;11:2-22.

Tan M, Meiri I. Hubungan kadar timbal dalam darah dengan kadar hemoglobin dan hematokrit pada petugas pintu tol Jagorawi. J Kesehatan Masyarakat Nasional 2011;6:35-41.

Devi OS, Suhartono E, Akbar IZ. Korelasi antara kadar glukosa darah dengan kadar kalsium tulang pada model tikus (Rattus novergicus) hiperglikemia. J Kedokter Yarsi 2010;18:114-

Patrick L. Lead toxicity Part II: The role of free radical damage and the use of antioxidants in the pathology and treatment of lead toxicity. Altern Med Rev 2006;1:114-27.

Prozialeck WC, Edwards JR, Nebert DW, Woods JM, Barchowsky A, Atchison WD. The vascular system as a target of metal toxicity. Toxicol Sci 2008;102:207–18.

Kaewboonchoo O, Morioka I, Saleekul S, Miyai N, Chaikittiporn C, Kawai T. Blood lead level and cardiovascular risk factors among bus drivers in Bangkok, Thailand. Ind Health 2010;48:61–5.

Ahmed YF, Mahmoud KGHM, Farghaly AA, Abo-Zeid MA, Ismail EM. Some studies on the toxic effects of prolonged lead exposure in male rabbits: chromosomal and testicular alterations.

Global Vet 2012;8:360-6.

Khan N, Naqvi A, Perveen K, Rafique M. Lead induced nephrotoxicity with special reference to proximal tubule in albino rats. Pakistan J Pharmacol 2008;25:29-35.

Adeniyi TT, Ajayi GO, Sado MA, Olopade HJ. Vitamin C and garlic (Allium sativum) ameliorate nephrotoxicity and biochemical

alterations induced in lead-exposed rats. J Med Med Sci 2012;3:273-80.

Vahedian M, Nabavizadeh F, Vahedian J, Keshavarz M, Nahrevanian H, Mirershadi F. Lead exposure changes gastric motility in rats: role of nitric oxide (NO). Arch Iran Med 2011;


Ahamed M, Akhtar MJ, Verma S, Kumar A, Siddiqui MKJ. Environmental lead exposure as a risk for childhood aplastic anemia. Bio Sci Trends 2011;5:38-43.

Todorovic T, Vujanovic D, Dozic I, Petkovic-Curcin A. Calcium and magnesium content in hard tissues of rats under condition of subchronic lead intoxication. Magnes Res 2008;21:43-50.

Martin RS, Henningsen RA, Suen A, Apparsundaram S, Leung B, Zhongjiang JZ, et al. Kinetic and thermodynamic assessment of binding of serotonin transporter inhibitors. J Pharmacol Exp Ther 2008;327:991-1000.

Bergethon PR. The physical basis of biochemistry. 2nd ed. New York: Springerlink;2010.

Toscano CD, Guilarte TR. Lead neurotoxicity: from exposure to molecular effects. Brain Res Rev 2005;49:529–54.

Conti MI, Bozzini C, Facorro GB, Lee CM, Mandalunis PM, Piehl LL, et al. Lead bone toxicity in growing rats exposed to chronic intermittent hypoxia. Bull Environ Contam Toxic 2012;89:693-8.

Fan G, Feng C, Li Y, Wang C, Yan J, Li W, et al. Selection of nutrients for prevention or amelioration of lead-induced learning and memory impairment in rats. Ann Occup Hyg 2009;53:341–51.

Mohamed HE, Alhaidary A, Beynen AC. Calcium metabolism in rats fed diets containing various concentrations of magnesium. Res J Biol Sci 2010;5:215-8.