The effect of oral administration of D-penicillamine on electrocardiogram parameters in pekin ducks poisoned with lead nitrate
Subject Areas : Journal of Comparative Pathobiologyhamed zarei 1 , Abdollah Kashani 2 , Azin Tavakoli 3
1 - Assistant Professor, Department of Physiology, Central Tehran Branch, Islamic Azad University, Tehran, Iran
2 - Department of Animal Sciences, Faculty of Agriculture, Garmsar Branch, Islamic Azad University, Garmsar, Iran
3 - Department of Clinical Sciences, Faculty of Veterinary Medicine, Garmsar Branch, Islamic Azad University, Garmsar, Iran
Keywords: D-penicillamine, Electrocardiography, Lead, Pekin duck,
Abstract :
Lead is known as one of the most important environmental pollutants for the body. The aim of this study is to evaluate the effect of oral administration of D-penicillamine on electrocardiogram parameters in ducks poisoned with lead nitrate. The number of 90 Pekin ducks divided into three groups of 30 including the negative control group, the positive control group (40 mg/kg of lead nitrate in the diet), and the treatment group (lead nitrate at a dose of 40 mg/kg + D-penicillamine at a dose of 20 mg/kg kg in the diet). In order to measure the height of the T, S, R complex components and the ST, RR, QT, QRS intervals and the electrical axis of the heart at the ages of 28 and 60 days, electrocardiogram strips were prepared from 8 chickens in each group. In the positive control group, the height of R, S, and T waves increased significantly compared to the negative control group (P<0.05). D-penicillamine prevented the abnormal increase of these waves in the treated groups, so that this reduction was significant in 60 days in the S wave of derivation III and aVF and the T wave in derivations II, III, aVF and aVR (P<0.05). Also, QRS and QT intervals increased significantly in some derivatives of the positive control group (P<0.05). In the group treated with D-penicillamine, no significant increase in these parameters was observed, so that this lack of increase in the QRS interval in lead II and aVF and in the ST interval of lead III was significant (P<0.05) at 60 days. Finally, it seems that the oral administration of D-penicillamine leads to the improvement of heart electrocardiogram indices in ducks suffering from lead nitrate poisoning.
1. Tuormaa TE. The adverse effects of lead. Journal of Nutritional Medicine. 1994;4(4):449-61.
2. Kurnia KA, Ruhyat K, Sofjan I, Diding L. Effect of phytate in diet and lead in drinking water on blood mineral and growth of ducks. Lucrari stiintifice Seria Zootehnie-Universitatea de Stiinte Agricole si Medicina Veterinara Ion Ionescu de la Brad (Romania). 2011.
3. Navas-Acien A, Guallar E, Silbergeld EK, Rothenberg SJ. Lead exposure and cardiovascular disease—a systematic review. Environmental health perspectives. 2007;115(3):472-82.
4. Ibrahim O, Al-sultan I, Makkawi T. Pathological changes induced by chromic exposure to lead acetate and treatment with
calcium disodium edetate in broilers. Published on line: 15th December. 2011.
5. Narayana K, Al-Bader M. Ultrastructural and DNA damaging effects of lead nitrate in the liver. Experimental and toxicologic pathology. 2011;63(1-2):43-51.
6. Revis N, Zinsmeister A, Bull R. Atherosclerosis and hypertension induction by lead and cadmium ions: an effect prevented by calcium ion. Proceedings of the National Academy of Sciences. 1981;78(10):6494-8.
7. van der Horst H, editor Poisoning with lead naphthenate after ingestion of aerosol lubricant in an African grey parrot. Proc Europ Conf Avian Med & Surg, The Netherlands; 1993.
8. Woerpel RW, Rosskopf W. HEAVY-METAL INTOXICATION IN CAGED BIRDS. 1. COMPENDIUM ON CONTINUING EDUCATION FOR THE PRACTICING VETERINARIAN. 1982;4(9):729-&.
9. Kirk RW, BONAGURA J. Current veterinary therapy IX. Small Animal Prac. 1986.
10. Degernes L, Frank R, Freeman M, Redig P, editors. Lead poisoning in trumpeter swans. Proc Annu Conf Assoc Avian Vet; 1989.
11. Martinez L, Jeffrey J, Odom T. Electrocardiographic diagnosis of cardiomyopathies in aves. Poultry and Avian Biology Reviews (United Kingdom). 1997.
12. Deng G, Zhang Y, Peng X, Guo D, Li C. Echocardiographic characteristics of chickens with ascites syndrome. British poultry science. 2006;47(6):756-62.
13. Kopp SJ, Perry Jr M, Glonek T, Erlanger M, Perry EF, Barany M, et al. Cardiac physiologic-metabolic changes after chronic low-level heavy metal feeding. American Journal of Physiology-Heart and Circulatory Physiology. 1980;239(1):H22-H30.
14. Arce-Menocal J, Avila-Gonzalez E, Lopez-Coello C, Martinez-Lemus L. Use of electrocardiography for genetic selection of broiler breeders: Effects on live performance and ascites incidence. Journal of applied poultry research. 2005;14(2):281-8.
15. Mao L, Huang C-H, Shao J, Qin L, Xu D, Shao B, et al. An unexpected antioxidant and redox activity for the classic copper-chelating drug penicillamine. Free Radical Biology and Medicine. 2020;147:150-8.
16. Lloyd M. Heavy metal ingestion: medical management and gastroscopic foreign body removal. Journal of the Association of Avian Veterinarians. 1992:25-9.
17. Maulik N, Engelman RM, Rousou JA, Flack III JE, Deaton D, Das DK. Ischemic preconditioning reduces apoptosis by upregulating anti-death gene Bcl-2. Circulation. 1999;100(suppl_2):II-369-Ii-75.
18. Lyle W. Penicillamine in metal poisoning. The Journal of rheumatology Supplement. 1981;7:96-9.
19. González-Ramírez D, Zuñiga-Charles M, Narro-Juárez A. Mobilization of lead in patients with chronic poisoning by that metal. Oral penicillamine. Archivos de Investigacion Medica. 1990;21(3):279-83.
20. Golalipour MJ, Roshandel D, Roshandel G, Ghafari S, Kalavi M, Kalavi K. Effect of lead intoxication and D-penicillamine treatment on hematological indices in rats. International Journal of Morphology. 2007;25(4):717-22.
21. Gurer H, Ercal N. Can antioxidants be beneficial in the treatment of lead poisoning? Free Radical Biology and Medicine. 2000;29(10):927-45.
22. Myerson RM, Eisenhauer JH. Atrioventricular conduction defects in lead poisoning. The American Journal of Cardiology. 1963;11(3):409-12.
23. Pirkle JL, Schwartz J, Landis JR, Harlan WR. The relationship between blood lead levels and blood pressure and its cardiovascular risk implications. American journal of epidemiology. 1985;121(2):246-58.
24. Myerburg RJ. Sudden cardiac death in persons with normal (or near normal) hearts. The American journal of cardiology. 1997;79(6):3-9.
25. Kopp S, Glonek T, Erlanger M, Perry E, Perry H, Barany M. Cadmium and lead effects on myocardial function and metabolism. J Environ Pathol Toxicol. 1980;4(3):205-27.
26. Kober TE, Cooper GP. Lead competitively inhibits calcium-dependent synaptic transmission in the bullfrog sympathetic ganglion. Nature. 1976;262(5570):704-5.
27. Silbergeld EK, Fales JT, Goldberg AM. Evidence for a junctional effect of lead on neuromuscular function. Nature. 1974;247(5435):49-50.
28. Kopp SJ, Baker JC, D'Agrosa LS, Hawley PL. Simultaneous recording of his bundle electrogram, electrocardiogram, and systolic tension from intact modified Langendorff rat heart preparations I: Effects of perfusion time, cadmium, and lead. Toxicology and applied pharmacology. 1978;46(2):475-87.
29. Read JL, Williams JP. Lead myocarditis: Report of a case. American Heart Journal. 1952;44(5):797-802.
30. Dey S, Swarup D, Singh G. Effect of experimental lead toxicity on cardiovascular function in calves. Veterinary and human toxicology. 1993;35(6):501-3.
31. Prentice RC, Kopp SJ. Cardiotoxicity of lead at various perfusate calcium concentrations: functional and metabolic responses of the perfused rat heart. Toxicology and applied pharmacology. 1985;81(3):491-501.
32. Kopp SJ, Barron JT, Tow JP. Cardiovascular actions of lead and relationship to hypertension: a review. Environmental Health Perspectives. 1988;78:91-9.
33. STEWART AFR. The ventricular myosin heavy chain found in chicken striated muscles: The University of Chicago; 1991.
34. Williams BJ, Hejtmancik Jr MR, Abreu M, editors. Cardiac effects of lead. Federation Proceedings; 1983.
