Histopathological Study of the Rat Liver Exposed with Lead Acetate as a Microscopic Survey
Animal and Veterinary Sciences
Volume 3, Issue 5, September 2015, Pages: 141-143
Received: Jun. 26, 2015; Accepted: Aug. 10, 2015; Published: Sep. 6, 2015
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Authors
Khatere Khosravian Dehkordi, Department of Animal Physiology, Islamic Azad University, Shahrekord Branch, Shahrekord, Iran
Soraya khosravian Dehkordi, Department of Basic Sciences, Azad University of Shahrekord, Shahrekord, Iran
Rahmat Allah Fatahian Dehkordi, Department of Basic Sciences, Faculty of Veterinary Medicine, University of Shahrekord, Shahrekord, Iran
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Abstract
Lead is one of the environmental pollutants that can effect on the life of living animates in several ways; it has a long half-life and is collected in the soft tissue and conduct to adverse effects in tissues. The present study was performed to investigate the histological effects caused by lead in the rat liver. The study was conducted on 20 rat, the animals were divided into 2 equal groups. The first group received distilled water and considered as a control group. The second groups were orally administered lead acetate 8.5 mg/l of body weight for 20 weeks. The rats were anesthetized, the liver were removed for histological studies. Histological changes which observed in the liver were vacuolation, fatty degeneration, congestion within central veins, hemorrhage and infiltration of inflammatory cells. In this study, harmful toxic effects observed in liver of rats.
Keywords
Lead, Histological Alterations, Liver
To cite this article
Khatere Khosravian Dehkordi, Soraya khosravian Dehkordi, Rahmat Allah Fatahian Dehkordi, Histopathological Study of the Rat Liver Exposed with Lead Acetate as a Microscopic Survey, Animal and Veterinary Sciences. Vol. 3, No. 5, 2015, pp. 141-143. doi: 10.11648/j.avs.20150305.14
References
[1]
Hurst, H. E., Martin, M. D. 2004. Toxicology in Yagiela, J. A. ; Dowd, F. I. Neidle, E. A. Pharmacology and Therapeutic for Dentistry. 5th Edn., Mosby, USA,. pp. 829-48.
[2]
Silbergeld, E. K. 2005. Learners and learning in the twenty-first century: what do we know about students’ attitudes towards and experiences of information and communication technologies that will help us design courses? Stud High Educ, 30(3): 257-74.
[3]
Riaz, F., Khan, U. A., Ayub, M., Shaukat, S. 2011. Protective role of ginger on lead induced derangement in plasma testosterone and luteinizing hormone levels of male Sprague Dawley rats. J Ayub Med Coll Abbottabad, 23(4).
[4]
Tian, L., Lawrence, D. A. 1995. Lead inhibits nitric oxide production in vitro by murine splenic macrophages. ToxicolApplPharmacol, 132(1): 156-63.
[5]
Kosnett, M. J. 2004. Heavy Metal Intoxication and Chelators. In Katzung, B. G. Basic and Clinical Pharmacology. Mc Graw-Hill, New York. pp. 970-81.
[6]
Meyer, P. A., Brown, M. J., Falk, H. 2008. Global approach to reducing lead exposure and poisoning. Mutat Res - Rev Mut Res, 659(1): 166-75.
[7]
Goyer, R. A., Clarkson, T. W. 1996. Toxic effects of metals. Casarett&Doull’s Toxicology The Basic Science of Poisons, Fifth Edition, Klaassen, CD [Ed] McGraw-Hill Health Professions Division, ISBN, 71054766: pp. 811-67.
[8]
Loghman-Adham, M. 1997. Renal effects of environmental and occupational lead exposure. Environmental Health Perspectives, 105(9): 923-8.
[9]
Gidlow, D. A. 2004. Lead Toxicity. Depth Review Occupational Medicine, 54: 76-81.
[10]
Plumlee, K. H. 2004. Metals and Minerals in Clinical Veterinary Toxicology, 1st Edn. Mosby, U.S.A. pp. 193-230.
[11]
Durgut, R., Koc, A., Gonenci, R., Bal, R., Celik, S., Guzel, M., et al. 2008. Effects of high dose lead toxication on liver, kidneys, heart, brain and blood in rabbits: an experimental study. Journal of Applied Biological Sciences, 2(2): 11-8.
[12]
US-EPA. 1986. Air quality criteria document for lead (Pb), Vol. 4. Washington DC: US Environmental Protection Agency. PP. 264-7.
[13]
Piasek, M., Kostial, K., Bunarević, A. 1989. The effect of lead exposure on pathohistological changes in the liver and kidney in relation to age in rats. Arhivzahigijenuradaitoksikologiju, 40(1): 15-21.
[14]
Kojima, M., Sekikawa, K., Nemoto, K., Degawa, M. 2005. Tumor necrosis factor-α-independent downregulation of hepatic cholesterol 7α-hydroxylase gene in mice treated with lead nitrate. Toxicological Sciences, 87(2): 537-42.
[15]
Calabrese, E. J., Baldwin, L. A. 1992. Lead-induced cell proliferation and organ-specific tumorigenicity. Drug Metabolism Reviews, 24(3): 409-16.
[16]
Suzuki, T., Morimura, S., Diccianni, M. B., Yamada, R., Hochi, S.-i., Hirabayashi, M., et al. 1996. Activation of glutathione transferase P gene by lead requires glutathione transferase P enhancer I. Journal of Biological Chemistry, 271(3): 1626-32.
[17]
Gajawat, S., Sancheti, G., Goyal, P. 2005. Vitamin; C against Concomitant Exposure to Heavy Metal and Radiation: A Study on Variations in Hepatic Cellular Counts. Asian Journal of Experimental Sciences, 19(2): 53-8.
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