A study of histopathological effects and functional tests in liver and kidney of laboratory male mice treated with ammonium chloride

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Int. J. Biosci. 2016 and thereby cause decreasing of serum creatinine (Kumar et al., 2010). Also, they cause oxidation of molecular protein in serum and this may result in decreasing the total protein in serum (Ujjwal and Dey, 2010). Mostafa et al. (2009) mentioned that the free radicals caused a significant decrease in plasma proteins. Previous reports stated that ammonium (chloride/ acetate) salt induces ammonia toxicity party via oxidative stress, which leads to lipid peroxidation and free- radical generation (Essa and Subramanian, 2006). Moreover, the excess of ammonia intoxication leads to excessive activation of N-methyl-D aspartate (NMDA) receptors leading to neuronal degeneration and death (Subash and Subramanian, 2010). Also, the elevated levels of circulatory liver- markers and lipid peroxidation products in ammonium chloride in rats might be due to the liver damage caused by ammoniainduced free radical generation (Essa and Subramanian, 2006; Thenmozhi and Subramanian, 2011). In the present study, the administration of ammonium chloride caused a significant increase in the levels of serum lipids (cholesterol and triglycerides as indicated in Table (3). These findings indicate that hyperammoemia may be accompanied by complication of atherosclerosis. Some studies showed that the levels of serum and tissue lipid were elevated during hyperammonemic conditions (Lena and Subramanian, 2004; Lena and Subramanian, 2004; Eassa et al. 2010; Subash and Subramanian, 2012). It has been reported that ammonium (chloride/acetate) salts may deplete levels of α-KG and other Krebs cycle intermediates (Lena and Subramanian; 2004; Essa and Subramanian, 2006) and thus elevate the levels of acetyl coenzyme A. This acetyl Co A may be used for the synthesis of fatty acids and cholesterol, since fatty acids of different sources are used as substrates for synthesizing triglycerides and phospholipids. The elevated levels of acetyl CoA may increase levels of lipid profile (free fatty acids, triacylglycerols, phospholipids and cholesterol). Another important function of α-KG occurs in the formation of carnitine (Vijayakumar and Subramanian, 2010). Carnitine acts as a carrier of fatty acids into cell mitochondria so that proper catabolism of fats can proceed. Conclusion In conclusion, ammonium chloride causes direct hepatotoxicity and nephrotoxicity. The results indicate that the exposure of male mice to ammonium chloride affects both liver and kidneys, and this may be due to the generation of free radicals by showing their toxicity on liver and kidneys. Acknowledgement We would like thank Dr. Farhan Mohsen for his remarks value in paper output. References Campall JW. 1991. Excretory nitrogen metabolism. In: Prosser, C.L. (Ed.). Environmental and metabolic animal physiology. Wiley- Liss Inc., New York: 277- 324. Cooper AJL, Plum F. 1987. Biochemistry and physiology of brain ammonia. Physiological Reviews 67, 440-519. http://dx.doi.org/10.1016/j.ab.2015.11.0030003- 2697/© Cotran RS, Kumar V, Collins T. 1999. Robbins pathologic basis of diseases 6 th ed., Saunders Co., 543p. Essa MM, Ali AA, Waly MI, Guillemin GJ, Subramanian P. 2010. Effect of leaves on serum lipids in ammonium chloride induced experimental hyperammonemic rats. International Journal of Biologcal and Medical Research 3, 71-73. Essa MM, Subramanian P. 2006. Pongamia pinnata modulates oxidant- antioxidant imbalance during hyperammonemic rats. Fundamental & Clinical Pharmacology 3, 299-303. http://dx.doi.org/10.1111/j.14728206.2006.00410.x 191 Al-Ali et al.
Int. J. Biosci. 2016 Essa MM, Subramanian P. 2007. Hibiscus sabdariffa affects ammonium chloride-induced hyperammonemic rats, Evidence-Based Complementary and Alternative Medicine (eCAM) 4(3), 321-325. http://dx.doi.org/10.1093/ecam/nel087 Foster Smith Pharmacy. 2010. Patient information sheet. 139-146. http://dx.doi.org/10.1016/S0008993(00)02785-2 Kosenko E, Kaminsky Y, Lopata O, Muravyov N, Kaminsky H, Hermenegilioto C, FelipoV. 1998. Nitroarginine, an inhibitor of nitric oxide syntheses, prevents changes in superoxide radical and antioxidant enzymes induced by ammonia intoxication. Metabolic Brain Disease 13, 29-41. Gewitz HS. 1987. Reconstitution and crystallization experiments with isolated split proteins from Bacillus stearothrmophilus ribosome’s. International Journal of Biochemistry 15(5), 887-895. Hall J. 2015. Guyton and Hall textbook of medical physiology. 13 th ed., Saunders, p1043p. Harikrishnan B, Subramanian P, Subash S. 2008. Antihyperammonemia effect of Withania somnifera on ammonia induced wistar rat. Cell and Tissue Research 8, 1417-1420. Humason GL. 1972. Animal tissue techniques. 3 rd ,Freeman and Company, San Francisco, 641 p. Jawad AAH. 1996. Ethological studies in assessing the anti- aggressive effects of some Iraqi medicinal plant in laboratory mice (Mus musculus). thesis College of Education, University of Basrah: 204 pp.(In Arabic). King PR, King EJ. 1954. Estimation of plasma phosphatase by determination of hydrolysed phenol with amino-antipyrine. Journal of Clinical Pathology 7, 322-326. Klaassen CD, Watkins JB. 1999. Casarett and Doull’s toxicology: The basic science of poisons, 5 th ed., McGraw Hill, New York: P816 p. Kosenko E, Kaminsky Y, Stavroskaya IG, Felipo V. 2000. Alternation of mitochondrial calcium by ammonia-reduced activation of NMDA receptor in rat brain in vivo. Brain Research 880, Kumar R, Malhotra S, Kumar D. 2010. Antibiotic and free radical scavenging bpotential of Euphorbia hirta flower extract. Journal of Pharmaceutical Sciences 72(4), 533-537. http://dx.doi.org/10.4103/0250-474X.73921 Lena PJ, Subramaninan P. 2004. Effects of melatonin on the levels of antioxidants and lipid peroxidation products in the rats treated with ammonium acetate. Pharmazie 59, 636-639. Monfort P, Felipo V. 2005. Long-term potentiation in hippocampus involves sequential activation of soluble guanylate cycleas, Cgmpdependent protein kinase and Cgmp-depending phosphodisterase alteration in hyperammonemia. BMC. Pharmacology 5(Suppl 1), 66 o. http://dx.doi.org/10.1186/1471-2210-5-S1-P66 Mori S, Kaneko H, Mitsuma T. 1998. Implications of gastric topical bioactive peptides in ammonia-induced acute gastric mucosal lesions in rats. Scandinavian Journal of Gastroenterology 33(4), 386-393. http://dx.doi.org/10.1080/00365529850171017 Mostafa A, Saleh M, Bassam A, Samera A. 2009. Oxidative in blood of camels (Camelus dromedarius) naturally infected with Trypanosoma evansi. Veterinary Parasitology 162(3-4), 192-199. http://dx.doi.org/10.1016/j.vetpar.2009.03.035 Nelson DL, Lehninger AL, Cox MM. 2008. Lehininger principles of Biochemistry. W. H. Freeman, London: 1100 p. 192 Al-Ali et al.
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