Hepatotoxicity Studies in the Progeny of Pregnant Dams Treated With Methimazole, Monocrotophos and Lead Acetate

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Authors

  • K. Vanisthasree
     Department of Pharmacology and Toxicology, College of Veterinary Science, Rajendranagar, Hyderabad - 500 030 ,IN
  • A. Gopala Reddy
     Department of Pharmacology and Toxicology, College of Veterinary Science, Rajendranagar, Hyderabad - 500 03 ,IN
  • B. Kalakumar
     Department of Pharmacology and Toxicology, College of Veterinary Science, Rajendranagar, Hyderabad - 500 03 ,IN
  • C. Haritha
     Department of Pharmacology and Toxicology, College of Veterinary Science, Rajendranagar, Hyderabad - 500 03 ,IN
  • B. Anilkumar
     Department of Pharmacology and Toxicology, College of Veterinary Science, Rajendranagar, Hyderabad - 500 03 ,IN

Keywords:

Hepatotoxicity, lead acetate, methimazole, monocrotophos, rats
Immunology

Abstract

An experimental study was conducted to evaluate the hepatotoxic effects in the progeny of dams treated with methimazole, monocrotophos (MCP) and lead acetate. Female pregnant albino rats of Wistar Kyoto strain were divided into five groups and treated as follows, from day 3 of pregnancy till weaning of pups on postnatal day (PND) 21. Group 1 served as sham control, group 2 received methimazole 0.02% in drinking water, group 3 received MCP (0.3 mg/kg orally), group 4 received lead acetate at 0.2% in drinking water and group 5 received MCP + lead acetate. Thyroid hormone profile was recorded on 14th day of gestation in dams. Eight pups from each group were euthanized on PND 21 and 90, and liver tissues were collected for analysis. Thiobarbituric acid reactive substances (TBARS), protein carbonyls and reduced glutathione (GSH) of liver were studied on PND 21 and 90, while the activities of Na+/K+ ATPase and Mg2+ATPase in the liver were studied on PND 90. T3, T4, GSH, Na+/K+ ATPase and Mg2+ATPase were significantly (P<0.05) decreased, while TBARS and protein carbonyls were significantly (P<0.05) increased in all the test groups as compared to group 1. From this study, it is concluded that both MCP and lead acetate have a possible influence on thyroid gland of dams as the thyroid profile was altered significantly and the hepatotoxic effects were comparable to those induced by methimazole.

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Published

2018-05-21

How to Cite

Vanisthasree, K., Reddy, A. G., Kalakumar, B., Haritha, C., & Anilkumar, B. (2018). Hepatotoxicity Studies in the Progeny of Pregnant Dams Treated With Methimazole, Monocrotophos and Lead Acetate. Toxicology International, 18(1), 67–69. Retrieved from https://informaticsjournals.com/index.php/toxi/article/view/21315

Issue

Volume 18, Issue 1, January-June 2011

Section

Original Research
Received 2018-05-21
Accepted 2018-05-21
Published 2018-05-21

 

References

Dundar B, Oktem F, Arslan MK, Delibas N, Baykal B, Arslan C, et al. The effect of long-term low-dose lead exposure on thyroid function in adolescents. Environ Res 2006;101:140-5.

Gardella C. Lead exposure in pregnancy: A review of the literature and argument for routine prenatal screening. Obstet Gynecol Surv 2001;56:231-8.

Roberto R, Peter VDH, Greet S, Wojtek H, Zusana R, Mario B, et al. Lead neurotoxicity in children: Is prenatal exposure more important than postnatal exposure? Acta Paediatr 2006;95:45-9.

Li PJ, Sheng YZ, Wang QY, Gu LY, Wang YL. Transfer of lead via placenta and breast milk in human. Biomed Environ Sci 2000;13:85-9.

Zaidi SS, Bhatnagar VK, Gandhi SJ, Shah MP, Kulkarni PK, Saiyed HN. Assessment of thyroid function in pesticide formulators. Human Exp Toxicol 2000;19:497-501.

Balasubramanian KA, Manohar M, Mathan VI. An unidentified inhibitor of lipid peroxidation in intestinal mucosa. Biochim Biophys Acta 1988;962:51-8.

Levine RL, Garland D, Oliver CN, Amici A, Climent I, Lenz AG, et al. Determination of carbonyl content in oxidatively modified proteins. Methods Enzymol 1990;186:464-78.

Moron MS, Depierre JW, Mannervik B. Levels of glutathione, glutathione reductase and glutathione S transferase in rat lung and liver. Biochem Biophys Acta 1979;582:67-8.

Kiku N, Shiusuke K, Makoto N. Adenosine triphosphatase activity of erythrocyte membrane in hereditary spheocytosis. Life Sci 1967;6:595-600.

Wallace HA. Principles and Methods of Toxicology. 4th ed. Unites Kingdom: Taylor and Francis; 2001.

Lowry OH, Rosenbrough MJ, Farr AL, Rawdell RA. Protein measurement with the Folin phenol reagent. J Biol Chem 1951;193:265-75.

Schell LM, Gallo MV, Denham M, Ravenscroft J, DeCaprio AP, Carpenter DO. Relationship of thyroid hormone levels of polychlorinated biphenyls, lead, p,p,-DDE and other toxicants in Akwesasne Mohawk youth. Environ Health Perspect 2008;116:806-13.

Kang JK, Sul D, Nam SY, Kim HJ, Lee E. Effects of lead exposure on the expression of phospholipid hydroperoxide glutathione peroxidase mRNA in the rat brain. Toxicol Sci 2004;82:228-36.

Mohammad A, Sara M, Shirin P, Shahin S. Oxidative stress and cholinesterase inhibition in saliva and plasma of rats following subchronic exposure to malathion. Comp Biochem Physiol 2004;137:29-34.

Elvira LM, Laura C, Maria TA. Oxidative damage in liver after perinatal intoxication with lead and/or cadmium. J Trace Ele Med Biol 2007;21:210-6.

Nigam D, Shukla GS, Agarwal AK. Glutathione depletion and oxidative damage in mitochondria following exposure to cadmium in rat liver and kidney. Toxicol Lett 1999;106:151-7.

Siddiqui MK, Mahboob M, Mustafa M. Hepatic and extra hepatic glutathione depletion and glutathione-S-transferase inhibition by monocrotophos and its two thiol analogues. Toxicol 1990;64:271-9.

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