Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury

Massaud S. Maamar; Mohamed A. Al-Griw; Rabia O. Al-Ghazeer; Seham A. Al-Azreg; Naser M. Salama; Emad M. Bennour

doi:doi:10.11648/j.ajbio.20160401.11

| Peer-Reviewed

Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury

Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, Emad M. Bennour

Published in American Journal of BioScience (Volume 4, Issue 1)

Received: 22 February 2016 Accepted: 1 March 2016 Published: 19 March 2016

Views: Downloads:

Download PDF

Share This Article

Twitter
Linked In
Facebook

Abstract

The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.

Published in	American Journal of BioScience (Volume 4, Issue 1)
DOI	10.11648/j.ajbio.20160401.11
Page(s)	1-8
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2016. Published by Science Publishing Group

Keywords

Environmental Toxicant, Spleen, Toxicity, Oxidative Stress, DNA Damage, Apoptosis, Mice

References

[1]	Wang, G., Wang, J., Ma, H., Ansari, G. A. S., and Khan, M. F. (2013) N-Acetylcysteine protects against trichloroethene-mediated autoimmunity by attenuating oxidative stress, Toxicology and Applied Pharmacology 273, 189-195.
[2]	Warren, D. A., Reigle, T. G., Muralidhara, S., and Dallas, C. (1998) Schedule-controlled operant behavior of rats during 1,1,1-trichloroethane inhalation: relationship to blood and brain solvent concentrations, Neurotoxicol Teratology 20, 143-153.
[3]	ATSDR:. Toxicological Profile for 1,1,1-trichloroethane (update). U. S. Department of Health and Human Services, Public Health Service. August 1995.
[4]	Mackay, C. J., Campbell, L., Samuel, A. M. (1987) Behavioral changes during exposure to 1,1,1-trichloroethane: time-course and relationship to blood solvent levels, American Journal Ind Medicine 11, 223–239.
[5]	Suttie, A. W. (2006) Histopathology of the Spleen, Toxicologic Pathology 34, 466-503.
[6]	Li, J. L., Li, H. X., Li, S., Tang, Z. X., Xu, S. W., Wang, X. L. (2010) Oxidative Stress-Mediated Cytotoxicity of Cadmium in Chicken Splenic Lymphocytes, Polish J. of Environ. Stud. 19, 947-956.
[7]	Gujral, J. S., Bucci, T. J., Farhood, A., and Jaeschke, H. (2001) Mechanism of Cell Death During Warm Hepatic Ischemia-Reperfusion in Rats: Apoptosis or Necrosis?, Histology 33, 397-405.
[8]	Gujral, J. S., Knight, T. R., Farhood, A., Bajt, M. L., and Jaeschke, H. (2002) Mode of cell death after acetaminophen overdose in mice: apoptosis or oncotic necrosis?, Toxicological Sciences 67, 322-328.
[9]	Khan, M. F., Wu, X., and Ansari, G. A. (2001) Anti-malondialdehyde antibodies inMRL+/+mice treatedwith trichloroethene and dichloroacetyl chloride: possible role of lipid peroxidation in autoimmunity, Toxicology Applied Pharmacology 170, 88-92.
[10]	Oates, J. C. (2010) The biology of reactive intermediates in systemic lupus erythematosus, Autoimmunity 43, 56-63.
[11]	Morgan, P. E., Sturgess, A. D., Davies, M. J. (2005) Increased levels of serum protein oxidation and correlation with disease activity in systemic lupus erythematosus, Arthritis Rheum 52, 2069-2079.
[12]	Ben Mansour, R., Lassoued, S., Elgaied, A., Haddouk, S., Marzouk, S., Bahloul, Z., Masmoudi, H., Attia, H., Aïfa, M. S., Fakhfakh, F. (2010) Enhanced reactivity to malondialdehydemodified proteins by systemic lupus erythematosus autoantibodies, Scand. J. Rheumatol 39, 247-253.
[13]	Wang, G., Pierangeli, S. S., Papalardo, E., Ansari, G. A., Khan, M. F. (2010) Markers of oxidative and nitrosative stress in systemic lupus erythematosus: correlation with disease activity, Arthritis Rheum 62, 2064-2072.
[14]	Melani, A., Pantoni, L., and Bordoni, F. (2003) The selective A2A receptor antagonist SCH 58261 reduces striatal transmitter outflow, turning behavior and ischemic brain damage induced by permanent focal ischemia in the rat, Brain Research 959, 243-250.
[15]	Lane, R. W., Riddle, B. L.; Borzelleca, J. F. (1982) Effects of 1,2-dichloroethane and 1,1,1-trichloroethane in drinking water on reproduction and development in mice., Toxicol Appl Pharmacology 63, 409–421.
[16]	Schalm, O. W., Jaim, N. C., and Carroll, E. J. (1975) Veterinary Haematology. 3rd (ed.) Lea. And Febiger, Philadelphia, U. S. A.
[17]	Burtis, C. A., Ashwood, E. R. (1999) Tietz Textbook of Clinical Biochemistry, 3rd. Ed., WB. Saunders Co, Tokyo. p.1034-54.
[18]	Zhang, Y. T., Zheng, Q. S., Pan, J., Zheng, R. L. (2004) Oxidative damage of biomolecules in mouse liver induced by morphine and protected by antioxidants, Basic Clin. Pharmacol. Toxicol. 95, 53-58.
[19]	Al-Griw, M. A., Salama, N. M., Treesh, S. A., Elnfati, A. H. (2015) Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk, International Journal of Genetics and Genomics 3, 43-49.
[20]	House, R. A., Liss, G. M., Wills, M. C., Holness, D. L. (1996) Paresthesias and sensory neuropathy due to 1,1,1-trichloroethane, Journal occupational environmental Medicine 38, 123-124.
[21]	Topham, J. C. (1980) Do induced sperm-head abnormalities in mice specifically identify mammalian mutagens rather than carcinogens, Mutat Res 74, 379-387.
[22]	Griffin, J. M., Blossom, S. J., Jackson, S. K., Gilbert, K. M., Pumford, N. R. (2000) Trichloroethylene accelerates an autoimmune response by Th1 T cell activation in MRL+/+ mice, Immunopharmacology 46, 123-137.
[23]	Wang, G., Cai, P., Ansari, G. A. S., and Khan, M. F. (2007) Oxidative and nitrosative stress in trichloroethene-mediated autoimmune response, Toxicology 229, 186–193.
[24]	Snyder, R., Andrews, L. S. (1996) Toxic effects of solvents and vapors. In: Klaassen, CD; ed. Casarett and Doull’s Toxicology: The Basis Science of Poisons, 5th ed. New York: McGraw-Hill.
[25]	Al-Griw, M. A., Salama, N. M., Treesh, S. A., Algadi, L. N., and Elnfati, A. H. (2015) Cell Death in Mouse Brain following Early Exposure to Trichloroethane (TCE), International Journal of Advanced Research 3, 1424-1430.
[26]	NTP. (2000) NTP technical report on the toxicity studies of 1,1,1-trichloroethane administered in microcapsules in feed to F344/N rats and B6C3F1 mice., National Toxicology Program. (41) NIH 004402.
[27]	EPA. (2007) Toxicological Review of 1,1,1-Trichloroethane (CAS No. 71-55-6) In Support of Summary Information on the Integrated Risk Information System (IRIS)., EPA/635/R-03/013. U. S. Environmental Protection Agency, Washington, DC..
[28]	WHO. (2003) 1,1,1-Trichloroethane in Drinking-water. Background document for development of
[29]	WHO Guidelines for Drinking-water Quality., World Health Organization WHO/SDE/WSH/03.04/65., 16.
[30]	ASTDR. (2006) 1,1,1 Trichloroethane, Agency for Toxic Substances and Disease Registry, 371.
[31]	Quast, J. F., Calhoun, L. L., and Frauson, L. E. (1988) 1,1,1-trichloroethane formulation: a chronic inhalation toxicity and oncogenicity study in Fischer 344 rats and B6c3F1 mice, Fundam Appl Toxicol 11, 611-625.
[32]	Tyson, C. A., Hawk-Prather, K., Story, D. L., and Gould, D. H. (1983) Correlations of in vitro and in vivo hepatotoxicity for five haloalkanes, Toxicol Appl Pharmacol 70, 289-302.
[33]	Bruckner, J. V., Kyle, G. M., Luthra, R., Acosta, D., Mehta, S. M., Sethuraman, S., and Muralidhara, S. (2001) Acute, short-term, and subchronic oral toxicity of 1,1,1-trichloroethane in rats, Toxicol Sci 60, 363-372.
[34]	Kinkead, E., and Leahy, H. (1987) Evaluation of the acute toxicity of selected groundwater contaminants., Harry G. Armstrong Aerospace Medical Research Lab (AAMRL-TR-87-021), 10.
[35]	Bogen, K., and Hall, L. ( 1989) Pharmacokinetics for regulatory risk analysis: The case of 1,1,1-trichloroethane (methyl chloroform)., Regul Toxicol Pharmacol 10, 26-50.
[36]	Hsu, H. C., Mountz, J. D. (2003) Origin of late-onset autoimmune disease, Immunol. Allergy Clin. North. Am 23, 65-82.
[37]	Balani, T., Agrawal, S., Thaker, A. M. (2008) Effects of imidacloprid a neonicotinoid insecticide on the immune system of white leghorn cockerels, Journal of Vet. Pharm. Toxicology 7, 27-30.
[38]	Eguchi, A., Wree, A., Feldstein, A. E. (2014) Biomarkers of liver cell death, Journal of Hepatology 60, 1063-1074.
[39]	Adedeji, O. B., Adeyemo, O. K., Agbede, S. A. (2009) Effects of diazinon on blood parameters in the African catfish (Clarias Gariepinus), Afr. J. Biotechnology 8, 3940-3946.
[40]	Hobara, T., Kobayashi, S., Higashihara, E. (1983) Changes in hematologic parameters with acute exposure to 1, l, l-trichloroethane, Ind Health 21, 255-261.

Cite This Article

Plain Text BibTeX RIS

APA Style

Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. (2016). Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. American Journal of BioScience, 4(1), 1-8. https://doi.org/10.11648/j.ajbio.20160401.11

Copy | Download

ACS Style

Massaud S. Maamar; Mohamed A. Al-Griw; Rabia O. Al-Ghazeer; Seham A. Al-Azreg; Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am. J. BioScience 2016, 4(1), 1-8. doi: 10.11648/j.ajbio.20160401.11

Copy | Download

AMA Style

Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am J BioScience. 2016;4(1):1-8. doi: 10.11648/j.ajbio.20160401.11

Copy | Download

@article{10.11648/j.ajbio.20160401.11,
  author = {Massaud S. Maamar and Mohamed A. Al-Griw and Rabia O. Al-Ghazeer and Seham A. Al-Azreg and Naser M. Salama and Emad M. Bennour},
  title = {Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury},
  journal = {American Journal of BioScience},
  volume = {4},
  number = {1},
  pages = {1-8},
  doi = {10.11648/j.ajbio.20160401.11},
  url = {https://doi.org/10.11648/j.ajbio.20160401.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbio.20160401.11},
  abstract = {The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.},
 year = {2016}
}

Copy | Download

TY - JOUR
T1 - Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury
AU - Massaud S. Maamar
AU - Mohamed A. Al-Griw
AU - Rabia O. Al-Ghazeer
AU - Seham A. Al-Azreg
AU - Naser M. Salama
AU - Emad M. Bennour
Y1 - 2016/03/19
PY - 2016
N1 - https://doi.org/10.11648/j.ajbio.20160401.11
DO - 10.11648/j.ajbio.20160401.11
T2 - American Journal of BioScience
JF - American Journal of BioScience
JO - American Journal of BioScience
SP - 1
EP - 8
PB - Science Publishing Group
SN - 2330-0167
UR - https://doi.org/10.11648/j.ajbio.20160401.11
AB - The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.
VL - 4
IS - 1
ER -

Copy | Download

Author Information

Massaud S. Maamar

Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Mohamed A. Al-Griw

Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Rabia O. Al-Ghazeer

Chemistry Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Seham A. Al-Azreg

Department of Pathology and Clinical Pathology, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya
Naser M. Salama

Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya
Emad M. Bennour

Department of Internal Medicine, Faculty of Veterinary Medicine, University of Tripoli, Tripoli, Libya

Download PDF

Sections

Plain Text BibTeX RIS

APA Style

Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. (2016). Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. American Journal of BioScience, 4(1), 1-8. https://doi.org/10.11648/j.ajbio.20160401.11

Copy | Download

ACS Style

Massaud S. Maamar; Mohamed A. Al-Griw; Rabia O. Al-Ghazeer; Seham A. Al-Azreg; Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am. J. BioScience 2016, 4(1), 1-8. doi: 10.11648/j.ajbio.20160401.11

Copy | Download

AMA Style

Massaud S. Maamar, Mohamed A. Al-Griw, Rabia O. Al-Ghazeer, Seham A. Al-Azreg, Naser M. Salama, et al. Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury. Am J BioScience. 2016;4(1):1-8. doi: 10.11648/j.ajbio.20160401.11

Copy | Download

@article{10.11648/j.ajbio.20160401.11,
  author = {Massaud S. Maamar and Mohamed A. Al-Griw and Rabia O. Al-Ghazeer and Seham A. Al-Azreg and Naser M. Salama and Emad M. Bennour},
  title = {Oxidative Stress Mediated Cytotoxicity of Trichloroethane in a Model of Murine Splenic Injury},
  journal = {American Journal of BioScience},
  volume = {4},
  number = {1},
  pages = {1-8},
  doi = {10.11648/j.ajbio.20160401.11},
  url = {https://doi.org/10.11648/j.ajbio.20160401.11},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajbio.20160401.11},
  abstract = {The present in vivo murine study was aimed to investigate the long-term effect of repeated administration of low-dose of the environmental toxicant trichloroethane (TCE) over three weeks on the spleen and peripheral blood cells, and the possible role of oxidative stress in TCE-induced toxicity. The results showed neither adverse clinical signs nor mortality on the TCE-treated mice. However, significant changes were noticed in the spleen of those animals. Grossly, the spleen of TCE-treated group was congested and enlarged (splenomegaly). Histpathologically, the splenic tissues of TCE-treated mice showed signs of toxicity as highly activated germinal centers of the white pulp with minimal apoptotic reaction as well as a prominent megakarocytosis and infiltration of the red pulp by comparatively increased number of eosinophiIs and mature lymphocytes were detected. In addition, lymphocyte numbers were decreased in peripheral blood as well as basophils. In contrast, there was an increase in monocyte numbers in the peripheral circulation. In addition, lipid peroxidation/ malondialdehyde formation, a biomarker of oxidative stress, was significantly induced by TCE treatment in the sera and spleen of mice, suggesting an overall increase in oxidative stress. These results provide further support to a role of oxidative stress in TCE-induced cell death, which could result in an impaired spleen function. This study concludes that attenuation of TCE-induced splenic damage in mice provides an approach for preventive and/or therapeutic strategies.},
 year = {2016}
}

Copy | Download