| Peer-Reviewed

Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk

Received: 19 August 2015     Accepted: 31 August 2015     Published: 9 September 2015
Views:       Downloads:
Abstract

Exposure to trichloroethane (TCE), a ambiguous environmental toxicant, has been negatively associated with male reproductive performance. The objective was to investigate, in-vivo, the mutagenic, carcinogenic or teratogenic effect of TCE maternal exposure on sperm quality and testicular cytoarchitecture of F1 generation of mice. A motile sperm separation technique was used to estimate sperm motility and a gelatin slide technique was used to measure the number of the halo around the acrosome of individual sperm as an acrosomal proteolytic enzyme (APA). Animals were followed up for signs of toxicity and mortality. Alterations in testicular tissues have been histopathology investigated. No adverse signs, symptoms and mortality were observed in the animals treated with TCE. Moreover, significant changes were seen in body and testis weight. Results of semen analysis revealed that TCE lead to low sperm count, abnormal sperm morphology, and frequently of sperm motility. These results were correlated with decrease in APA when pre-leptotene or spermatogonial cells were tested, indicating a transgenerational toxic effects. Histopathological examination revealed that TCE insult marked alterations in the microstructures of testicular tissues appeared as severe morphological abnormal spermatozoa and vacuoles. Taken together, these results suggest that early exposure to TCE causes testicular toxicity and poor semen quality. The sperm phenotypes utilized in this study may increase the value of sperm for detection mutagenic developmentally active agents, and agent with anti-fertility effects in mammals. This in-vivo animal model represents a unique platform for assessing human reproductive toxicity potential and genetic risk of various environmental mutagens, carcinogens and teratogens in a rapid, efficient, and unbiased format.

Published in International Journal of Genetics and Genomics (Volume 3, Issue 5)
DOI 10.11648/j.ijgg.20150305.11
Page(s) 43-49
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), 2015. Published by Science Publishing Group

Keywords

Trichloroethane, Transgenerational Genetic Effect, Sperm Quality, Testicular Toxicity, Mice

References
[1] Sadowski, R. N., Wise, L. M., Park, P. Y., Schantz, S. L., Jurask, J. M. (2014) Early Exposure to Bisphenol A alters Neuron and Glia Number in the Rat Prefrontal Cortex of Adult Males, but not Females, Neuroscience 279, 122-131.
[2] Nomura, T. (2008) Transgenerational effects from exposure to environmental toxic substances, Mutation Research 659 185-193.
[3] Nadea, J. H. (2009) Transgenerational genetic effects on phenotypic variation and disease risk, Human Molecular Genetics 18, R202-R210.
[4] Anway, M. D., Cupp, A. S., Uzumcu, M., and Skinner, M. K. (2005) Epigenetic transgenerational actions of endocrine disruptors and male fertility, Science 308, 1466-1469.
[5] Rakyan, V., and Whitelaw, E. (2003) Transgenerational epigenetic inheritance, Curr Biol 13, R6.
[6] Anway, M. D., Memon, M. A., Uzumcu, M., and Skinner, M. K. (2006) Transgenerational effect of the endocrine disruptor vinclozolin on male spermatogenesis, J Androl 27, 868-879.
[7] Skinner, M. K. (2007) Endocrine disruptors and epigenetic transgenerational disease etiology, Pediatr Res 61, 48R-50R.
[8] Anway, M. D., Leathers, C., and Skinner, M. K. (2006) Endocrine disruptor vinclozolin induced epigenetic transgenerational adult-onset disease, Endocrinology 147, 5515-5523.
[9] Easley IV, C. A., Bradner, J. M., Mosera, A., Rickmana, C. A., McEachina, Z. T., Merritt, M. M., Hansenc, J. M., and Caudle, W. M. (2015) Assessing reproductive toxicity of two environmental toxicants with a novel in vitro human spermatogenic model, Stem Cell Research 14, 347-355.
[10] Aitken, R. J., Koopman, P., and Lewis, S. E. M. (2004) Seeds of concern, Nature 432, 48-52.
[11] Wong, E. W. (2010) Cell junctions in the testis as targets for toxicants. In: Richburg, JH.; Hoyer, P.,editors. , Comprehesive toxicology. Academic Press, P167-188.
[12] Sharpe, R. M. (2010) Environmental/lifestyle effects on spermatogenesis, Philos Trans R Soc Lond B Biol Science 365, 1697-1712.
[13] 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.
[14] 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.
[15] York, R. G., Sowry, B.M., Hastings, L., Manson, J.M. (1982) Evaluation of teratogenicity and neurotoxicity with maternal inhalation exposure to methyl chloroform, Journal of Toxicol. environ. Health 9, 251-266.
[16] Wang, W., Hafner, K. S., and Flaws, J. A. (2014) In utero bisphenol A exposure disrupts germ cell nest breakdown and reduces fertility with age in the mouse, Toxicology and Applied Pharmacology 276, 157-164.
[17] Khan, M. F., Kaphalia, B. S., Prabhakar, B. S., Kanz, M. F., and Ansari, G. A. (1995) Trichloroetheneinduced autoimmune response in female MRL+/+ mice, Toxicology Applied Pharmacology 134, 155-160.
[18] 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.
[19] Salama, N. M., Ficsor, G., Block, K. K., McIntire, C. L., and Ginsberg, L. C. (1982) Germ cell specific decrease of acrosomal proteolytic activity, sperm motility and number in Mitomycin C treated mice, Teratogenic and Carcinogenic 2, 13-18.
[20] Zhang, H., Wang, H., Ji, Y.L., Ning, H., Yu, T., Zhang, C., Zhang, Y., Zhao, X.F., Wang, Q., Liu, P., Meng, X.H., Xu, D.X. (2009) Lactational fenvalerate exposure permanently impairs testicular development and spermatogenesis in mice, Toxicol Lett 191, 47-56.
[21] Organization, W. H. (1999) WHO laboratory manual for the examination of human semen and sperm-cervical mucus interaction. 4th ed. Cambridge: Cambridge University Press, 128 p.
[22] Ginsberg, L. C., Johnson, S. C., Salama, N. M., and Ficsor, G. (1981) Acrosomal proteolytic assay for detection of mutagens in mammals, Mutation Research 91, 413-418.
[23] Bancroft, J. D., and Gamble, M. (2008) Theory and practice of histological techniques. 6th ed. Philadelphia ,PA: Churchill Livingstone.
[24] Wong, E. W. P., and Cheng, C. Y. (2011) Impacts of environmental toxicants on male reproductive dysfunction, Trends Pharmacol Science 32, 290-299.
[25] Manikkam, M., Guerrero-Bosagna, C., Tracey, R., Haque, M. M., and Skinner, M. K. (2012) Transgenerational actions of environmental compounds on reproductive disease and identification of epigenetic biomarkers of ancestral exposures, PLoS One 7, e31901.
[26] Hauser, R., and Sokol, R. (2008) Science linking environmental contaminant exposures with fertility and reproductive health impacts in the adult male, Fertil Steril 89, e59-65.
[27] Kjellstrom, T., and Nordberg, G. F. (1978) A kinetic model of cadmium metabolism in the human being, Environ Research 16, 248-269.
[28] 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..
[29] WHO. (2003) 1,1,1-Trichloroethane in Drinking-water. Background document for development of
[30] WHO Guidelines for Drinking-water Quality., World Health Organization WHO/SDE/WSH/03.04/65., 16.
[31] ASTDR. (2006) 1,1,1 Trichloroethane, Agency for Toxic Substances and Disease Registry, 371.
[32] Prodi, G., Collacci, A., and Grilli, S. (1988) Comparison of the covalent binding of various chloroethanes with nucleic acids. In: Feo, F; ed. Chemical carcinogenesis: models and mechanisms. , PNew York, NY: Plenum Press; . 93–102.
[33] Turina, M., Colacci, A., and Grilli, S. (1986) Short-term tests of genotoxicity for 1,1,1-trichloroethane. , Res Commun Chem Pathol Pharmacol 52, 305–320.
[34] 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.
[35] Ahammad, M. U., Nishino, C., Tatemoto, H., Okura, N., Kawamoto, Y., Okamoto, S., and Nakada, T. (2011) Maturational changes in motility, acrosomal proteolytic activity, and penetrability of the inner perivitelline layer of fowl sperm, during their passage through the male genital tract, Theriogenology 76, 1100-1109.
[36] Quast, J. F., Calhoun, L. L., Frauson, L. E. (1988) 1,1,1-trichloroethane formulation: a chronic inhalation toxicity and oncogenicity study in Fischer 344 rats and B6c3F1 mice Fundamental and applied toxicology: official journal of the Society of Toxicology 11, 611-625.
[37] Adams, E., Spencer, H., Rowe, V. (1950) Vapor toxicity of 1,1,1-trichloroethane (methylchloroform) determined by experiments on laboratory animals, Arch Ind Hyg Occup Med 2, 225-236.
[38] Shire, J. G. M., and Bartke, A. (1972) Strain differences in testicular weight and spermatogenesis with special reference to C57HL/10J and DBA/2J mice., Journal of Endocrinology 55, 163-171.
[39] Joshi, S. C., Mathur, R., Gulati, N.. (2007) Testicular toxicity of chlorpyrifos (an organophosphate pesticide) in albino rat, Toxicol Ind Health 23, 439-444.
[40] ElMazoudy, R. H., Attia, A. A., El-Shenawy, N. S. (2011) Protective role of propolis against reproductive toxicity of chlorpyrifos in male rats, Pestici Biochem Phys 101, 175-181.
[41] Wu, P. F., Chiang, T. A., Chen, M. T., Lee, C. P., Chen, P. H., Ko, A. M., Yang, K. J., Chang, P. Y., Ke, D. S., Ko, Y. C. A. J. (2010) characterization of the antioxidant enzyme activity and reproductive toxicity in male rats following sub-chronic exposure to areca nut extracts, Hazard Mater 178, 541-546.
Cite This Article
  • APA Style

    Mohamed A. Al-Griw, Naser M. Salama, Soad A. Treesh, Abdul Hakim Elnfati. (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(5), 43-49. https://doi.org/10.11648/j.ijgg.20150305.11

    Copy | Download

    ACS Style

    Mohamed A. Al-Griw; Naser M. Salama; Soad A. Treesh; Abdul Hakim Elnfati. Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk. Int. J. Genet. Genomics 2015, 3(5), 43-49. doi: 10.11648/j.ijgg.20150305.11

    Copy | Download

    AMA Style

    Mohamed A. Al-Griw, Naser M. Salama, Soad A. Treesh, Abdul Hakim Elnfati. Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk. Int J Genet Genomics. 2015;3(5):43-49. doi: 10.11648/j.ijgg.20150305.11

    Copy | Download

  • @article{10.11648/j.ijgg.20150305.11,
      author = {Mohamed A. Al-Griw and Naser M. Salama and Soad A. Treesh and Abdul Hakim Elnfati},
      title = {Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk},
      journal = {International Journal of Genetics and Genomics},
      volume = {3},
      number = {5},
      pages = {43-49},
      doi = {10.11648/j.ijgg.20150305.11},
      url = {https://doi.org/10.11648/j.ijgg.20150305.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ijgg.20150305.11},
      abstract = {Exposure to trichloroethane (TCE), a ambiguous environmental toxicant, has been negatively associated with male reproductive performance. The objective was to investigate, in-vivo, the mutagenic, carcinogenic or teratogenic effect of TCE maternal exposure on sperm quality and testicular cytoarchitecture of F1 generation of mice. A motile sperm separation technique was used to estimate sperm motility and a gelatin slide technique was used to measure the number of the halo around the acrosome of individual sperm as an acrosomal proteolytic enzyme (APA). Animals were followed up for signs of toxicity and mortality. Alterations in testicular tissues have been histopathology investigated. No adverse signs, symptoms and mortality were observed in the animals treated with TCE. Moreover, significant changes were seen in body and testis weight. Results of semen analysis revealed that TCE lead to low sperm count, abnormal sperm morphology, and frequently of sperm motility. These results were correlated with decrease in APA when pre-leptotene or spermatogonial cells were tested, indicating a transgenerational toxic effects. Histopathological examination revealed that TCE insult marked alterations in the microstructures of testicular tissues appeared as severe morphological abnormal spermatozoa and vacuoles. Taken together, these results suggest that early exposure to TCE causes testicular toxicity and poor semen quality. The sperm phenotypes utilized in this study may increase the value of sperm for detection mutagenic developmentally active agents, and agent with anti-fertility effects in mammals. This in-vivo animal model represents a unique platform for assessing human reproductive toxicity potential and genetic risk of various environmental mutagens, carcinogens and teratogens in a rapid, efficient, and unbiased format.},
     year = {2015}
    }
    

    Copy | Download

  • TY  - JOUR
    T1  - Transgenerational Genetic Effect of Trichloroethane (TCE) on Phenotypic Variation of Acrosomal Proteolytic Enzyme and Male Infertility Risk
    AU  - Mohamed A. Al-Griw
    AU  - Naser M. Salama
    AU  - Soad A. Treesh
    AU  - Abdul Hakim Elnfati
    Y1  - 2015/09/09
    PY  - 2015
    N1  - https://doi.org/10.11648/j.ijgg.20150305.11
    DO  - 10.11648/j.ijgg.20150305.11
    T2  - International Journal of Genetics and Genomics
    JF  - International Journal of Genetics and Genomics
    JO  - International Journal of Genetics and Genomics
    SP  - 43
    EP  - 49
    PB  - Science Publishing Group
    SN  - 2376-7359
    UR  - https://doi.org/10.11648/j.ijgg.20150305.11
    AB  - Exposure to trichloroethane (TCE), a ambiguous environmental toxicant, has been negatively associated with male reproductive performance. The objective was to investigate, in-vivo, the mutagenic, carcinogenic or teratogenic effect of TCE maternal exposure on sperm quality and testicular cytoarchitecture of F1 generation of mice. A motile sperm separation technique was used to estimate sperm motility and a gelatin slide technique was used to measure the number of the halo around the acrosome of individual sperm as an acrosomal proteolytic enzyme (APA). Animals were followed up for signs of toxicity and mortality. Alterations in testicular tissues have been histopathology investigated. No adverse signs, symptoms and mortality were observed in the animals treated with TCE. Moreover, significant changes were seen in body and testis weight. Results of semen analysis revealed that TCE lead to low sperm count, abnormal sperm morphology, and frequently of sperm motility. These results were correlated with decrease in APA when pre-leptotene or spermatogonial cells were tested, indicating a transgenerational toxic effects. Histopathological examination revealed that TCE insult marked alterations in the microstructures of testicular tissues appeared as severe morphological abnormal spermatozoa and vacuoles. Taken together, these results suggest that early exposure to TCE causes testicular toxicity and poor semen quality. The sperm phenotypes utilized in this study may increase the value of sperm for detection mutagenic developmentally active agents, and agent with anti-fertility effects in mammals. This in-vivo animal model represents a unique platform for assessing human reproductive toxicity potential and genetic risk of various environmental mutagens, carcinogens and teratogens in a rapid, efficient, and unbiased format.
    VL  - 3
    IS  - 5
    ER  - 

    Copy | Download

Author Information
  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Department of Histology and Medical Genetics, Faculty of Medicine, University of Tripoli, Tripoli, Libya

  • Division of Developmental Biology, Zoology Department, Faculty of Science, University of Tripoli, Tripoli, Libya

  • Sections