Protective Influence of Zinc sulphate on some histological changes in Male mice embryo belongs to mother injected with lead acetate

Nisreen Flayyih; Ban Thabit Saeed; Rana A. Al-Saadi; Zahraa Alzaidi

doi:10.28969/IJEIR.v14.i2.r2.24

Authors

Nisreen Flayyih The High Institute for Infertility Diagnosis and Assisted Reproductive Technologies
Ban Thabit Saeed The High Institute for Infertility Diagnosis and Assisted Reproductive Technologies https://orcid.org/0000-0002-0137-8713
Rana A. Al-Saadi The High Institute for Infertility Diagnosis and Assisted Reproductive Technologies
Zahraa Alzaidi The High Institute for Infertility Diagnosis and Assisted Reproductive Technologies https://orcid.org/0000-0003-1195-5796

DOI:

https://doi.org/10.28969/IJEIR.v14.i2.r2.24

Keywords:

lead, zink, testes development teratogenicity

Abstract

Abstract:

Background:

Lead is a heavy metal toxicant, present widely in our environment and workplaces. Zinc has been shown to reduce the toxicity of lead. The present experimental animal study was designed to observe the changes in the testes due to excessive use of lead. This study aims to detect the effect of antioxidant (zinc) on the toxicity of high dose of lead on the reproductive organs of male mice embryo compared to the control group, as a model for human representative.

Materials and methods:

Thirty mature female mice were used (Swiss-Webster), as a mammalian model. They were divided into three groups, 10 mice/group after labeling them. They were randomly assigned into two experimental groups (G1) was injected with 50 mg/kg of body weight of lead acetate from the first day for three days. While (G2) was given 0.5 mg zinc/kg b.w./d orally as zinc sulphate during the 3 weeks period of the experiment(gestation)from the first day of gestation for 3 days, and One control group G3 (n= 10) received distilled water and. Total number of embryos and there weight were recorded for all groups. Then the testes of these embryos excised and processed for histological observations.

Results:

The recorded results showed significant decrease in the weight of the embryo of treated group compared with control group. However, no significant differences in number of the fetus for treated group compared to control one. The histological features of the embryo testes of treated group showed irregular testes cords with prominent degenerative changes and undescended testes compared to that of control group numbers of the embryos belongs to mother Injection with lead acetate and orally administrated with zinc sulphate showed no significant changes in comparison to control group. When mice are administrated to lead for three days, the testicular cords of their testes are disarranged, the primordial germ cells are severe degeneration and descending of the testes remained adjacent to the kidneys (metanephron) at the upper part of the abdominal cavity in comparison with control group.

Conclusion:

It is now generally accepted that the mammalian testes are very sensitive to lead, leading to changes in the testicular biochemical function. Testicular morphology was severely affected in embryo of mice Lead induces production of ROS and reduces the activity of ant oxidative enzymes, thereby causing oxidative damage to the testes. Testicular morphology was severely affected in embryo of mice exposed to lead acetate. Zinc could significantly compete for and effectively reduce the availability of binding sites for lead acetate uptake. Therefore, it plays important role in preventing lead induced reproductive or testes damage in mice. The recorded results of this study assess the presence of teratogenic effect of lead on the developing testes and position of testes of the mice exposed to leads.

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References

Reference

Altshuler, N. (2003). Children’s environmental exposures. DCHP paper Series on Children’s Health and the environmental. Washington, D.C. USA; Us Environmental Protection Agency.

Suk WA, Murray K, Avakian MD. Environmental hazards to children's health in the modern world. Mutat Res. 2003 Nov;544(2-3):235-42. doi: 10.1016/j.mrrev.2003.06.007. PMID: 14644325.

2 RÍsovÁ V. The pathway of lead through the mother's body to the child. Interdiscip Toxicol. 2019 Sep;12(1):1-6. doi: 10.2478/intox-2019-0001. Epub 2020 Feb 20. PMID: 32189981; PMCID: PMC7061448.

M. M. El-Tohamy and W. S. El-Nattat, “Effect of Antioxidant on Lead-Induced Oxidative Damage and Reproductive Dysfunction in Male Rabbits,” Journal of American Science, Vol. 6, No. 1, 2010, pp. 613-622.

Abadin H, Ashizawa A, Stevens YW, Llados F, Diamond G, Sage G, Citra M, Quinones A, Bosch SJ, Swarts SG. Toxicological Profile for Lead. Atlanta (GA): Agency for Toxic Substances and Disease Registry (US); 2007 Aug. PMID: 24049859.

Moniem A, Dkhil M, Al-Quraishy S: Protective role of flaxseed oil against lead acetate induced oxidative stress in testes of adult rats. Afr J Biotechnol 2010, 9(42):7216–7223.

Singh RP, Shashwat S, Suman K: Free Radicals and Oxidative Stress in Neurodegenerative Diseases: Relevance of Dietary Antioxidants. Journal of Indian Academy of Clinical Medicine JIACM 2004, 5(3):218–225.

Mishra M, Acharya UR: Protective action of vitamins on the spermatogenesis in lead-treated Swiss mice. J Trace Elem Med Biol 2004, 18(2):173–178.

Sebahat T, Bünyamin K, Günfer T, Gülten E and Osman G. Effects of cadmium and zinc on plasma levels of growth hormone, insulin-like growth factor I, and insulin-like growth factor-binding protein 311. Biological Trace Element Research, 2005; 108: 197-204.

Gundacker C, Hengstschläger M. The role of the placenta in fetal exposure to heavy metals. Wien Med Wochenschr. 2012 May;162(9-10):201-6. doi: 10.1007/s10354-012-0074-3. PMID: 22717874.

Greenpeace (2005). A Chinese child sits amongst a pile of wires and- waste, picture. Pp 53-82.

Walker, P.M. Ischemia /reperfusion injury in skeletal; muscle. Ann. Vasc. Surg, 1991; 5:399-402. Fridovich, I. Superoxide dismutase, regularities and irregularities. Harvey Lect., 1985; 79:51-75.

Baker, H.W.G., Brindle, J., Irvine, D.S. and Aitken, J. Protective effect of antioxidants on the impairment of sperm motility by activated polymorphonuclear leukocytes. Fertil. Steril., 1996; 65:411-419.

Kurpisz, M., Miesel, R., Sanocka, D. and Jendrzejczyk, P. Seminal plasma can be a predictive factor for male infertility. Hum. Reprod., 1996; 11: 1223–1226.

Henkel, R.R., Defosse, K. and Koyro, H.W. Estmate of oxygen consumption and intercellular zinc concentration of human spermatozoa in relation to motility: Asian, J.Anodrol., 2003; 5:3-8.

Vish wanath, M. Inorganic elements in: Sardesai, Vish wanath, M., Introduction to clinical Nutrition. 2nd Ed. New York, 1998; 98-100.

Klauder DS, Murthy L, Petering HG. Effect of dietary intake of lead acetate on copper metabolism in male rats. In: Hemphill DD, ed. Trace substances in environmental health. Columbia, MO: University of Missouri; 1973:131. 9. Six KM,

Conrad ME, Barton JC. Factors affecting the absorption and excretion of lead in the rat. Gastroenterology. 1978;74:731±40.

Barltrop D, Khoo HE. The influence of dietary mineral and fat on the absorption of lead. Science Tot Environ. 1976;6:265±73.

Flora SJS, Jain VK, Behari JR, Tandon SK. Protective role of trace metals in lead intoxication. Toxicol Lett. 1982;13:51±6.

Kagi JHR, Vallee BL. Metallothionein, a cadmium and zinc containing protein from equine renal cortex. J Biol Chem. 1961; 236:2435±42.

. Papaioannou RA, Sohler A, Pfeiffer CC. Reduction of blood lead levels in battery workers by zinc and vitamin C. J Orthomol Psychiat. 1978;7:1±13.

Flora SJS, Singh S, Tondon SK. Thiamine and zinc in prevention or therapy of lead intoxication. J Internat Med Res. 1989;17:68± 75.

Aitken, R.J., Fisher, H.M., Fulton, N., Gomez, E., Knox, W., Lewis, B., and Irvine, S. Reactive oxygen species generation by human spermatozoa is induced by exogenous NADPH and inhibited by the flavor protein inhibitors diphenylene iodonium and quinacrine. Mol Reprod Dev.,1987; 47: 468 -482.

Corpas, I.; Gaspar, I.; Martinez, S.; Codesal, J.; and Candelas, S. (1995). Testicular alteration in rats due to gestational and early lactation administration of lead. Reprod. Toxicol. 9: 307-313.

Homan, C.S. and Brogan, G.X. (1993). Lead Toxicity. In; Hand book of Medical Toxicology. Viccellio, P. (ed.). Little, Brown and company, London. Pp: 271-273.

McGivern, R.F; Sokol, R.Z. and Berman, N.G. (1991). Prenatal lead exposure in the rat during the third week of gestation; Long-term behavioral, physiological and anatomical effects associated with reproduction. Toxicol. Appl. Pharmacol. 110: 206-215.

Gonzale-Cossio, T.; Peterson, K.E.; Sanin, L.; Fishbein, S.E.; Palazuelos, E.; Aro, A.; Hernandez-Avila, M. and Hu, H. (1997). Decrease in birth weight in relation to maternal bone lead burden. Pediatrics. 100: 856-862.

(IPCS) (1995). International Panel of Chemical Safety. Inorganic lead-Environmental Health Criteria 165. International Programme on Chemical Safety. World Health Organization, Geneva, Switzerland.

Brent, R.L. (2004). Environmental causes of human congenital malformations, the pediatrician's role in dealing with these complex clinical problems caused by a multiplicity of environmental and genetic factors. Pediatrics. 113(4 suppl). 957-68.

Danielson, B.R.; Dencker, L. and Lindgren, A. (1983). Transplacental movement of inorganic lead in early and late gestation in the mouse. Arch. Toxicol. 54: 97-107.

Odiette, W.O. (1999). Environmental physiology of animals and pollution. Diversified resources Ltd. Lagos. P 261.

Guyton, A.C. and Hall, J.E. (2016). Text Book of Medical Physiology, Used, Elsevier Saunders, Philadelphia, Pennsylvania. Pp: 1017-1018.

Heap, R.B.; Flint, A.P.; Hartmann, P.E.; Gadsby, J.E.; Staples, L.D.; Ackland, N. and Hamon, M. (1981). Oestrogen production in early pregnancy. J. Endocrinol. 89 (Suppl). 77 -94.

Bowman, P. and McLaren, A. (1970). Cleavage rate of mouse embryos in vivo and in vitro. J. Embryol. Exp. Morphol. 24: 203-207.

Dey, S.K. (2003). Fertility study shows increased estrogen shortens window of implantation in mice. Vanderbilt University Medical Center, [email protected]: 322-4747.

Tchernitchen, N.N.; Villagra, A. and Tchernitchen, A.N. (1998). Antiestrogenic activity of lead. Environ. Toxicol. Water Qual. 13: 43-53.

Pinon- Lataillaade, G.; Thoreux-Manlay, A.; Coffigny, H.; Masse, R. and Soufir, J.C. (1995). Reproductive toxicity of chronic lead exposure in male and female mice. Hum. Experiment. Toxicol. 14: 872-878.

Kostial, K. and Momcilovic, B. (1974). Transport of lead 203 and Calcium 47 from mother to offspring. Arch. Environ. Health. 29: 28-30.

Silbergeld, E.K. (1983). Experimental studies of lead neurotoxicity. Biol. Reprod. 33: 722-728.

Moorman, W.J.; Skaggs, S.R.; Clarck, J.C. and Simon, S.D. (1998). Male reproductive effects of lead including species extrapolation for the rabbit model. Reprod. Toxicol. 12: 333-46.

McGivern, R.F; Sokol, R.Z. and Berman, N.G. (1991). Prenatal lead exposure in the rat during the third week of gestation; Long-term behavioral, physiological and anatomical effects associated with reproduction. Toxicol. Appl. Pharmacol. 110: 206-215.

Liu, D. Y. and Baker, H. W. G. Tests of human sperm function and fertilization in vitro. Fertil. Steril., 1992; 58:465–483.

Robert, K. M., Daryl, K.G., Peter, A. M., and Victor, W. K. Harpers Biochemistry.24th Ed .Appleton &Lange, 1997; Pp.155-521.

Aitken, R.J., Fisher, H.M., Fulton, N., Gomez, E., Knox, W., Lewis, B., and Irvine, S. Reactive oxygen species generation by human spermatozoa is induced by exogenous NADPH and inhibited by the flavor protein inhibitors diphenylene iodonium and quinacrine. Mol Reprod Dev., 1987; 47: 468.

Irvine, D.S. Glutathione as a treatment of male infertility. Rev Reprod., 1996; 1: 6-12.

Behrman, R.E.; Kliegman, R.M. and Arvin, A.M. (1996). Nelson Textbook of Pediatrics, 15th ed. Philadelphia, WB Saunders, PP 343.

Bernstein, L.; Pike, M.C.; Depue, R.H.; Ross, R.K.; Moore, J.W. and Henderson, B.E. (1988). Maternal hormone levels in early gestation of crypt orchid males: A case-control study. Br.J. Cancer. 58: 379-381.

Hutson, J.M.; Baker, M.; Terada, M.; Zhou, B. and Paxton, G. (1994). Hormonal control of testicular descent and the cause of cryptorchidisim. Reprod. Fertil. Dev. 6: 151-156.

Thoreux-Manlay, A.; Velezdelacalle, J.F.; Olivier, M.F.; Soufir, J.C.; Masse, R. and Pinon-Lataillade, G. (1995). Impairment of testicular endocrine function after lead intoxication in the adult rat. Toxico. 100; 101-109.