The protective effect of ascorbic acid and thiamine supplementation against damage caused by lead in the testes of mice

  • Guang Shan (陕 光)
  • Tian Tang (唐 甜)
  • Xiaobin Zhang (张孝斌)
Article

Summary

Lead is a ubiquitous environmental and industrial pollutant that may have toxic effects on the male. Vitamins may protect against toxic effects of lead in the liver and reproductive system, which is confirmed by our initial research. The aim of this study was to further investigate the protective effects of vitamins (ascorbic acid combined with thiamine) on lead acetate (Pb)-induced reproductive toxicities in mice and study the possible mechanisms underlying these effects. Forty-five male mice were randomly divided into 3 groups, 15 mice in each and received daily intragastric administration with control, Pb (20 mg/kg), and Pb+vitamins (ascorbic acid of 420 mg/kg+thiamine of 30 mg/kg) for 6 weeks, respectively. The Pb-treated animals showed significant decreases in the epididymal sperm count and motility compared to the control group, while the Pb+vitamins group had significant increases for these variables. Moreover, an increasing apoptosis of germinal cells induced by Pb was reduced by vitamin treatment. Pb induced the activation of Caspase-3, Fas/Fas-L and Bcl-2 with elevated levels, and the adaptor protein primarily regulated signaling through Fas and required for Fas-induced apoptosis. In conclusion, ascorbic acid combined with thiamine exhibited protective effect on reproductive system by inhibiting Pb-induced excessive cell apoptosis.

Key words

lead ascorbic acid thiamine reproductive toxicity apoptosis 

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References

  1. 1.
    Adhikari N, Sinha N, Narayan R, et al. Lead-induced cell death in testes of young rats. J Appl Toxicol, 2001, 21(4):275–277PubMedCrossRefGoogle Scholar
  2. 2.
    Richburg JH. The relevance of spontaneous- and chemically-induced alterations in testicular germ cell apoptosis to toxicology. Toxicol Lett, 2000,112–113:79–86PubMedCrossRefGoogle Scholar
  3. 3.
    Hernández-Ochoa I, García-Vargas G, López-Carrillo L, et al. Low lead environmental exposure alters semen quality and sperm chromatin condensation in northern Mexico. Reprod Toxicol, 2005,20:221–228PubMedGoogle Scholar
  4. 4.
    Wang C, Zhang Y, Liang J, et al. Impacts of ascorbic acid and thiamine supplementation at different concentrations on lead toxicity in testis. Clin Chim Acta, 2006, 370(1–2):82–88PubMedCrossRefGoogle Scholar
  5. 5.
    Oliveira H, Loureiro J, Filipe L, et al. Flow cytometry evaluation of lead and cadmium effects on mouse spermatogenesis. Reprod Toxicol, 2006,22(3):529–535PubMedCrossRefGoogle Scholar
  6. 6.
    Ramanathan K, Balakumar BS, Panneerselvam C. Effects of ascorbic acid and alpha-tocopherol on arsenic-induced oxidative stress. Hum Exp Toxicol, 2002,21(12):675–680PubMedCrossRefGoogle Scholar
  7. 7.
    Krishnamoorthy G, Venkataraman P, Arunkumar A, et al. Ameliorative effect of vitamins (alpha-tocopherol and ascorbic acid) on PCB (Aroclor 1254) induced oxidative stress in rat epididymal sperm. Reprod Toxicol, 2007, 23(2):239–245PubMedCrossRefGoogle Scholar
  8. 8.
    Gruss-Fischer T, Fabian I. Protection by ascorbic acid from denaturation and release of cytochrome C, alteration of mitochondrial membrane potential and activation of multiple caspases induced by H2O2, in human leukemia cells. Biochem Pharmacol, 2002,63(7):1325–1335PubMedCrossRefGoogle Scholar
  9. 9.
    Dhawan M, Kachru DN, Tandon SK. Influence of thiamine and ascorbic acid supplementation on the antidotal efficacy of thiol chelators in experimental lead intoxication. Arch Toxicol, 1988,62(4):301–304PubMedCrossRefGoogle Scholar
  10. 10.
    Flora SJ, Tandon SK. Preventive and therapeutic effects of thiamine, ascorbic acid and their combination in lead intoxication. Acta Pharmacol Toxicol, 1986, 58(5):374–378Google Scholar
  11. 11.
    Wang C, Liang J, Zhang C, et al. Effect of ascorbic Acid and thiamine supplementation at different concentrations on lead toxicity in liver. Ann Occup Hyg, 2007,51(6):563–569PubMedCrossRefGoogle Scholar
  12. 12.
    Mihich E, Schimke RT. Apoptosis. New York: Plenum Press, 1994.1–265Google Scholar
  13. 13.
    Li LH, Wine RN, Chapin RE. 2-Methoxyacetic acid (MAA)-induced spermatocyte apoptosis in human and rat testes: an in vitro comparison. J Androl, 1996,17(5):538–549PubMedGoogle Scholar
  14. 14.
    Blanchard KT, Allard EK, Boekelheide K. Fate of germ cells in 2, 5-hexanedione-induced testicular injury. I. Apoptosis is the mechanism of germ cell death. Toxicol Appl Pharmacol, 1996,137(2):141–148PubMedCrossRefGoogle Scholar
  15. 15.
    Nagata S. Apoptosis by death factor. Cell, 1997,88:355–365PubMedCrossRefGoogle Scholar
  16. 16.
    Wyllie AH, Morris RG. Hormone-induced cell death. Purification ad properties of thymocytes undergoing apoptosis after glucocorticoid treatment. Am J Pathol, 1982,109(1):78–87PubMedGoogle Scholar
  17. 17.
    Meikrantz W, Schlegel R. Apoptosis and the cell cycle. J Cell Bioch, 1995, 58:160–174CrossRefGoogle Scholar
  18. 18.
    Williams GT, Smith CA. Molecular regulation of apoptosis: genetic controls on cell death. Cell, 1993,74(5):777–779PubMedCrossRefGoogle Scholar
  19. 19.
    Nair R, Shaha C. Diethylstilbestrol induces rat spermatogenic cell apoptosis in vivo through increased expression of spermatogenic cell Fas/FasL system. J Biol Chem, 2003,278(8):6470–6481PubMedCrossRefGoogle Scholar
  20. 20.
    World Health Organization. WHO Laboratory Manual for the Examination of Human Semen and Sperm-cervical Mucus Interaction. 4th ed. Cambridge: Cambridge University Press, 1999Google Scholar
  21. 21.
    Latchoumycandane C, Chitra KC, Mathur PP. The effect of methoxychlor on the epididymal antioxidant system of adult rats. Reprod Toxicol, 2002,16(2):161–172PubMedCrossRefGoogle Scholar
  22. 22.
    Peirce EJ, Breed WG. A comparative study of sperm production in two species of Australian arid zone rodents (Pseudomys australis, Notomys alexis) with marked differences in testis size. Reproduction, 2001,121(2): 239–247PubMedCrossRefGoogle Scholar
  23. 23.
    Marchlewicz M, Wiszniewska B, Gonet B, et al. Increased lipid peroxidation and ascorbic Acid utilization in testis and epididymis of rats chronically exposed to lead. Biometals, 2007,20(1):13–19PubMedCrossRefGoogle Scholar
  24. 24.
    Marchlewicz M, Protasowicki M, Rózewicka L, et al. Effect of long-term exposure to lead on testis and epididymis in rats. Folia Histochem Cytobiol, 1993, 31(2):55–62PubMedGoogle Scholar

Copyright information

© Huazhong University of Science and Technology and Springer-Verlag GmbH 2009

Authors and Affiliations

  • Guang Shan (陕 光)
    • 1
  • Tian Tang (唐 甜)
    • 2
  • Xiaobin Zhang (张孝斌)
    • 1
  1. 1.Department of UrologyRenmin Hospital of Wuhan UniversityWuhanChina
  2. 2.Department of Cancer Radio-Chemotherapy, Zhongnan Hospital and Cancer Research CenterWuhan UniversityWuhanChina

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