Advertisement

Bulletin of Experimental Biology and Medicine

, Volume 156, Issue 1, pp 15–18 | Cite as

Role of Cytochrome P450-Dependent Monooxygenases and Polymorphic Variants of GSTT1 and GSTM1 Genes in the Formation of Brain Lesions in Individuals Chronically Exposed to Mercury

  • Yu. I. ChernyakEmail author
  • V. B. Itskovich
  • O. A. D’yakovich
  • S. I. Kolesnikov
Article

The metabolic test with antipyrine was performed, the relationship between genotypes of GSTT1 and GSTM1 polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxication. The changes in the parameters of antipyrine test were studied in linked samples (N = 62, 4 year interval); in patients with chronic mercury intoxication, the disease stage was taken into account. Inhibition of antipyrine metabolism, increased frequency of combination of GSTT1(0/0)/GSTM1(+) genotypes in patients with chronic mercury intoxication, and the specificity of cytochrome P450 inhibition with mercury suggest that disease progression is related to inhibition of cytochrome P450 isoforms in the brain that catalyze regulation of endogenous substrates.

Key Words

cytochromes P450 antipyrine metabolism genetic polymorphism glutathione-S-transferase chronic mercury intoxication 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Yu. I. Chernyak, V. B. Itskovich, B. K. Baduev, and G. B. Borovskii, Bull. Exp. Biol. Med., 154, No. 1, 68–72 (2012).PubMedCrossRefGoogle Scholar
  2. 2.
    Yu. I. Chernyak, V. B. Itskovich, and S. I. Kolesnikov, Bull. Exp. Biol. Med., 151, No. 4, 445–448 (2011).PubMedCrossRefGoogle Scholar
  3. 3.
    C. B. Ambrosone, C. Sweeney, B. F. Coles, et al., Cancer Res., 61, No. 19, 7130–7135 (2001).PubMedGoogle Scholar
  4. 4.
    F. Dutheil, P. Beaune, and M. A. Loriot, Biochimie, 90, No. 3, 426–436 (2008).PubMedCrossRefGoogle Scholar
  5. 5.
    C. S. Ferguson, and R. F. Tyndale, Trends Pharmacol. Sci., 32, No. 12, 708–714 (2011).PubMedCentralPubMedCrossRefGoogle Scholar
  6. 6.
    C. Gundacker, M. Gencik, and M. Hengstschlager, Mutat. Res., 705, No. 2, 130–140 (2010).PubMedCrossRefGoogle Scholar
  7. 7.
    S. Kezic, F. Calkoen, M. A. Wenker, et al., Toxicol. Ind. Health, 22, No. 7, 281–289 (2006).PubMedCrossRefGoogle Scholar
  8. 8.
    M. Korbas, J. L. O’Donoghue, G. E. Watson, et al., ACS Chem. Neurosci., 1, No. 12, 810–818 (2010).PubMedCrossRefGoogle Scholar
  9. 9.
    S. Miksys, E. Hoffmann, and R. F. Tyndale, Biochem. Pharmacol., 59, No. 12, 1501–1511 (2000).PubMedCrossRefGoogle Scholar
  10. 10.
    T. Nakahama, Y. Inouye, and M. Fukuhara, J. Health Sci., 47, No. 1, 14–20 (2001).CrossRefGoogle Scholar
  11. 11.
    O. Pelkonen, J. Maenpaa, P. Taavitsainen, et al., Xenobiotica, 28, No. 12, 1203–1253 (1998).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Yu. I. Chernyak
    • 1
    Email author
  • V. B. Itskovich
    • 1
  • O. A. D’yakovich
    • 1
  • S. I. Kolesnikov
    • 1
  1. 1.Angara Affiliated Department of East Siberian Center of Human EcologySiberian Division of the Russian Academy of Medical SciencesMoscowRussia

Personalised recommendations