Lead induces Siberian tiger fibroblast apoptosis by interfering with intracellular homeostasis

References

• Alavian, K.N., et al., 2011. Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase. Nature Cell Biology, 13, 1224–1234.
   PubMed Web of Science ®Google Scholar
• Ariza, M.E., and Williams, M.V., 1996. Mutagenesis of AS52 cells by low concentrations of lead(II) and mercury(II). Environmental and Molecular Mutagenesis, 27, 30–33.
   PubMed Web of Science ®Google Scholar
• Chen, L., Yang, X., and Jiao, H., 2003. Tea catechins protect against lead-induced ROS formation, mitochondrial dysfunction, and calcium dysregulation in PC12 cells. Chemical Research in Toxicology, 16, 1155–1161.
   PubMed Web of Science ®Google Scholar
• Dominguez, C., Solé, E., and Fortuny, A., 2002. In vitro lead-induced cell toxicity and cytoprotective activity of fetal calf serum in human fibroblasts. Molecular and Cellular Biochemistry, 237, 47–53.
   PubMed Web of Science ®Google Scholar
• Dong, S., et al., 2009. The role of MAPK and FAS death receptor pathways in testicular germ cell apoptosis induced by lead. Acta Biochimica et Biophysica Sinica, 4, 800–807.
   Web of Science ®Google Scholar
• Dong, S., Shan, Y., and Lu, M., 2005. Study on DNA damage and proliferation of testicular cells with lead exposed. Chinese Journal of Public Health, 21, 1216–1218.
   Google Scholar
• EI-Sokkary, G.H., Kamel, E.S., and Reiter, R.J., 2003. Prophylactic effect of melatonin in reducing lead induced neurotoxicity in the rat. Cellular and Molecular Biology Letters, 8, 461–470.
   PubMed Web of Science ®Google Scholar
• Ercal, N., et al., 1996. In vivo indices of oxidative stress in lead-exposed C57BL/6 mice are reduced by treatment with meso-2,3-dimercaptosuccinic acid or N-acetylcysteine. Free Radical Biology &Amp; Medicine, 21, 157–161.
   PubMed Web of Science ®Google Scholar
• Fehsel, K., et al., 1995. Nitric oxide induces apoptosis in mouse thymocytes. Journal of Immunology, 155, 2858–2865.
   PubMed Web of Science ®Google Scholar
• Friesen, C., and Fulda, S., 1997. Deficient activation of the CD 95(Apo1/Fas) system in drug resistant cells. Leukemia, 11, 1822–1841.
   Web of Science ®Google Scholar
• Gerber, G.B., Leonard, A., and Jacquet, P., 1980. Toxicity, mutagenicity and teratogenicity of lead. Mutation Research, 76, 115–141.
   PubMed Web of Science ®Google Scholar
• Goyer, R.A., 1993. Lead toxicity: current concerns. Environmental Health Perspectives, 100, 177–187.
   PubMed Web of Science ®Google Scholar
• IARC. 1987. Overall evaluation of carcinogenicity: an updating of IARC monographs. In IARC Monographs on the Evaluation of Carcinogenic Risks to Human, Vol. 1–42, Supplement 7. International Agency for Research on Cancer, Lyon, 230–232.
   Google Scholar
• Iavicoli, I., Carelli, G., and Sgambato, A., 2001. Lead inhibits growth and induces apoptosis in normal rat fibroblasts. Alternatives to Laboratory Animals: Atla, 29, 461–469.
   PubMed Web of Science ®Google Scholar
• Kulms, D., and Schwarz, T., 2002. Independent contribution of three different pathways to ultraviolet-B-induced apoptosis. Biochemical Pharmacology, 64, 837–841.
   PubMed Web of Science ®Google Scholar
• Kurochkin, I.O., et al., 2011. Top-down control analysis of the cadmium effects on molluscan mitochondria and the mechanisms of cadmium-induced mitochondrial dysfunction. American Journal of Physiology – Regulatory, Integrative and Comparative Physiology, 300, R21–R31.
   PubMed Web of Science ®Google Scholar
• Kwong, W.T., Friello, P., and Semba, R.D., 2004. Interactions between iron deficiency and lead poisoning: epidemiology and pathogenesis. The Science of the Total Environment, 330, 21–37.
   PubMed Web of Science ®Google Scholar
• Matyushkin, E. N., et al., 1999. Distribution and numbers of Amur tigers in the Russian Far East in the mid-1990s. In: A.A. Aristova, ed. Rare mammal species of Russia and neighboring territories (in Russian). Moscow: Russian Academy of Sciences Therological Society, 242–271.
   Google Scholar
• Mielke, H.W., and Reagan, P.L., 1998. Soil is an important pathway of human lead exposure. Environmental Health Perspectives, 106, 217–229.
   PubMed Web of Science ®Google Scholar
• Miquelle, D. G., and Pikunov, D. G., 2003. Status of the Amur tiger and Far Eastern leopard. In: J.P. Newell, ed. The Russian Far East: A Reference Guide for Conservation and Development. McKinleyville, CA: Daniel and Daniel Publishers, 106–109.
   Google Scholar
• Orrenius, S., Zhivotovsky, B., and Nicotera, P., 2003. Regulation of cell death: the calcium-apoptosis link. Nature Reviews – Molecular Cell Biology, 4, 552–565.
   PubMed Web of Science ®Google Scholar
• Roncal, C., et al., 2007. Lead, at low levels, accelerates arteriolopathy and tubulointerstitial injury in chronic kidney disease. American Journal of Physiology – Renal Physiology, 293, F1391–F1396.
   PubMed Web of Science ®Google Scholar
• Roy, N.K., and Rossman, T.G., 1992. Mutagenesis and comutagenesis by lead compounds. Mutation Research, 298, 97–103.
   PubMed Web of Science ®Google Scholar
• Russello, M.A., et al., 2004. Potential genetic consequences of a recent bottleneck in the Amur tiger of the Russian far-east. Conservation Genetics, 5, 707–713.
   Web of Science ®Google Scholar
• Srianujata, S., 1998. Lead- the toxic metal to stay with human. The Journal of Toxicological Sciences, 23, 237–240.
   PubMedGoogle Scholar
• Valencia-Cruz, G., et al., 2009. Kbg and Kv1.3 channels mediate potassium efflux in the early phase of apoptosis in Jurkat T lymphocytes. American Journal of Physiology – Cell Physiology, 297, C1544–C1553.
   PubMed Web of Science ®Google Scholar
• Van Wijngaarden, E., and Dosemeci, M., 2006. Brain cancer mortality and potential occupational exposure to lead: findings from the national longitudinal mortality study, 1979–1989. International Journal of Cancer, 119, 1136–1144.
   PubMed Web of Science ®Google Scholar
• Villeda-Hernandez, J., et al., 2006. Morphometric analysis of brain lesions in rat fetuses prenatally exposed to low-level lead acetate: correlation with lipid peroxidation. Histology and Histopathology, 21, 609–617.
   PubMed Web of Science ®Google Scholar
• Xu, J., 2008. Study on the pathways of lead acetate-induced apoptosis in PC12 cells. Dissertation, Zhejiang University.
   Google Scholar
• Xu, J., Ji, L.X., and Li, H., 2006. Lead-induced apoptosis in PC 12 cells: Involvement of p53, Bcl-2 family and caspase-3. Toxicology Letters, 166, 160–167.
   PubMed Web of Science ®Google Scholar
• Yanamandra, N., et al., 2011. Tipifarnib-induced apoptosis in acute myeloid leukemia and multiple myeloma cells depends on Ca2+ influx through plasma membrane Ca2+ channels. The Journal of Pharmacology and Experimental Therapeutics, 337, 636–643.
   PubMed Web of Science ®Google Scholar
• Yang, J.L., Yeh, S.C., and Chang, C.Y., 1996. Lead acetate mutagenicity and mutational spectrum in the hypoxanthine guanine phosphoribosyltransferase gene of Chinese hamster ovary K1 cells. Molecular Carcinogenesis, 17, 181–191.
   PubMed Web of Science ®Google Scholar
• Yin, F., and Huang, J.H., 1999. The status of the tiger and it’s induced risk factors. China Wildlife, 20, 26–27.
   Google Scholar
• Yu, X., Kubota, H., and Wang, R., 2001. Involvement of Bcl-2 family genes and Fas signaling system in primary and secondary male germ cell apoptosis induced by 2-bromopropane in rat. Toxicology and Applied Pharmacology, 174, 35–48.
   PubMed Web of Science ®Google Scholar
• Zelikoff, J.T., et al., 1988. Genetic toxicology of lead compounds. Carcinogenesis, 9, 1727–1732.
   PubMed Web of Science ®Google Scholar