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Environmental Exposure to Lead as a Risk for Prostate Cancer

Environmental Exposure to Lead as a Risk for Prostate Cancer
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摘要 Objective To evaluate the possible role of environmental exposure to lead as a risk factor for prostate pathology in patients suffering from prostate cancer (PCA) and benign prostate hyperplasia (BPH). Methods Blood lead (BPb) level was determined in PCA and BPH cases using a graphite furnace Atomic Absorption Spectrophotometer and compared with those in a control group living in the similar socioeconomic environment. Results BPb was significantly higher in PCA and BPH cases than in normals (P<0.05). Blood levels of zinc and copper were significantly lower in PCA and BPH cases when compared with controls (P<0.05). In all the three groups, a statistically significant positive correlation between lead and thiobarbituric acid reactive substances (TEARS) measured as malondialdehyde, and negative correlation between blood lead and antioxidant GSH level, indicative of possible generation of reactive oxygen species, were also observed after adjusting for age as a possible confounders. However, positive association between blood lead and TEARS was relatively higher in PCA patients (r=0.77, P<0.05) than in BPH (r=0.32, P<0.05) and normal (r=0.30, P<0.05). Conclusion These results with limited power seem to suggest for the first time that environmental exposure of aging males to lead may be a risk factor for prostate cancer and/or benign prostate hyperplasia possibly through generation of reactive oxygen species and/or reducing the level of zinc which acts as a cellular growth protector. Objective To evaluate the possible role of environmental exposure to lead as a risk factor for prostate pathology in patients suffering from prostate cancer (PCA) and benign prostate hyperplasia (BPH). Methods Blood lead (BPb) level was determined in PCA and BPH cases using a graphite furnace Atomic Absorption Spectrophotometer and compared with those in a control group living in the similar socioeconomic environment. Results BPb was significantly higher in PCA and BPH cases than in normals (P<0.05). Blood levels of zinc and copper were significantly lower in PCA and BPH cases when compared with controls (P<0.05). In all the three groups, a statistically significant positive correlation between lead and thiobarbituric acid reactive substances (TEARS) measured as malondialdehyde, and negative correlation between blood lead and antioxidant GSH level, indicative of possible generation of reactive oxygen species, were also observed after adjusting for age as a possible confounders. However, positive association between blood lead and TEARS was relatively higher in PCA patients (r=0.77, P<0.05) than in BPH (r=0.32, P<0.05) and normal (r=0.30, P<0.05). Conclusion These results with limited power seem to suggest for the first time that environmental exposure of aging males to lead may be a risk factor for prostate cancer and/or benign prostate hyperplasia possibly through generation of reactive oxygen species and/or reducing the level of zinc which acts as a cellular growth protector.
出处 《Biomedical and Environmental Sciences》 SCIE CAS CSCD 2002年第4期298-305,共8页 生物医学与环境科学(英文版)
基金 Correspondence should be addressed: Dr. M.K.J. Siddiqui, Industrial Toxicology Research Centre, Post Box No. 80, M.G Marg, Lucknow-226001, India. Telephone: 0522-227586, Fax: 91522 228227, E-mail: itrc@ sanchamet.in
关键词 Benign prostate hyperplasia Prostate cancer Blood lead Atomic Absorption Spectrophotometer Benign prostate hyperplasia Prostate cancer Blood lead Atomic Absorption Spectrophotometer
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  • 1[1]Wingo, P.A., Landis, S., and Ries, I.A. (1997). An adjustment to the 1997 estimate for new prostate cancer cases. Cancer80, 1810-1813.
  • 2[2]Yeole, B.B. and Jussawala, DJ. (1997). Descriptive epidemiology of the cancers of male genital organs in greater Bombay. Indian J. Cancer 34, 30-34.
  • 3[3]Wilson, M.J. (1995). Proteases in prostate development, function and pathology. Microse. Res. Tech. 30, 305-318.
  • 4[4]Anumuller, G., Scitz, J., and Riva, A. (1994). Functional Morphplogy of Prostate Gland, in Ultrastructre of Male Urogeniatal Glands: Prostate Seminal Vesicles, Urethral, and Bulbourethral Glands. (A. Riva, F. Testa Riva and P. M. Motta, Eds.), pp. 61-112, Kluwer Academic Publishers, Hingham.
  • 5[5]Nogueira, E. (1987). Rat renal carcinogenesis after chronic simultaneous exposure to lead acetate and Nnitrosodiethylamine. Virch. Arch. B 53, 365-374.
  • 6[6]Zawirska, B. and Medras, K. (1972). The role of the kidneys in disorders of porphyrin metabolism during carcinogenesis induced with lead acetate. Arch. Immunol. Ther. Exp. 20, 257-272.
  • 7[7]Blakley, B.R. (1987). The effect of lead on chemical- and viral-induced tumor production in mice. J. Appl.Toxicol. 7, 167-172.
  • 8[8]Steenland, K. and Boffetta, P. (2000). Lead and cancer in humans: Where are we Now? Am. J. Indus. Med. 38,295-299.
  • 9[9]Winder, C. and Bonin, T. (1993). The genotoxicity of lead. Mutation Res. 285, 117-124.
  • 10[10]Hartwig, A.R., Schlepegrell, and Beyersmann, D. (1990). Indirect mechanism of lead induced genotoxicity in cultured mammalian cells. Mutation Res. 241, 75-82.

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