• صفحه اصلی
  • Blood Lead Level and Δ-Aminolevulinic Acid Dehydratase Activity in Pre-Menopausal and Postmenopausal Women

اشتراک گذاری

آدرس مقاله


کد مقاله : JCHR-43 بازدید : 135 صفحه: 0 - 0

10.22034/jchr.2012.543989

نوع مقاله: پژوهشی

Blood Lead Level and Δ-Aminolevulinic Acid Dehydratase Activity in Pre-Menopausal and Postmenopausal Women

محورهای موضوعی :

I.R Elezaj 1 , K.Rr. Letaj 2 , Q.I. Selimi 3 , A. Rrustemi 4 , D. Zogaj 5 , L. Sefaja 6

1 - Department of Biology, University of Prishtina, Republic of Kosovo
2 - Department of Biology, University of Prishtina, Republic of Kosovo
3 - Department of Biology, University of Prishtina, Republic of Kosovo
4 - Department of Biology, University of Prishtina, Republic of Kosovo
5 - Institute of National Public Health, University of PrishtinaP.O.Box 10.000 Prishtinë, Republic of Kosovo
6 - Institute of National Public Health, University of PrishtinaP.O.Box 10.000 Prishtinë, Republic of Kosovo

تاریخ دریافت : 1391/04/22 تاریخ پذیرش : 1397/08/07 تاریخ انتشار : 1391/03/12

کلید واژه: Women, blood, Lead, Menopause, ALAD, Hct,

چکیده مقاله :

To describe the relationship of blood lead levels (BLL) and blood, δ-aminolevulinic acid dehydratase(ALAD) activity and haematocrit value(Hct) to menopause , were examined 17 pre-or perimenopausal (PreM) and 17 postmenopausal women (PosM)from Prishtina City, the capital ofRepublic Kosovo. The mean age of the PreM women was 28.8 years (21-46), with a mean blood lead level of 1.2 μg/dL (SD=0.583 μg/dL ) , the mean blood ALAD activity53.2 U/LE (SD= 2.8 U/LE) and haematocrit value42.1 % (SD= 4.3 %). The mean age of the PosM women was 53.6 years (43-67), with a mean blood lead level1.9 μg/dL (SD=0.94 μg/dL), the mean blood ALAD activity 44.4 U/LE(SD=7.2 U/LE) and haematocrit value 42.1 % ( SD= 4.3 %) and 42.2 % (SD=4.4 %). The BPb level of PosM women was significantly higher (P<0.001) in comparison with the BPb level in PreM women. The blood ALAD activity of PosM was significantly inhibited (P<0.002) in comparison with blood ALAD activity in PreM women. The haematocrit values were relatively unchanged. There was established significantly negative correlation between BPb and blood ALAD activity (r=- 0.605; P<0.01) in the PreM women.These results support the hypothesis that release of bone lead stores increases during menopause and constitutes an internal source of exposure possibly associated with adverse health effects on women in menopause transition.

چکیده انگلیسی:

منابع و مأخذ:
  1. Brody D.J., Kramer R.A., et al. Blood lead levels
  2. in the U.S. population. Phase 1of the Third
  3. National Health and Nutritional Examination
  4. Survey (NHABES, 1988to 1991) . JAMA 1994;
  5. .283 -272:277
  6. Silbergeld E.K., Schwartz J., Mahaffey K. 1988.
  7. Lead and osteoporosis: mobilization on lead from
  8. bone in postmenopausal women. Environ Res. 47:
  9. .94 -79
  10. Symanski E., Hertz P.I. 1995. Blood lead level in
  11. relation to menopause, smoking, and pregnancy
  12. history. Am J Epidemiol. 141: .158 -1047
  13. Rabinowitz M.B., Wetherill G.W., Kopple J.D.
  14. : Kinetic analysis of lead metabolism in
  15. healthy humans, J Clin Invest. 58: .270 -260
  16. Robison C.J., Hall J., Beshir S.O. 1983.
  17. Hormonal modulation of mineral metabolism in
  18. reproduction. Proc Nutr Soc. .180 -42:169
  19. Oââ‚‌™Flaherty E.J. 1991. Physiologically models
  20. for bone ââ‚‌“seeking elements. I. Rat skeletal and
  21. bone growth. Toxicol Appl Pharmacol .111:
  22. .312 -299
  23. Oââ‚‌™Flaherty E.J. 1991. Physiologically models
  24. for bone ââ‚‌“seeking elements. II. Kinetics of lead
  25. deposition in rats. Toxicol Appl Pharmacol
  26. .111: .331 -313
  27. Oââ‚‌™Flaherty E.J. 1991. Physiologically models
  28. for bone ââ‚‌“seeking elements. III. Human skeletal
  29. and bone growth. Toxicol Appl Pharmacol.
  30. .341 -111:332
  31. Garel J.M. 1987. Hormonal control of calcium
  32. metabolism during the reproductive cycle in
  33. mammals. Physiol Rev. 67: .66 -1
  34. Berkowitz G.S. Moline J., Todd A.C., 1999.
  35. Methodological issues related to studies of lead
  36. mobilization during menopause. Salud Publica
  37. de Mexico. Vol.41, suplemento 2. s88-s.92
  38. Luckey M., Meier D., Wallenstein S., Lapinski
  39. R. 1992. Racial differences in early
  40. postmenopausal bone loss: A longitudinal
  41. study. J Bone Miner Res. 7: S .140
  42. Silbergeld E., Watson L. 1991. Lead in bone:
  43. implications for toxicology during pregnancy
  44. and lactation. Environ Health Perspect. 91: -63
  45. .70
  46. Rosen J.F., Pounds J.G. 1988. The cellular
  47. metabolism of lead and calcium: a kinetic
  48. analysis in cultured osteoclastic bone cells.
  49. Contrib Nephrol. ,.82 -64:74
  50. Pounds J.G., Long G.J., Rosen J.F. 1991.
  51. Cellular and molecular toxicity of lead in bone .
  52. environ Health Perspect. 91: .32 -17
  53. Pounds J.G. 1984. Effect of lead interaction on
  54. calcium homeostasis and calcium-mediated cell
  55. function: a review. Neurotoxicology. 5: -295
  56. .331
  57. Simons T.J. 1993. Lead-calcium interactions in
  58. cellular lead toxicity. Neurotoxicity. 14: .85 -77
  59. Berglund M., Akesson A., Bjellerup P. , et al.
  60. Metal-bone interactions. Toxicol Lett.
  61. -112: .225 -219
  62. Manton W.I. 1985. Total contribution of
  63. airborne lead to blood lead. Br J Ind Med.
  64. .172 -42:168
  65. Bronner F. 1992. Bone and calcium
  66. homeostasis. Neurotoxicology. 13: .782 -775
  67. Wittmers L.J. Aufderheide A.C. Wallgren J.
  68. Lead in bone. I. Distribution of lead in
  69. human skeleton. Arch Environ Health. 43: -381
  70. .391
  71. Inskip M.J., Franklin C.A., Subramanian K.S.
  72. et. al. 1992. Sampling of cortical and trabecular
  73. bone for lead analysis: method development in
  74. stady of lead mobilization during pregnancy.
  75. Neurotoxicology. 13: .834 -825
  76. Gulson B.L., Mizon K.J., Korsch M.J. et. al.
  77. Mobilization of lead from human bone
  78. tissue during pregnancy and lactation-a
  79. summary of long-term research. Sci Total
  80. Environ. 303: .104 -79
  81. Vahter M., Berglund M., Akesson A., et al.
  82. Metals and womenââ‚‌™s health. Environ Res.
  83. : .155 -145
  84. Lindquist O, Bengtsson C, Hansson T. et al.,
  85. Bone mineral content in relation to age
  86. and menopause in middle-age women: a study
  87. of bone density in lumbar vertebrae by dual
  88. photon absorptiometry in a population sample
  89. of women. Scand J Clin Lab Invest. 41: -215
  91. Riggs B.L., Melton L.D. 1986. Involutional
  92. osteoporosis. N Engl J Med Lancet. 314: -1676
  93. .1686
  94. Sharp D.S., Becker C.E., Smith A.H. 1987.
  95. Chronic low ââ‚‌“ level lead exposure: its role in
  96. the pathogenesis of hypertension. Med Toxicol.
  97. .232 -2:210
  98. Nash D., Magder L., Lustberg M., et al., 2003.
  99. Blood lead , blood pressure and hypertension in
  100. perimenopausal and postmenopausal women.
  101. JAMA. 289: .1532 -1523
  102. Payton M., Riggs K.M, Spiro A. et al. 1988.
  103. Relations of bone and blood lead to cognitive
  104. function. The VA Normative Aging Study.
  105. Neurotoxicol Teratol. 20: .27 -19
  106. Lustberg M., Silbergeld E. 2002. Blood lead
  107. levels and mortality. Arch Intern Med. 162:
  108. . 2449 -2443
  109. Morita Y., Sakai T., Araki T.,
  110. Masuayama.1993. Usefulness of δ-
  111. aminolevulinic acid in blood as an indicator of
  112. lead exposure. Jpn J Ind Health. .118 -35:112
  113. Sakai T. 2000. Biomarkers of Lead Exposure.
  114. Industrial Health.38; .142 -127
  115. .32 Berlin D., Schaller K.K.1974. European
  116. standardized method for the determination of δ-
  117. aminolevulinic acid dehydratase activityin
  118. blood. Z. Klin. Chem. Biochem. 12: .390 -389
  119. Nash D., Magder L.S., Sherwin R., Rubin R.J.
  120. and Silbergeld E.K. 1994. Bone Density-related
  121. Predictions of Blood Lead Level among Periand
  122. Postmenopausal Women in the United
  123. States. American Journal of Epidemiology.
  124. Vol.160, Issue 9; .911 -901
  125. Latorre F.G., Hernandez-Avila M., Orozco J.T.,
  126. medina C.A, Aro A., Palazuelos E., H. H. 2003.
  127. Relationship of Blood and Bone Lead to
  128. Menopause and Bone Mineral density among
  129. Middle-Age Women in Mexico City.
  130. Environmental Health Perspectives. Vol.11, N 0
  131. : 636 -631
  132. Hernandez ââ‚‌“Avila M. Villalapondo VG,
  133. Palazuelos R. et al. 2000. Determinations of
  134. blood and bone lead levels across the
  135. menopausal transition. Arch. Environ Health.
  136. : 360 -355
  137. Sun Y., Sun D., Zhou Z., Zhu G., Zhang H.,
  138. Chang X., Lei L., Jin T. 2008. Osteoporosis in
  139. Chinese Population Due to Occupational
  140. Exposure to Lead. AMERICAN JOURNAL OF
  141. INDUSTRIAL MEDICINE. .442 -51:436
  142. Smith D.R., Osterioh J.D., Fegal A.R. 1996. use
  143. of endogenous stable lead isotope to determine
  144. release of lead from the skeleton. Environ
  145. Health Perspect. .66 -104:60
  146. Murata K., Iwata T., Dakeishi M., Karita K.
  147. Lead Toxicity: Does the Critical Level of
  148. lead Resulting in Adverse Effects Differ
  149. between Adults and Children ?. .12 -51:1
  150. Murata K., Sakai T., Morita Y., Iwata T.,
  151. Dakeishi M. 2003. Critical Dose of Lead
  152. Affecting δ-Aminolevulinic Acid Levels. J
  153. Occup Health. 45: (.214 -209

سکوی نشر دانش

سند یا سکوی نشر دانش ،سامانه ای جهت مدیریت حوزه علمی و پژوهشی نشریات دانشگاه آزاد می باشد

پیوندهای سایت

مراکز مرتبط

پشتیبانی

صفحات رسمی

حقوق این وب‌سایت متعلق به سامانه مدیریت نشریات دانشگاه آزاد اسلامی است.
حق نشر © 1403-1400

صفحه اصلی| عضویت/ ورود| درباره سند| تماس با ما|
[English] [العربية] [en] [ar]