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MeSH Review

Lead Poisoning

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Disease relevance of Lead Poisoning


Psychiatry related information on Lead Poisoning

  • The resultant mental incompetence and especially the rapidly declining birth rate among the ruling class are now believed to have been major factors in the decline of the Roman Empire. Epidemic outbreaks of lead poisoning have occurred repeatedly throughout history and still occur today [6].
  • However, coexposure to lead and ethanol could result in more serious depletion of calcium and magnesium, and this could be the cause of suspected synergism between alcohol consumption and lead poisoning [7].

High impact information on Lead Poisoning


Chemical compound and disease context of Lead Poisoning

  • The mean Kis of lead for glucose-6-phosphate and nicotinamide adenine dinucleotide phosphate (NADP) for G6PD were 1.5 microM and 2.1 microM, respectively, which is within the range of intraerythrocytic lead concentrations found in clinical lead poisoning [1].
  • In chronic demyelination caused by lead poisoning, the cellular and extracellular distribution of apolipoproteins was similar to Te neuropathy; the amount of apo E accumulation and the macrophage density were proportional to the prevalence of active demyelination in teased fibers [13].
  • Published recommendations (1985) for the management of childhood lead poisoning suggest the use of ethylenediaminetetraacetic acid (EDTA) provocation testing and chelation as the mainstay of treatment for blood lead levels between 25 and 55 micrograms/dL [14].
  • Effects of calcium disodium versenate (CaNa2EDTA) chelation in moderate childhood lead poisoning [15].
  • Excess dietary selenium did protect partially against lead poisoning in vitamin E-deficient rats, but the levels of selenium used were toxic in themselves [16].

Biological context of Lead Poisoning


Anatomical context of Lead Poisoning


Gene context of Lead Poisoning


Analytical, diagnostic and therapeutic context of Lead Poisoning


  1. Inhibition of the pentose phosphate shunt by lead: a potential mechanism for hemolysis in lead poisoning. Lachant, N.A., Tomoda, A., Tanaka, K.R. Blood (1984) [Pubmed]
  2. Autoantibody against erythrocyte protein 4.1 in a patient with autoimmune hemolytic anemia. Wakui, H., Imai, H., Kobayashi, R., Itoh, H., Notoya, T., Yoshida, K., Nakamoto, Y., Miura, A.B. Blood (1988) [Pubmed]
  3. Mechanism of oxidative DNA damage induced by delta-aminolevulinic acid in the presence of copper ion. Hiraku, Y., Kawanishi, S. Cancer Res. (1996) [Pubmed]
  4. DNA damage by 3,6-dihydropyrazine-2,5-dipropanoic acid, the cyclic dimerization product of 5-aminolevulinic acid. Teixeira, P.C., Onuki, J., Medeiros, M.H., Dörnemann, D., Di Mascio, P. Biol. Chem. (2001) [Pubmed]
  5. Hemolytic anemia associated with lead poisoning from shotgun pellets and the response to Succimer treatment. Aly, M.H., Kim, H.C., Renner, S.W., Boyarsky, A., Kosmin, M., Paglia, D.E. Am. J. Hematol. (1993) [Pubmed]
  6. A perspective of lead poisoning in antiquity and the present. Woolley, D.E. Neurotoxicology (1984) [Pubmed]
  7. Combined exposure to lead and ethanol on tissue concentration of essential metals and some biochemical indices in rat. Flora, S.J., Kumar, D., Sachan, S.R., Das Gupta, S. Biological trace element research. (1991) [Pubmed]
  8. Saturnine gout among Roman aristocrats. Did lead poisoning contribute to the fall of the Empire? Nriagu, J.O. N. Engl. J. Med. (1983) [Pubmed]
  9. Lead poisoning: altered urinary catecholamine metabolites as indicators of intoxication in mice and children. Silbergeld, E.K., Chisolm, J.J. Science (1976) [Pubmed]
  10. Lead poisoning among low-income children in Orange County, California. A need for regionally differentiated policy. Gellert, G.A., Wagner, G.A., Maxwell, R.M., Moore, D., Foster, L. JAMA (1993) [Pubmed]
  11. Acute lead poisoning in two users of illicit methamphetamine. Allcott, J.V., Barnhart, R.A., Mooney, L.A. JAMA (1987) [Pubmed]
  12. Treatment of lead poisoning by 2,3-dimercaptosuccinic acid. Friedheim, E., Graziano, J.H., Popovac, D., Dragovic, D., Kaul, B. Lancet (1978) [Pubmed]
  13. Macrophage apolipoprotein synthesis and endoneurial distribution as a response to segmental demyelination. Gelman, B.B., Goodrum, J., Bouldin, T.W. J. Neuropathol. Exp. Neurol. (1991) [Pubmed]
  14. Management of childhood lead poisoning: a survey. Glotzer, D.E., Bauchner, H. Pediatrics (1992) [Pubmed]
  15. Effects of calcium disodium versenate (CaNa2EDTA) chelation in moderate childhood lead poisoning. Markowitz, M.E., Bijur, P.E., Ruff, H., Rosen, J.F. Pediatrics (1993) [Pubmed]
  16. Comparative effects of selenium and vitamin E in lead-poisoned rats. Levander, O.A., Morris, V.C., Ferretti, R.J. J. Nutr. (1977) [Pubmed]
  17. An artificial gene for human porphobilinogen synthase allows comparison of an allelic variation implicated in susceptibility to lead poisoning. Jaffe, E.K., Volin, M., Bronson-Mullins, C.R., Dunbrack, R.L., Kervinen, J., Martins, J., Quinlan, J.F., Sazinsky, M.H., Steinhouse, E.M., Yeung, A.T. J. Biol. Chem. (2000) [Pubmed]
  18. Pharmacokinetics of meso-2,3-dimercaptosuccinic acid in patients with lead poisoning and in healthy adults. Dart, R.C., Hurlbut, K.M., Maiorino, R.M., Mayersohn, M., Aposhian, H.V., Hassen, L.V. J. Pediatr. (1994) [Pubmed]
  19. Lead poisoning from an unexpected source in a 4-month-old infant. Shannon, M. Environ. Health Perspect. (1998) [Pubmed]
  20. Metabolism of meso-2,3-dimercaptosuccinic acid in lead-poisoned children and normal adults. Asiedu, P., Moulton, T., Blum, C.B., Roldan, E., Lolacono, N.J., Graziano, J.H. Environ. Health Perspect. (1995) [Pubmed]
  21. 2,3-Dimercaptosuccinic acid: a new agent for the treatment of lead poisoning. Graziano, J.H., Leong, J.K., Friedheim, E. J. Pharmacol. Exp. Ther. (1978) [Pubmed]
  22. Pyrimidine-specific 5' nucleotidase activity in bovine erythrocytes: effect of phlebotomy and lead poisoning. George, J.W., Duncan, J.R. Am. J. Vet. Res. (1982) [Pubmed]
  23. Carbonic anhydrase isozymes, hemoglobin-F and glutathione levels in lead-exposed workers. Taniguchi, N., Sato, T., Kondo, T., Tamachi, H., Saito, K. Clin. Chim. Acta (1975) [Pubmed]
  24. Alteration of glucose metabolism in the spinal cord of experimental lead poisoning rats: microdetermination of glucose utilization rate and distribution volume. Yokoyama, K., Araki, S., Akabayashi, A., Kato, T., Sakai, T., Sato, H. Industrial health. (2000) [Pubmed]
  25. Damage to rat liver mitochondria promoted by delta-aminolevulinic acid-generated reactive oxygen species: connections with acute intermittent porphyria and lead-poisoning. Hermes-Lima, M., Valle, V.G., Vercesi, A.E., Bechara, E.J. Biochim. Biophys. Acta (1991) [Pubmed]
  26. Effect of lead chelation therapy with EDTA in children on erythrocyte pyrimidine 5'-nucleotidase and with cytidine triphosphate levels. Swanson, M.S., Angle, C.R., Stohs, S.J. International journal of clinical pharmacology, therapy, and toxicology. (1982) [Pubmed]
  27. Lead toxicity as related to glutathione metabolism. Hsu, J.M. J. Nutr. (1981) [Pubmed]
  28. A molecular epidemiological study of childhood lead poisoning in lead-polluted environment. Zheng, Y., Leng, S., Song, W., Wang, Y., Niu, Y., Zhang, W., Yan, H., Liu, Y., Huang, Q., Wu, Y. Zhonghua Liu Xing Bing Xue Za Zhi (2002) [Pubmed]
  29. delta-Aminolevulinic acid dehydratase isozymes and lead toxicity. Astrin, K.H., Bishop, D.F., Wetmur, J.G., Kaul, B., Davidow, B., Desnick, R.J. Ann. N. Y. Acad. Sci. (1987) [Pubmed]
  30. Identification of community flour mills as the source of lead poisoning in West Bank Arabs. Eisenberg, A., Avni, A., Grauer, F., Weissenberg, E., Acker, C., Hamdallah, M., Shahin, S., Moreb, J., Hershko, C. Arch. Intern. Med. (1985) [Pubmed]
  31. The presence of lead decreases the availability of meso-2, 3-dimercaptosuccinic acid for analysis in the monobromobimane assay. Lever, S.Z., Parsons, T.L. Chem. Res. Toxicol. (1999) [Pubmed]
  32. The effect of 2,3 dimercaptosuccinic acid in the treatment of lead poisoning in adults. Lifshitz, M., Hashkanazi, R., Phillip, M. Ann. Med. (1997) [Pubmed]
  33. Does vitamin C intake protect against lead toxicity? Houston, D.K., Johnson, M.A. Nutr. Rev. (2000) [Pubmed]
  34. Choosing area based socioeconomic measures to monitor social inequalities in low birth weight and childhood lead poisoning: The Public Health Disparities Geocoding Project (US). Krieger, N., Chen, J.T., Waterman, P.D., Soobader, M.J., Subramanian, S.V., Carson, R. Journal of epidemiology and community health. (2003) [Pubmed]
  35. Aminolevulinic acid dehydratase genotype mediates plasma levels of the neurotoxin, 5-aminolevulinic acid, in lead-exposed workers. Sithisarankul, P., Schwartz, B.S., Lee, B.K., Kelsey, K.T., Strickland, P.T. Am. J. Ind. Med. (1997) [Pubmed]
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