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  1. NTU Theses and Dissertations Repository
  2. 生命科學院
  3. 動物學研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/75454
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dc.contributor.authorJwo-Sheng Chenen
dc.contributor.author陳卓昇zh_TW
dc.date.accessioned2021-07-01T08:13:17Z-
dc.date.available2021-07-01T08:13:17Z-
dc.date.issued1982
dc.identifier.citation1. Abbrecht, P., D. Mouw. A. Vander and K. Kalitis. 1978. The effect of chronic, low-level lead poisoning on the erythropoietin response to hypoxia. Proc. Soc. Expt. Biol. Med., 158, 109-112.
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4. Becker, K.L. 1976. Endocrine and metabolic disorders. In THE LABORATORY IN CLINICAL MEDICINE: INTERPRETATION AND APPLICATION ed. by J.A. Halsted. W.B. Saunders Co. Philadelphia. pp. 665-747.
5. Bridord, K. and H.P. Blejer. 1978. Prophylatic chelation therapy in occupational lead poisoning: A review. Am. Ind. Hyg. Assoc. J., 38, 536-542.
6. Burch, H.B. and A.L. Siegel. 1971. Improved method for measurement of delta-aminolevulinic acid dehydratase activity of human erythrocytes. Clin. Chem., 17, 1038-1041.
7. Bushinell, P.J. and H.F. DeLuca. 1981. Lactose facilitates the intestinal absorption of lead in weanling rats. Sci., 211, 61-63.
8. Caspers, M.L. and G.J. Siegel. 1980. Inhibition by lead of human erythrocyte (Na++K+)-adenosine triphosphatase associated with binding of 210-Pb to membrane fragments. Biochim. Biophys. Acta, 600, 27-35.
9. Chang, M.H. and D.W. King. 1982. Effects of cadmium chloride on the activity of the alkaline and acid phosphatases in the bone of the mouse. Proc. Natl. Sci. Counc. (R.O.C.), 6, 85-92.
10. Chiba,M. and M. Kikuchi. 1979. 5-aminolevulinate dehydratase activity in blood of rabbits given tin or lead. Brit. J. Ind. Med., 36, 323-325.
11. Chisolm, J.J., Jr. 1968. The use of chelating agents in the treatment of acute and chronic lead intoxication in childhood. J. Pediat., 73, 1-38.
12. Chisolm, J.J., Jr., M.B. Barrett and E.D. Mellitis. 1975. Dose effect and dose-response relationships for lead in children. J. Pediat., 87, 1152-1160.
13. De Barreiro, O.C. 1967. 5-aminolevulinate dehydratase from yeast isolation and purification. Biochim. Biophys. Acta, 139, 479-486.
14. Dresel, E.I.B. and J.E. Falk. 1956a. Studies on the biosynthesis of blood pigments. 2. Haem and porphyrin formation in intact chicken erythrocytes. Biochem. J., 63, 72-79.
15. Idem, 1956b. Studies on the biosynthesis of blood pigments. 3. Haem and porphyrin formation from δ-aminolevulinic acid and from porphobilinogen in haemolysed chicken erythrocytes. Biochem. J., 63, 80-87.
16. Fernley, H.N. 1970. Mammalian alkaline phosphatases. In THE ENZYME ed. by P.D. Boyer, Acad. Press, New York. Vol. 4, pp. 417.
17. Frankel, S., S. Reitman and A.C. Sonnenwirth. 1970. GRADWOHL'S LABORATORY METHODS AND DIAGNOSIS 7th ed. The C.V. Mosby Co. St. Louis. Vol. I, pp. 58, 112-115.
18. Gelman, B.B., I.A. Michaelson and J.S. Bus. 1978. The effect of lead on oxidative hemolysis and erythrocyte defense mechenism in the rat. Toxicol. Appl. Pharmacol., 45, 119-129.
19. Gibson, K.D., A. Neuberger and J.J. Scott. 1955. The purification and properties of δ-aminolevulinic acid dehydratase. Biochem. J., 61, 618-629.
20. Goldberg, A., H. Ashenbrucker, G.E. Cartwright and M.M. Wintrobe. 1956. Studies on the biosynthesis of home in vitro by avian erythrocytes. Blood, 11, 821-833.
21. Gurba, P.E., R.E. Sennett and R.D. Kobes. 1972. Studies on the mechenism of action of δ-aminolevulinate. dehydratase from bovine and rat liver. Arch. Biochim. Biophys., 150, 130-136.
22. Hamilton, A. and H.L. Hardy. 1974. Lead. In INDUSTRIAL TOXICOLOGY 3rd. ed. Publishing Sciences Group, Inc. Acton, Mass. U.S.A. pp. 85-121.
23. Howard, J.K. 1974. Human erythrocyte glutathione reductase and glucose-6-phosphate dehydrogenase activities in normal subjects and persons exposed to lead. Clin. Sci. Mol. Med., 47, 515-520.
24. Hsieh, C.C. 1982. Long-term lead effects on the activities of adenosine triphosphatase, alkaline phosphatase and acetyl-choline esterase of the mouse brain. Bachelor thesis, National Taiwan University.
25. Hsu, J.M. 1981. Lead toxicity as related to glutathione metabolism. J. Nutr., 111, 26-33.
26. Javitt, N.B. 1961. Glutathione role in conjugation in the liver. Am. J. Med., 30, 341-344.
27. Jugo, S. 1977. Metabolism of toxic heavy metals in growing organism: A review. Environ. Res., 13, 36-46.
28. Keller, C.A. and R.A. Doherty. 1980. Effect of dose on lead retention and distribution in suckling and adult female mice. Toxicol. Appl. Pharmacol. 52, 285-293.
29. King, D.W., D.C.C. Chen, A.W.S. Wung, J.L. Hsu, J.M. Lai, H.N. Chiang and G.R. Lu. 1980. Interrelationships of zinc, cadmium and lead in chick embryogenesis. Proc. Natl. Sci. Counc. (R.O.C.), 4, 55-64.
30. King, D.W. and J.L. Hsu. 1976. Effect of lead acetate on chick embryogenesis. BioScience (R.O.C.), 9, 41-54.
31. Kokarovtseva, M.G. 1980. Interrelationship between the biotransformation of acetylcysteine and its detoxifying capacity. Khim-Farm. Zh., 13, 15-18. (Abst.)
32. Lazdunski, C., C. Petetelere and M. Lazdunski. 1968. Structure-function relationships for some metalloalkaline phosphatase of E. coli.. Eur. J. Biochem., 8, 501-517.
33. Lenz, G.R. and A.E. Martell. 1964. Metal chelates of some sulfur-containing amino acid. Biochemistry, 3, 745-750.
34. Li, N.C. and R.A. Manning. 1955. Some metal complexes of sulfur-containing amino acid. J. Am. Chem. Soc., 77, 5225-5228.
35. Lin-Fu, J.S. 1973. Vulnerability of children to lead exposure and toxicity. N. Eng. J. Med., 289, 1289-1293.
36. Lorenzo, A.V., M. Gewirtz, C. Maher and L.I. Davidowski. 1977. The equilibration of lead between blood and milk of lactating rabbits. Life Sci., 21, 1679-1683.
37. Lorenzo, A.V., M. Gewirtz and D. Averill. 1978. CNS lead toxicity in rabbit offspring. Environ. Res., 17, 131-150.
38. Lowry, O.H., N.J. Rosebrough, A.L. Farr and R.J. Randa. 1951. Protein measurement with the folin phenol reagent. J. Biol. Chem., 193, 265-275.
39. Lowry, O.H., N.R. Roberts, M.-L. Wu, W.S. Hixon and E.J. Crawford. 1954. Quantitative histochemistry of brain. II. Enzyme measurements. J. Biol. Chem., 207, 19-37.
40. Mauras, Y. and P.Allain. 1979. Inhibition of delta-aminolevulinc acid dehydratase in human red blood cells by lead and activation by zinc and cysteine. Enzyme, 24, 181-187. (Abst.)
41. McNiff, E.F., L.K. Cheng, H.C. Woodfield and H.L. Fung. 1978. Effect of L-cysteine, L-cysteine derivatives and ascorbic acid on lead excretion in rats. Res. Commun. Chem. Pathol. Pharmacol., 20, 131-137.
42. Michaelson, I.A. and M.W. Sauerhoff. 1974. An improved model of lead-induced brain dysfunction in the suckling rat. Toxicol. Appl. Pharmacol., 28, 88-96.
43. Mitema, E.S., F.w. Oehme and L. Penumarthy. 1980. Effect of chronic lead on the haematology, blood glutathione and bone marrow non-haem iron of dogs. Acta Pharmacol. Toxicol., 46, 250-256.
44. Mylroie, A.A., L. Moore and U. Erogbogbo. 1977. influence of dietary factors on blood and tissue lead concentrations and lead toxicity. Toxicol. Appl. Pharmacol., 41, 361-367.
45. Natelson, S., M.L. Scott and C. Beffa. 1951. A rapid method for the estimation of urea in biological fluids by means of the reaction between diacetyl and urea. Am. J. Clin. Path., 21, 275-281.
46. Plock, D.J. and B.L. Vallee. 1962. Interaction of alkaline phosphatase of E. coli. with metal irons and chelating agents. Biochemistry, 1,1039-1044.
47. Sastry, K.V. and P.K. Gupta. 1979. Alternation in the activities of three peptidase and lipases in the digestive system of the fish Channa punctatus exposed to lead nitrate. Bull. Environ. Contam. Toxicol. 21, 190-195.
48. Schwarz, K. 1977. Essentiality versus toxicity of metals. In CLINICAL CHEMISTRY AND CHEMICAL TOXICOLOGY OF METALS ed. Brown, S.S.. Elsevier/North-Holland Biochemical Press. Amsterdam. pp.3-22.
49. Sheard, C. and A.H. Sanford. 1929. A photoelectric hemoglobinometer. Clinical applications of the principles of photo-electric photometer to the measurement of hemoglobin. J. Lab. Clin. Med., 14, 558-574.
50. Sidbury, J.B., Jr. 1955. Lead poisoning Am. J. Med. 18, 932-946.
51. Sidbury, J.B., Jr., J.C. Bynum and L.L. Fetz. 1953. Effect of chelating agent on urinary lead excretion. Comparison of oral and intravenous administration. Proc. Sec. Expt. Biol. Med., 82, 226-228.
52. Singh, N.P., I.S. Thind, L.F. Vitale and M. Parvlow. 1976. Lead content of tissues of baby rat born of and nourished by lead-poisoned mother. J. Lab. Clin. Med., 87, 273-280.
53. Sugimura, K. and A. Mizutani. 1979. Histochemical and cytochemical studies of alkaline phosphatase activity in the synapses of rat brain. Histochemistry, 61, 123-129.
54. Thompson, J., D.D. Jones and W.H. Beasley. 1977. The effect of metal irons on the activuty of δ-aminolevulinic acid dehydratase. Brit. J. Ind. Med., 34, 32-36.
55. Tsuchiya, K. 1979. Lead. In HANDBOOK ON THE TOXICOLOGY OF METALS ed. by L. Friberg, G.F. Nordberg and V. Vouk. Elsevier/North-Holland Biomed. Press. Amsterdam, pp. 451-484.
56. Tsukamoto, I., T. Yoshinaga and S. Sano. 1979. The role of zinc with special reference to the essential thiol group in δ- amino-levulinic acid dehydratase (EC 4.2.1. 24) of bovine liver. Biochim. Biophys. Acta, 570, 167-178.
57. Tucker, R.K. and A. Matte. 1980. In vitro effects of cadmium and lead on ATPases in the gill of the rock crab, Cancer irroratus. Bull. Environ. Contam. Toxicol., 24, 847-852.
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64. Wapnir, R.A., S.A. Moak, F. Lifshitz and S. Teichberg. 1979. Alterations of intestinal and renal functions in rats after intraperitoneal injections of lead acetate. J. Lab. Clin. Med., 94, 144-151.
65. Wong, P.W.K. and R. Fresco. 1972. Tissue cystathionine in mice treated with cysteine and homocysteine. Pediat. Res., 6, 172-181.
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68. Zucconi, T.D., G.E. Janauer, S. Donahe and C. Lewkowicz. 1979. Acid dissociation and metal complex formation constants of penicillamine, cysteine and antiarthritic gold complexes at stimulated biological condition. J. Pharmacol. Sci., 68, 426-432.
dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/75454-
dc.description.abstract本實驗在研究含硫胺基酸——半胱胺酸(Cysteine, Cys.)對鉛中毒小白鼠之影響。將剛出生之ICR種系小白鼠用含鉛(醋酸鉛)500 ppm之飲水處理,斷奶前餵給母鼠,斷奶後由幼鼠自行攝取。四週後檢查,小白鼠已有明顯之鉛中毒。第五週起,停止鉛處理,以不同劑量之Cys.(0,25,50,100,400及800毫克/公斤)由腹腔注射處理,每兩週三次。對於鉛中毒小白鼠(PbM),在第六週,Cys.劑量為800毫克/公斤(用Cys. 800-6表示)時,可使5-胺基-4-酮戊酸脫水?(δ-Aminolevulinic acid dehydratase, ALAD)之活性?升。在Cys.400-6下,血容比(Hematocrit, Hct)也?升。血紅素(Hemoglobin,Hb)在Cys.50-6及Cys.100-8下也有?升現象,但在高劑量(Cys.400-8及Cys.800-8)下,反而降低。對正常小白鼠(OPbM)而言,Hb在Cys.25-6, Cys.50-6及Cys.100-6下,有升高之現象。Hct在Cys.800-6下則有降低之結果。Cys.可抑制OPbM及PbM之血清,肝及腎臟之酸性磷酸酯解?(Acid phosphatase,AcPase)之活性,也可抑制PbM血清及肝臟之鹼性磷酸酯解?(Alkaline phosphatase, AlPase)之活性。但不論OPbM或PbM, Cys.可提高腎臟AlPase之活性。Cys.亦可提高OPbM血清AlPase之活性。
因此,Cys.在適當的劑量及處理時間下,可以改善血液中鉛中毒的一些症狀。但同時也影響血清、肝及腎臟內AlPase及AcPase之活性。
zh_TW
dc.description.abstractThe effect of a sulfur-containing amino acid, cysteine, on lead toxicity was investigated in 4-week-old to 8-week-old ICR strain mice. Neonatal mice were lactated by lead-treated dams receiving normal diet and drinking water containing 500 ppm of lead acetate from the day of parturition. After weanling (about 3 weeks old), the pups were supplied with the same water as their mothers' for one more week. After 4 weeks treatment, the mice were intoxicated obviously, including the decrease in the hematocrit (Hct) and the activity of δ-aminolevulinic acid dehydratase (ALAD) and changes in some other parameters examined. From the 5th week to the 8th week, all the normal and lead-treated mice (OPbM and PbM) were provided with tap water and subjected to i.p. injections of various doses of cysteine (0, 25, 50, 100, 400 and 800 mg/kg of body weight, in 0.2 ml distilled water) three times every two weeks. In PbM, the activity of ALAD and Hct were increased at Cys.800-6 (i.e. the dose of cysteine was 800 mg/kg, in 6-week-old mice) and Cys.400-6 respectively. At Cys.50-6 and Cys.100-8, the hemoglobin (Hb) concentration was raised, but at Cys.400-8 and Cys.800-8, it was decreased. In OPbM, the increase in the Hb concentration was also observed at Cys.25-6, Cys.50-6 and Cys.100-6. Nevertheless, the Hct was decreased at Cys.800-6. Cysteine inhibited the alkaline phosphatase (AlPase) activities of the serum and the liver in PbM, and the acid phosphatase (AcPase) activities of the serum, the liver and the kidney in both OPbM and PbM. Cysteine, however, enhanced the activities of the kidney AlPase in both OPbM and PbM and the activity of the serum AlPase in OPbM.
Thus, some of the deleterious effects on hematological changes in lead intoxication might be ameliorated by using proper doses of cysteine for a proper time. However, the activities of AlPase and AcPase of the serum, the liver and the kidney might be affected simultaneously.
en
dc.description.provenanceMade available in DSpace on 2021-07-01T08:13:17Z (GMT). No. of bitstreams: 0
Previous issue date: 1982
en
dc.description.tableofcontentsⅠ、誌謝………………………………………i
Ⅱ、目次………………………………………ii
Ⅲ、圖表次………………………………………iii
Ⅳ、內容:
中文摘要………………………………………1
第一章 前言………………………………………3
第二章 材料與方法………………………………………6
一、實驗動物及處理方法………………………………………6
二、測定分析及樣品之準備………………………………………7
(一)樣品之準備………………………………………7
(二)測定方法………………………………………7
(三)統計分析………………………………………13
第三章 結果………………………………………15
第四章 討論………………………………………39
英文摘要………………………………………46
參考文獻………………………………………47
dc.language.isozh-TW
dc.title半胱胺酸對鉛中毒小白鼠之影響zh_TW
dc.titleThe Effect of Cysteine on the Lead Toxicity to Miceen
dc.date.schoolyear70-2
dc.description.degree碩士
dc.relation.page53
dc.rights.note未授權
dc.contributor.author-dept生命科學院zh_TW
dc.contributor.author-dept動物學研究所zh_TW
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