Abstract
Lead was administered to adult male rabbits in drinking water at a 0.1% concentration for four and five week periods. The lead contents were determined in the central and peripheral nervous tissues and in the liver, kidney, and intestinal mucosa. The conduction velocity of sciatic nerve and the activities of drug metabolizing enzymes in other tissues were determined. The lead concentration in the blood was at a steady state at four to five weeks of exposure. Lead accumulated in all tissues except the brain. The brain lead concentration was 40 to 50% of that in the blood, indicating the existence of a blood-brain barrier. However, the lead concentration in the sciatic nerve increased significantly from four to five weeks of exposure and exceeded that in the blood. This indicates the lack of a blood-nervous tissue barrier in the sciatic nerve allowing a continuous accumulation of lead. This accumulation affected the function of the sciatic nerve; motor nerve conduction velocity decreased from the control level (58.3±7.4 m/sec) to 43.8±6.3 m/sec after the four-week exposure and to 35.0 ± 1.3 m/sec at 5 weeks of exposure. After five weeks of exposure, no changes in the hepatic, intestinal, or renal drug metabolizing enzyme activites were found. These results suggest that motor nerve conduction velocity is affected by lead exposure prior to any influence on biotransformation enzymes.
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Aitio, A.: A simple and sensitive assay of 7-ethoxycoumarin deethylation. Anal. Biochem.85, 488 (1978).
Barltrop, D., and F. Meek: Absorption of different lead compounds. Postgrad. Med. J.51, 805 (1975).
Calop, J., M.-E. Burchkart, and R. Fontanges: Etude de I'influence des éléments traces sur I'hydroxylation du benzo(a)pyrene. Eur. J. Toxicol.9, 27 (1976).
Conrad, M. E., and J. C. Barton: Factors affecting the absorption and excretion of lead in the rat. Gastroenterology74, 731 (1978).
Cremer, J. E., L. D. Braun, and W. H. Oldendorf: Changes during development in transport processes of the blood-brain barrier. Biochim. Biophys. Acta448, 633 (1976).
Der, R., Z. Fahim, M. Yousef, and M. Fahim: Environmental interaction of lead and cadmium on reproduction and metabolism of male rats. Res. Commun, in Chem. Path. Pharmacol.14, 689 (1976).
Dyck, P. J., P. O'Brien, and A. Ohnishi: Lead neuropathy: 2. Random distribution of segmental demyelination among “old internodes” of myelinated fibers. J. Neuropath. exp. Neurol.36, 570 (1977).
Feldman, R. G., M. K. Hayes, R. Younes, and F. D. Aldrich: Lead neuropathy in adults and children. Arch. Neurol. (Chic.)34, 481 (1977).
Fischbein, A., A. P. Alvares, K. E. Anderson, S. Sassa, and A. Kappas: Lead intoxication among demolition workers: The effect of lead on the hepatic cytochrome P-450 system in humans. J. Toxicol. Environ. Health3, 431 (1977).
Fishbein, L.: Environmental metallic carcinogens: An overview of exposure levels. J. Toxicol. Environ. Health2, 77 (1976).
Goldstein, G. W., A. K. Asbury, and I. Diamond: Pathogenesis of lead encephalopathy. Arch. Neurol. (Chic.)31, 382 (1974).
Gornall, A. G., C. J. Bardawill, and M. M. David: Determination of serum proteins by means of the biuret reaction. J. Biol. Chem.177, 751 (1949).
Hänninen, O.: On the metabolic regulation in the glucuronic acid pathway in the rat tissues. Ann. Acad. Sci. Fenn.A2, (No 142), 1 (1968).
Henry, R. A., and K. H. Byington: Inhibition of glutathione-S-aryltransferase from rat liver by organogermanium, lead, and tin compounds. Biochem. Pharmacol.25, 2291 (1976).
Hirano, A., and J. A. Kochen: Further observations on the effects of lead implantation in rat brains. Acta Neuropath. (Berl.)34, 87 (1976).
Iannaccone, A., P. Boscolo, and G. Bombardieri: Comparative effects of experimental lead poisoning on enzymatic activities of kidney and liver in rat. Life Sci.19, 427 (1976).
Isselbacher, K. J.: Enzymatic mechanisms of hormone metabolism. II. Mechanism of hormonal glucuronide formation. Recent Progr. in Horm. Res.12, 134 (1956).
Lancranjan, J., H. I. Popescu, O. Gavanescu, I. Klepsch, and M. Serbanescu: Reproductive ability of workmen occupationally exposed to lead. Arch. Environ. Health30, 396 (1975).
Levander, O.A.: Metabolic interactions between metals and metalloids. Environ. Health Perspect.25, 77 (1978).
Low, P. A., and P. J. Dyck: Increased endoneurial fluid pressure in experimental lead neuropathy. Nature (Lond.)269, 427 (1977).
Nebert, D. W., and H. V. Gelboin: Substrate-inducible microsomal aryl hydrocarbon hydroxylase in mammalian cell culture. J. Biol. Chem.234, 6242 (1968).
Netter, K. J.: Eine Methode zur direkten Messung derO-demethylierung Lebermikrosomen und ihre Anwendung auf die Mikrosomen hemmwirkung von SKF 525-A. Naunyn-Schmiedeberg's Arch. Pharmacol.238, 292 (1960).
Nordberg, G. F. (ed.): Effects and dose-response relationships of toxic metals. Amsterdam: Elsevier (1976).
Omura, T., and R. Sato: The carbon-monoxide binding pigment of liver microsomes. II. Solubilization, purification, and properties. J. Biol. Chem.239, 2379 (1964).
O'Tuama, L. A., C. S. Kim, J. T. Gatzy, M. R. Krigman, and P. Mushak: The distribution of inorganic lead in guinea pig brain and neural barrier tissues in control and lead-poisoned animals. Toxicol. appl. Pharmacol.36, 1 (1976).
Pardridge, W. M., and W. H. Oldendorf: Transport of metabolic substrates through the blood-brain barrier. J. Neurochem.28, 5 (1977).
Phillips, A. H., and R. G. Langdon: Hepatic triphosphopyridine nucleotide-cytochrome c reductase: Isolation, characterization and kinetic studies. J. Biol. Chem.237, 2653 (1962).
Sassa, S., J. L. Granick, S. Granick, A. Kappas, and R. D. Levere: Studies in lead poisoning I: Microanalysis of erythrocyte protoporphyrin levels by spectrofluorometry in the detection of chronic lead intoxication in the subclinical range. Biochem. Med.8, 135 (1973).
Savolainen, H., and J. Kilpiö: Brain and blood lead in acute intoxication. Scand. J. Work Environ. Hlth.3, 104 (1977).
Seppäläinen, A. M., and S. Hernberg: Sensitive technique for detecting subclinical lead neuropathy. Brit. J. Ind. Med.29, 443 (1972).
Seppäläinen, A. M., and I. Linnoila: Electrophysiological studies on rabbits in long-term exposure to carbon disulfide. Scand. J.Work Environ. and Health1, 178 (1975).
Seppäläinen, A. M., S. Tola, S. Hernberg, and B. Kock: Subclinical neuropathy at “Safe” levels of lead exposure. Arch. Environ. Health30, 180 (1975).
Sunderman, Jr., F. W.: Carcinogenic effects of metals. Fed. Proc.37, 40 (1978).
Ullrich, V., and P. Weber: The O-dealkylation of 7-ethoxycoumarin by liver microsomes. A direct fluorometric test. Hoppe-Seyler's Z. physiol. Chem.353, 1171 (1972).
Wattenberg, L. W., J. L. Leong, and P. J. Strand: Benzpyrene hydroxylase activity in the gastrointestinal tract. Cancer Res.22, 1120 (1962).
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Hietanen, E., Kilpiö, J., Närhi, M. et al. Biotransformational and neurophysiological changes in rabbits exposed to lead. Arch. Environ. Contam. Toxicol. 9, 337–347 (1980). https://doi.org/10.1007/BF01057413
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DOI: https://doi.org/10.1007/BF01057413