Skip to main content
  • Published:

The Effect of Experimental Methyl Mercury Poisoning on the Distribution of Acid Phosphatase During Autolysis in Cat Liver

Inverkan av metylkvicksilverförgiftning på fördelning av surt fosfatas under autolys i kattlever

Summary

Seven healthy male cats weighing between 2.35 and 4.30 kg were daily fed a diet which contained Hg203 labelled methyl mercury hydroxide in liver homogenate. Eight additional cats were kept as controls on a similar diet without methyl mercury hydroxide. The daily amount of methyl mercury hydroxide fed to the cats, expressed as inorganic mercury, varied between 3.75 and 4.33 mg per cat. When the animals had developed neurological symptoms typical of methyl mercury poisoning, they were decapitated and their livers removed for the determination of the mercury content, the distribution of acid phosphatase during autolysis at 37°G, the pH and the total bacterial count before and after a 24 hr. period of autolysis. Similar determinations except for the mercury were made from the livers of the control animals. The total amount of methyl mercury hydroxide fed to the cats varied between 29.14 and 40.12 mg Hg++ per kg of body weight, and the mercury content in their livers between 102.5 and 128.7 mg Hg++ per kg of liver wet weight.

The share of un sedimentable activity of acid phosphatase out of the total immediately after decapitation was found to be significantly (P < 0.001) greater in the livers of the methyl mercury-fed cats than in the livers of the control animals. After 12 to 24 hrs. of autolysis at 37 °G the unsedimentable activity accounted for 100 % of the total acid phosphatase activity in the livers of 6 of the 7 methyl mercury-fed animals, while in the livers of the controls the corresponding percentages varied after 24 hrs. of incubation between 42 and 73, the mean being 57.4 ± 11.4 %. The mean pH of the livers of the methyl mercury fed animals was found to be significantly higher before (P< 0.001) and after (P < 0.001) a 24 hr. incubation at 37 °G than the corresponding mean pH values of the control animals.

Because of the injection of antibiotics given to the cats before sacrifice the total bacterial count of the livers, which was checked before and after a 24 hr. incubation at 37°G, was found to be zero.

Sammanfattning

Sju hankatter, vars vikter varierade mellan 2,35 och 4,30 kg utfodrades dagligen med ett foder som innehöll Hg203 märkt metylkvicksilverhy droksid blandat med leverhomogenat. Åtta katter, „ kontrollerna”, fick samma foder utan metylkvicksilver. Den dagliga givan av metylkvicksilver uttryckt som Hg++ per katt varierade mellan 3,75 och 4,33 mg. När djuren visade grava för metylkvicksilverförgiftning typiska neurologiska symptom avlivades de och deras levrar tillvaratogs för kvicksilverbestämning, för bestämning av pH och det totala bakterietalet före och efter en 24 timmars inkubation vid 37° G. Samma bestämningar med undantag av kvicksilveranalys utfördes på kontrollkatternas levrar. Totalmängden av metylkvicksilver som utfodrades till katterna varierade mellan 29,14 och 40,12 mg Hg++ per kg kroppsvikt och det motsvarande kvicksilverinnehållet i levrarna mellan 102,5 och 128,7 mg Hg++ per kg lever.

Omedelbart efter avlivandet av katterna var det sytoplasmatiska sura fosfatasets andel av det totala signifikant (P < 0,001) större i de med metylkvicksilver utfodrade katternas levrar jämnfört med kontrollernas levrar. Efter 12 till 24 timmars inkubation vid 37° G var den sytoplasmatiska aktivitetens andel av den totala aktiviteten 100 % i sex av de sju med metylkvicksilver utfodrade katterna. Motsvarande andel var hos kontrollerna efter 24 timmars inkubation 57 ± 11,4 %. Levrarnas genomsnittliga pH-värde var signifikant (P < 0,001) större hos de med metylkvicksilver utfodrade katterna än hos kontrollerna både före och efter en 24 timmars inkubation vid 37° G.

På grund av antibiotikum injektion omedelbart före avlivandet var det totala bakterietalet noll med den användade metoden både före och efter en 24 timmars inkubation vid 37° C.

References

  • Beafay H. E. von Campenhaut & C. de Duve: Tissue fractionation studies. II. Influence of various hepatoxic treatments on the state of some bound enzymes in rat liver. Biochem. J. 1959, 73, 617–623.

    Article  Google Scholar 

  • Dingle J.T.: Action of vitamin A on the stability of lysosomes in vivo and in vitro. In Lysosomes. Ciba foundation symposium, ed. V. S. de Reuck & M. P. Cameron. J. & A. Churchill, Ltd., London 1963, 384–398.

    Chapter  Google Scholar 

  • de Duve C.: The Lysosome concept. In Lysosomes. Giba foundation symposium, ed. V. S. de Reuck & M. P. Cameron. J. & A. Churchill, Ltd., London 1963, 1–35.

    Google Scholar 

  • Fong C. T. O. J. L. Schwartz, E. A. Popence, L. Silver & M. A. Schoessler: On the molecular bounding of lysine vasopressin at its venal receptor site. J. Amer. ehem. Soc. 1959, 81, 2592.

    Article  CAS  Google Scholar 

  • Goto T. & M. Fujino: Counteraction of sulfhydryls (SH) in rats against mercury. I. Influence of methionine on the growth of rats given a diet containing mercury pestisides, and SH in liver. J. Jap. Soc. Fd Nutr. 1969, 22, 73–77.

    CAS  Google Scholar 

  • Hegner D.: Funktionelle Bedeutung von SH-Gruppen in Membranen von Lysosomalen Granula aus polymorphkernigen Rinderleuco-cyten. (Functional importance of sulfhydryl groups in membranes of lysosomal granules of bovine polymorphonuclear leucocytes). Naunyn-Schmiedeberg’s Arch. exp. Path. Pharmak. 1968, 261, 239–251.

    Article  CAS  Google Scholar 

  • Häsänen E.: Determination of mercury in biological material by neutron activation analysis. Acta chem. fenn. 1970, 43A, 251–254.

    Google Scholar 

  • Irukayama K. F. Kai, T. Kondo, S. Ushikusa, M. Fujiki & S. Tajima: Toxicity and metabolism of metlryl mercury compounds in animals - especially in relation to Minamata disease. Jap. J. Hyg. 1965, 20, 11–21.

    Article  CAS  Google Scholar 

  • Kominz D. R.: Molecular changes in myosin caused by methyl-mercuric hydroxide. Biochim. biophys. Acta (Amst.) 1961, 51, 456–463.

    Article  CAS  Google Scholar 

  • Kośmider St.: Untersuchungen über den toxischen Wirkungsmechanismus des metallischen Quecksilbers. (Studies on the toxic mechanism of action of the metallic mercury). Arch. Gewerbe-path. Gewerbehyg. 1965, 21, 282–314.

    Article  Google Scholar 

  • Kurland L. T. S. N. Faro & H. Siedler: Minamata disease. The outbreak of a neurological disorder in Minimata Japan and its relationship to the ingestion of seafood contaminated by mercuric compounds. Wld Neurol. 1960, 1, 370–391.

    CAS  Google Scholar 

  • Munder P. G. E. Ferber & H. Fischer: Untersuchungen über die Abhängigkeit der cytolytischen Wirkung des Lysolecithins von Membranenzymen. (Studies on the dependence between the cytolytic effect of the lysolecithins and the membrane enzymes). Z. Naturforsch. 1965, 20b, 1048.

    Article  Google Scholar 

  • Netter K. J.: Sulfhydrylgruppen in Lebermikrosomen. (The sulfhydryl groups of the liver microsomes). Naunyn-Schmiedeberg’s Arch, exp. Path. Pharmak. 1966, 253, 76.

    Google Scholar 

  • Neubert D.: Einfluss von Pharmaka auf energieliefernde Reaktionen des Stoffwechsels. (The effect of drugs on the energy producing reactions of the metabolism). Naunyn-Schmiedeberg’s Arch, exp. Path. Pharmak. 1963, 246, 101–132.

    CAS  Google Scholar 

  • Nomura S.: Epidemiology of Minamata disease. In Minamata Disease. Study group of Minamata disease, ed. M. Kutsuna. Kumamoto University, Japan 1968, 5–36.

    Google Scholar 

  • Norseth T.: The intracellular distribution of mercury in rat liver after methoxyethylmercury intoxication. Biochem. Pharmacol. 1967, 16, 1645–1654.

    Article  CAS  Google Scholar 

  • Norseth T.: The intracellular distribution of mercury in rat liver after at single injection of mercuric chloride. Biochem. Pharmacol. 1968, 17, 581–593.

    Article  CAS  Google Scholar 

  • Pekkanen T. J.: Distribution of acid phosphatase during autolysis in bovine liver. Acta vet. scand. 1970, 11, 283–294.

    CAS  PubMed  Google Scholar 

  • Swensson Å. & U. Ulfvarson: Toxicology of organic mercury compounds used as fungicides. Occup. Hlth Rev. 1963, 15, 5–11.

    CAS  Google Scholar 

  • Takeuchi T.: Experiments with organic mercury, particularly with methyl mercury compounds; Similarities between experimental poisoning and Minamata Disease. In Minamata Disease. Study group of Minamata disease, ed. M. Kutsuna. Kumamoto University, Japan 1968, 229–252.

  • Taylor N. S.: Histochemical studies of nephrotoxicity with sublethal dose of mercury in rats. Amer. J. Path. 1965, 46, 1–14.

    CAS  PubMed  Google Scholar 

  • Timm F. Ch. Naundorf & M. Kraft: Zur Histochemie und Genese der chronischen Quecksilbervergiftung. (On the histochemistry and development of the chronic mercury poisoning). Arch. Ge-werbepath. Gewerbehyg. 1966, 22, 236–245.

    Article  CAS  Google Scholar 

  • Ushikusa S.: Supplementary experiments on the toxicity of methyl-mercuric chloride in cats administered per os. Kumamoto med. J. 1965, 39, 33–39.

    CAS  Google Scholar 

  • Webb J. L.: Mercurials. Chapter 7. In Enzyme and Metabolic Inhibitors. Acad. Press. New York and London 1966, Vol. II, a 746–768; b 892-916; c 815-820; d 830-859, 874.

    Google Scholar 

  • Weissmann G. & L. Thomas: Studies on lysosomes. I. The effects of endotoxin, endotoxin tolerance and cortisone on the release of acid hydrolases from a granular fraction of rabbit liver. J. exp. Med. 1962, 116, 433–450.

    Article  CAS  Google Scholar 

  • Östlund K.: Extraction of mercury compounds from organic material. In Studies on the Metabolism of Methyl Mercury and Dimethyl Mercury in Mice. Acta pharmacol. (Kbh.) 1969, 27, Suppl. 1, 38.

    Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Rights and permissions

Reprints and permissions

About this article

Cite this article

Pekkanen, T.J. The Effect of Experimental Methyl Mercury Poisoning on the Distribution of Acid Phosphatase During Autolysis in Cat Liver. Acta Vet Scand 12, 523–535 (1971). https://doi.org/10.1186/BF03547721

Download citation

  • Received:

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1186/BF03547721