Histochemical response of mice to mistletoe lectin I (ML I)

Journal/Book: Histochemistry 94 (5), 531-537. 1991;

Abstract: The acute toxicity of lectin ML I from the toxic drug, mistletoe, wasdemonstrated in previous experiments. Because the reason for thisextremely high toxicity is not yet clear, mice were studiedhistochemically at different times after treatment with various doses ofML I, ML I A or ML I B chain separately, or recombinations of ML I A andML I B. Various plasma membrane-associated hydrolases as well as Golgiapparatus-and endoplasmic reticulum-linked hydrolases, peroxisomal andextraperoxisomal oxidases, lysosomal hydrolases, mitochondrialdehydrogenases, the cytoskeletal proteins keratin and vimentin as wellas iron, glycogen and lipids were analysed in all organs and tissues offemale mice. Irrespective of the dose, a clear-cut response was onlyobserved in the liver. After ML I treatment, glycogen disappearedcompletely from all hepatocytes, and this effect did not depend on theML I-concentration and exposure time. The increase in activity ofGolgi-associated thiamine pyrophosphatase in hepatocytes and ofnon-specific alkaline phosphatase in the sinusoidal endothelial cellsdepended on the applied ML I concentration and the time of treatment.Doses of 600 or 900 ng ML I/kg drastically increased the phosphataseactivities. These clear-cut changes of glycogen and enzyme activitieswere not observed after administration of the ML I B chain alone, andless so when the mice were treated only with the ML I A chain, or weretreated with a recombination of ML I A and ML I B even at concentrationshigher than that of ML I.(ABSTRACT TRUNCATED AT 250 WORDS) Author.

Keyword(s): ALKALINE-PHOSPHATASE/ME (metabolism)

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