Arylsulfatase A and β-galactosidase activities in leukocytes and lymphocytes from normal and psychiatric subjects

Shantilal N. Shah1, Ronald C. Johnson1, Kyungtak Minn2, Frank Schoenfeld3
1Brain Behavior Research Center, Sonoma Developmental Center, University of California, San Francisco, Eldridge
2Napa State Hospital, Napa
3Veterans Administration Medical Center, San Francisco

Tóm tắt

Arylsulfatase A (ASA) and cerebroside-β-galactosidase activities in leukocytes serve as a diagnostic tool for determining the presence of metachromatic leukodystrophy and globoid cell leukodystrophy, respectively. It has not been demonstrated whether a delay in blood processing and the presence of mixed cell types in different proportions in leukocytes affect the activities of the two enzymes in these cells. We have in the present study determined the specific activity in leukocytes and lymphocytes (T-cells) prepared from blood samples processed immediately after, 4, and 24 h after collection. In order to determine whether the enzyme activitiies in lymphocytes reflect expression of genetic trait, and not environmental or “state” influence, the activities of the two enzymes in interleukin 2-stimulated T-cells and resting T-cells were compared. A delay of up to 24 h in blood processing did not significantly change the specific activities of the two enzymes in both leukocytes and lymphocytes. The specific activity of ASA and β-galactosidase in lymphocytes was 1.4–1.8 times that in leukocytes. The activities of the two enzymes in interleukin 2-stimulated T-cells did not differ from those in resting T-cells. These results indicate that blood-processing delay had no significant effects on ASA and β-galactosidase activity. The data further indicate that the ASA and β-galactosidase activity in interleukin 2-stimulated T-cells was not significantly different from resting lymphocytes from either normal or psychiatric subjects exposed to various medications. The activity levels in lymphocytes from psychiatric subjects thus reflect expression of genetic trait, rather than environmental or state influence.

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Tài liệu tham khảo

Adolph K., Kucey M. T., Hodges S. T., Carter R. J., and Snyder F. F. (1988) Interleukin 2-dependent T lymphocytes for the diagnosis and investigation of inherited metabolic disorders.Clin. Chim. Acta 173, 147–156.

Baum H., Dodgson K. S. and Spencer B. (1959) The assay of arylsulfatase A and B in human urine.Clin. Chim. Acta 4, 453–455.

Bennett E. R. Yedgar S., Lerer B., and Ebstein R. P. (1991) Phospholipase A2 activity in Epstein-Barr virus-transformed lymphoblast cells from schizophrenia patients.Biol. Psychiat. 29, 1058–1062.

Folch-Pi J., Lees M., and Sloane Stanley G. (1957) A simple method for the isolation and purification of total lipides from animal tissues.J. Biol. Chem. 226, 497–509.

Georgopoulos D. and Manowitz P. (1982) Arylsulfatase A activity and electrophoresis banding patterns from isolated human blood fractions.Biochem. Genet. 20, 907–918.

Herska M., Moscovich D. G., Kalian M., Gottlieb D., and Bach G. (1987) Arylsulfatase A deficiency in psychiatric and neurological patients.Am. J. Med. Genet. 26, 629–635.

Kamatani N., Yamanaka H., Nishioka K., Nakamura T., Nakano K., Tanimoto K., Mizuno T., and Nishida Y. (1984) A new method for the detection of Lesch-Nyhan heterozygotes by peripheral blood T cell culture using T cell growth factor.Blood 63, 912–916.

Kolodny E. H. and Mumford R. (1976) Human leukocyte acid hydrolases: characterization of eleven lysosomal enzymes and study of reaction conditions for their automated analysis.Clin. Chim. Acta 70, 247–257.

Lejoyeux M. and Maziére J. (1991) Lack of interaction between arylsulfatase and neuroleptics: Confirmation in human cultured fibroblasts.Psychiat. Res. 38, 93–94.

Lowry O. H., Rosebrough N. J., Farr A. L., and Randall R. J. (1951) Protein measurement with the Folin phenol reagent.J. Biol. Chem. 193, 265–275.

Manowitz P., Goldstein L., and Nora R. (1981) An arylsulfatase A variant in schizophrenic patients: preliminary report.Biol. Psychiat. 16, 1107–1113.

Mills P. J., Dimsdale J. E., and Ziegler M. (1989) Short-term delay in blood processing does not alter basal or isoproterenol-stimulated cyclic AMP accumulation in human lymphocytes.Life Sci. 44, 1917–1920.

Percy A. K., and Brady R. O. (1968) Metachromatic leukodystrophy: Diagnosis with samples of venous blood.Science 161, 594–595.

Pilz H. (1972) Late adult metachromatic leukodystrophy: Arylsulfatase A activity of leukocytes in two families.Arch. Neurol. 27, 87–90.

Poulos A., and Pollard A. C. (1976) A rapid method for the estimation of β-galactocerebrosidase, β-glucocerebrosidase and sphingomyelinase activities in leukocytes.Clin. Chim. Acta 72, 327–335.

Propping, P., Frieldl W., Huschka M., Schlor K. H., Reimer F., Lee-Vaupel M., Conzelman E., and Sandhoff K. (1986) The influence of low arylsulfatase a activity on neuropsychiatric morbidity: A large scale screening in patients.Hum. Genet. 75, 144–248.

Radin N. S., Hof L., Bradley R. M., and Brady R. O. (1969) Lactosylceramide galactosidase: Comparison with other sphingolipid hydrolases in developing rat brain.Brain Res. 14, 497–505.

Raghavan S. S., Gajewski A., and Kolodny E. H. (1981) Leukocyte sulfatidase for the reliable diagnosis of metachromatic leukodystrophy.J. Neurochem. 36, 724–731.

Shah S. N., Johnson R. C., Stone R. K. and Mahon-Haft H. (1985) Prevalence of partial cerebroside sulfate sulfatase (Arylsulfatase A) defect in adult psychiatric patients.Biol. Psychiat. 20, 50–57.

Snyder R. A. and Brady R. O. (1969) The use of white cells as a source of diagnostic material for lipid storage diseases.Clin. Chim. Acta 23, 331–338.

Stolc V. and Krause J. R. (1989) Regulation of total leukocyte, neutrophil and lymphocyte concentrations in human blood by major effectors.Hum. Hered. 39, 240–247.

Suzuki K., Suzuki Y., and Fletcher T. F. (1972) Further studies on galactocerebroside β-galactoside in globoid cell leukodystrophy, inSphingolipids, Sphingolipidoses and Allied Disorders, vol. 19 (Volk and Aronson, eds.), Plenum, New York, pp. 487–498.

Svennerholm L., Hakansson G., Mansson J-E., and Vanier M. (1979) The assay of sphingolipid hydrolases in white blood cells with labelled natural substrates.Clin. Chim. Acta 92, 53–64.

Von Figura K., Steckel F., and Haslik A. (1983) Juvenile and adult metachromatic leukodystrophy: partial restoration of arylsulfatase A (cerebroside sulfatase) activity by inhibitors of thiol proteinases.Proc. Nal. Acad. Sci. USA 80, 6066–6070.