Year: 1977
Type: article
Abstract: In their report describing low adenosine deaminase (ADA) activity in chronic lymphocytic leukaemia, Ramot el al(1977) pose the question of whether the low ADA activity is a primary defect of the cells or represents a property of the proliferating leukaemic lymphocytes.We have been interested in the activity of enzymes necessary for purine reutilization and have measured the activity of adenosine deaminase (ADA) and purine nucleoside phosphorylase (NP) in lymphocytes.Table I lists the ADA activity present in: B-lymphoblastoid cells lines (LCL) obtained by in viho Epstein-Barr virus infection (Nilsson, 1976); T-lymphoblastoid cell lines (Royston et al, 1975); normal human bone marrow; normal human thymocytes; and peripheral blood lymphocytes (containing 90% T-lymphocytes as determined by E-rosette formation) obtained from a patient with Bruton's X-linked agammaglobulinaemia.These data show that human B-LCL and bone marrow contain significantly less (P<o.oI)ADA activity than T-LCL, thymocytes and peripheral blood T-lymphocytes.No significant difference in N P activity (B-LCL, 0.040 k0.01 compared with T-LCL and thymocytes 0.039 k0.01) was detected between the different lymphoid populations.TABLE I. Adenosine deaminase activity in human lymphoid populations
Source: British Journal of Haematology
Institution: University of Washington
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W1986800868
