High impact information on NSC19173

• Supplemental copper but not zinc or iron prevented the potentiation of the H(2)O(2)-induced oxidative DNA damage caused by 2,3,2-tet [1].
• The somatostatin analog Demotate 1 (Tyr(3)-octreotate conjugated to the 1,4,8,11-tetraazaundecane chelator) was used for chelation of the positron emitter (94m)Tc (half-life, 52 min) and targeting to SSTR2 [2].
• Finally, incubation of human peripheral blood mononuclear cells (PBMC) with 2,3,2-tet decreased mitogen-induced IL-2 production by 50% compared with untreated controls [3].
• Moreover, binding of diferric transferrin (Tf) and cellular uptake of Tf-59Fe by Jurkat cells were not increased by 2,3,2-tet, indicating that chelator-treated cells were not iron deficient [3].
• To address these matters, we have developed an in vitro model of cellular copper deficiency by treating Jurkat, a human T-lymphocyte cell line, with low concentrations of 2,3,2-tetraamine (2,3,2-tet), a high affinity copper chelator [3].

Anatomical context of NSC19173

• Incubation of copper-overloaded hepatocytes with the copper chelator, 2,3,2-tetramine, had a partial protective effect [4].

Associations of NSC19173 with other chemical compounds

• Exposure to 5-20 micromol/L 2,3,2-tet for 35 h decreased cell copper and the activity of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) by 30-40% and IL-2 production by 60-70% in cultures activated with phytohemagglutinin and phorbol myristate acetate [3].

Gene context of NSC19173

• During the chase, the cellular depletion curves for apolipoprotein A-I, apolipoprotein B and total protein were not altered by 2,3,2-tetramine treatment [5].

References