Abstract
In several mouse tumour models iron given parenterally not only inhibited the transport of 67Ga by plasma transferrin but also accelerated the binding of 67Ga in tumour tissue, particularly during the first hour after 67Ga injection. By 30 min, the tumour had already attained a high concentration though the 67Ga accumulated was still potentially reversible. With the passage of time equally high 67Ga concentrations were attained in tumour in iron-treated and untreated animals alike, and were maintained high as 67GA was totally cleared from the plasma. Given IV, 125-I-human transferrin was not preferentially bound in tumour whereas in muscle tissue loaded with transferrin, 67Ga was accumulated locally during the immediate post-injection phase and to an enhanced degree in iron-treated animals. A hypothesis is presented which, by drawing attention to the role of extravascular transferrin in binding and presenting 67Ga for cellular uptake, helps resolve the apparent contradictions between in vivo and cell culture findings.
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