ArticleEuropean journal of nuclear medicine and molecular imaging2003
Sestamibi is a substrate for MDR1 and MDR2 P-glycoprotein genes.
Article in European journal of nuclear medicine and molecular imaging, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
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- Evaluation of 11C-acetate and 18F-FDG PET/CT in mouse multidrug resistance gene-2 deficient mouse model of hepatocellular carcinoma.BMC medical imaging · 2015Article
- Imaging of multidrug resistance in cancer.Cancer imaging : the official publication of the International Cancer Imaging Society · 2011Review
- Effect of cyclosporin A administration on the biodistribution and multipinhole muSPECT imaging of [123I]R91150 in rodent brain.European journal of nuclear medicine and molecular imaging · 2009Article
- Systemic and local release of inflammatory cytokines regulates hepatobiliary excretion of 99mTc-mebrofenin.Nuclear medicine communications · 2008Article
- Abnormal intense skeletal radiotracer uptake on myocardial perfusion imaging with Tc-99m sestamibi.Journal of nuclear cardiology : official publication of the American Society of Nuclear CardiologyArticle
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Technetium-99m sestamibi has attracted interest for assessment of the function of P-glycoproteins, which are well expressed in the liver and have roles in biliary transport and the removal of chemotherapeutic drugs. To further examine the cross-reactivity of (99m)Tc-sestamibi for P-glycoprotein family members, we conducted studies in animals. Hepatobiliary secretion of (99m)Tc-sestamibi was determined in normal FVB/N mice, mutant mice with specific P-glycoprotein deficiencies in the FVB/N background, normal Long-Evans Agouti (LEA) rats, and Long-Evans Cinnamon (LEC) rats with abnormal copper transport and liver disease but intact P-glycoprotein expression. After intrasplenic injection, (99m)Tc-sestamibi was rapidly incorporated in the mouse and rat liver, with maximal accumulation after 102+/-31 and 109+/-16 s, respectively ( P=NS). In normal mice and rats, 55%+/-11% and 55%+/-6%, respectively, of the maximal sestamibi activity was retained in the liver after 1 h ( P=NS). In double knockout mice lacking both mdr1a and mdr1b homologs of the human MDR1 ( ABCB1) gene, 88%+/-11% of maximal sestamibi activity was retained in the liver after 1 h ( P<0.001). In knockout mice deficient in either mdr1a gene or mdr2 ( ABCB4) gene, biliary sestamibi excretion was also impaired, although this impairment was relatively less pronounced in ABCB4-deficient mice than in double knockout mice lacking both ABCB1 gene homologs ( P<0.03). Hepatobiliary sestamibi excretion in LEC rats was not different from that in control normal rats, despite the presence of significant liver disease in the former. Hepatobiliary sestamibi excretion requires P-glycoproteins and is unperturbed in chronic liver disease. Sestamibi appears to be a substrate for both ABCB1 and ABCB4 genes, although the former utilizes it far more efficiently. Assessment of P-glycoprotein activity with sestamibi should consider how regulation of ABCB1 and related family members might modulate sestamibi incorporation.
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