Basis of Radiopharmaceutical Localization


Radiopharmaceutical

Application

Indication for imaging

Radiolabeled particles

99mTc-MAA, 10–50 μm

Capillary blockade

Lung perfusion

99mTc-DTPA, aerosol, 1–4 μm

Sedimentation in bronchioles

Lung ventilation

99mTc-Sulfur colloid, 0.1–1.0 μm

Reticuloendothelial function

Liver, spleen, and bone marrow

99mTc-SC, filtered 0.1–0.3 μm

Lymphatic drainage

Breast cancer and melanoma

99mTc-HSA (nanocolloid), 0.02 μm

Lymphatic drainage

Breast cancer and melanoma

99mTc-Antimony sulfide colloid, 0.1 μm

Lymphatic drainage

Breast cancer and melanoma

Radiolabeled gases

133Xe, 127Xe, 81mKr

Alveolar transit–capillary diffusion

Lung ventilation

99mTc-Technegas, 0.004–0.25 μ

Alveolar transit–capillary diffusion

Lung ventilation

Radiolabeled chelates

99mTc-MDP, HDP

Bone formation

Metastatic bone disease, neuroblastoma, osteosarcoma

99mTc-DTPA

Blood–brain barrier disruption

Brain tumors
 
Renal function glomerular filtration

Renal blood flow and renogram

99mTc-MAG3

Renal function, tubular secretion

Renogram

99mTcIII-DMSA

Binding to renal parenchyma

Renal scan

99mTcV-DMSA

Tumor cell uptake

Medullary carcinoma of thyroid

99mTc-Disofenin and mebrofenin

Hepatobiliary function

Hepatobiliary imaging

99mTc-Ceretec and Neurolite

Blood flow

Brain imaging

99mTc-sestamibi and tetrofosmin

Blood flow

Myocardial perfusion

99mTc-sestamibi, and tetrofosmin

Tumor viability and multidrug resistance, MDR (Pgp expression)

Breast cancer, parathyroid adenoma, brain tumor

111In-DTPA

CSF flow

Cisternogram

111In-oxine

Radiolabeling white cells

Labeled leukocyte thrombus imaging

67Ga-citrate

Tumor viability, capillary leakage

Tumor and infection imaging

Radiotracers as ions

99mTc-pertechnetate (TcO4 )

Thyroid function (trapping)

Thyroid imaging

123I,131I-sodium iodide (I)

Thyroid function (trapping)

Thyroid uptake, imaging therapy

82Rb-chloride, Rb+

Blood flow

Myocardial perfusion

201Tl-thallous chloride, Tl(OH)2 +

Blood flow

Myocardial perfusion
 
Tumor viability

Tumor imaging (brain, parathyroid, thyroid)

Radiolabeled cells

111In-leukocytes

Cell migration and phagocytosis

Infection imaging

111In-platelets

Cell incorporation in thrombus

Thrombus imaging

51Cr-RBCs

Dilution in blood compartment

RBC mass and blood volume

99mTc-RBCs

Cardiac function

Cardiac ejection fraction, wall motion
 
Blood pool

Hemangioma, GI bleeding

99mTc-RBC (heat denatured)

Spleen

Accessory splenic tissue

Receptor binding radiotracers

111In-pentetreotide, Octreoscan

Somatostatin receptors

Neuroendocrine tumors

99mTc-P829, NeoTect

Somatostatin receptors

Lung cancer, NE tumors

99mTc-P280, Acutect

GP IIb/IIIa receptors

Thrombus imaging, DVT

99mTc-TRODAT-1

Dopamine transporter

Brain imaging-dopamine D2 receptors

123I-VIP

VIP receptors

Gastrointestinal tumors

131I-NP-59

LDL receptor, cholesterol metabolism

Adrenal carcinoma, adenoma, Cushing’s syndrome

123I- or 131I-MIBG

Presynaptic adrenergic receptors

Myocardial failure
 
Adrenergic tissue uptake

Tumor imaging (pheochromocytoma, neuroendocrine, neuroblastomas)

[11C]Raclopride

Dopamine D2 receptors

Brain imaging-dopamine D2 receptors

123I-IBZM

Dopamine D2 receptors

Brain imaging-dopamine D2 receptors, tumor imaging, malignant melanoma

[18F]fluoro-estradiol (FES)

Estrogen receptors

Breast tumor imaging

Radiolabeled monoclonal antibodies

111In-OncoScint, B72.3 IgG

TAG-72 antigen

Colorectal and ovarian cancer

111In-ProstaScint, 7E11-C5.3 IgG

PSMA (intracellular epitope)

Prostate cancer

99mTc-CEA-Scan, IMMU-4 Fab’

CEA

Colorectal cancer

99mTc-Verluma, NR-LU-10 Fab’

Cell surface GP as antigen

Small-cell lung cancer

99mTc-fanolesomab (CD15)

Granulocyte antigen CD15

Appendicitis

111In-antimyosin

Antimyosin

Acute myocardial infarction, heart transplant rejection

Radiolabeled metabolic substrates

18F-fluorodeoxyglucose, FDG

Tumor viability and metabolism

Tumor imaging
 
Glucose metabolism

Brain and cardiac imaging

18F-fluorothymidine

Cell proliferation

Tumor imaging and monitoring treatment

11C-choline

Cell proliferation

Brain tumors

[11C] or 123I-methyltyrosine

Protein synthesis, protein upregulation

Brain tumors

11C-methionine

Amino acid transport

Brain and pancreatic tumors

[11C]-thymidine

DNA synthesis, cell proliferation

Brain tumors

[18F] and 123I-fatty acids

Myocardial metabolism

Cardiac imaging

[57Co]-vitamin B12

Vitamin B12 absorption

Pernicious anemia

18F-fluoromisonidazole

Hypoxia and oxidative metabolism

Tumors selected for radiotherapy

18F-fluoroethyltyrosine(FET)

Amino acid transporter

Brain tumors



Radiopharmaceutical agents exhibit a huge range of physical and chemical properties and may be classified into different categories. The most important factors that influence the transport, uptake, and retention of radiopharmaceuticals in different organs and tissues include the chemical and biochemical nature of the carrier molecule transporting the radionuclide of choice to the targeted area.

The use of radiopharmaceuticals to deliver therapeutic doses of ionizing radiation has been extensively investigated. Targeted radionuclide therapy by systemic administration of a radiopharmaceutical provides a potential to treat widely disseminated cancer tissue. A number of radiopharmaceuticals (Table 3.2) are now available for the treatment of different malignancies or palliation of pain due to bony metastases. Tumor-specific radiopharmaceuticals that are clinically useful for noninvasive imaging of tumors are being modified for radionuclide therapy of tumors.


Table 3.2
Radiopharmaceuticals for therapy
































































Radiopharmaceutical

Application

Specific tumors

131I-sodium iodide

Thyroid function

Differentiated thyroid carcinoma

131I-MIBG

Adrenergic tissue

Colorectal cancer metastatic to liver and bladder cancer

131I-anti-B1 antibody

Anti-CD22 antigen

Lymphoma

90Y-MXDTPA-anti-B1 antibody

Anti-CD22 antigen

Lymphoma

32P-chromic phosphate (colloid)

Cell proliferation and protein synthesis

Peritoneal metastases, recurrent malignant ascites

32P-orthophosphate

Cell proliferation and protein synthesis

Polycythemia vera

89Sr chloride

Exchanges with Ca in bone

Palliation of pain due to bony metastases

153Sm-EDTMP

Binds to hydroxyapatite

Palliation of pain due to bony metastases

117mSn-DTPA

Binds to hydroxyapatite

Palliation of pain due to bony metastases

186Re-HEDP

Binds to hydroxyapatite

Palliation of pain due to bony metastases

90Y-DOTA-Tyr3-octreotide

Somatostatin receptors

Neuroendocrine tumors

90Y-DOTA-lanreotide

Somatostatin receptors

Neuroendocrine tumors

90Yb-ibritumomab

Lymphocyte antigen CD20

Lymphoma


A number of these therapeutic radionuclides also have gamma rays which are used for imaging. These radiopharmaceuticals are referred to as theranostic, and they include the following radionuclides, 68Ga (a PET imaging radionuclide) 131I, 153Sm, 186/188Re, and 117mSn



3.2 Mechanism(s) of Radiopharmaceutical Localization


The uptake and retention of radiopharmaceuticals by different tissues and organs involve many different mechanisms, as summarized in Table 3.3. The pharmacokinetics, biodistribution, and metabolism of the radiopharmaceutical are very important to understanding the mechanisms of radiopharmaceutical localization in the organ or tissue of interest. Injury to a cell or tissue significantly alters the morphology and molecular biology compared with that of normal tissue or organs.


Table 3.3
Mechanisms of radiopharmaceutical localization



















































































































Mechanism

Radiopharmaceutical

1. Isotope dilution

125I-HSA, 51Cr-RBC, and 99mTc-RBC

2. Capillary blockade

99mTc-MAA

3. Physicochemical adsorption

99mTc-MDP, HDP

4. Cellular migration

111In- and 99mTc-leukocytes, 111In-platelets

5. Cell sequestration

Heat denatured 99mTc-RBC

6. Simple diffusion

133Xe, 81mKr, 99mTc-pertechnegas

 Diffusion and mitochondrial binding

99mTc-sestamibi and tetrofosmin

 Diffusion and intracellular binding

99mTc-Ceretec and Neurolite

 Diffusion and increased capillary permeability

67Ga-citrate

7. Facilitated diffusion and transport, protein upregulation

[18F]-FDG, radiolabeled amino acids

8. Active transport

Radioiodide, 99mTcO4 , 201Tl thallous cation
 
[18F]-FDG, radiolabeled amino acids

 Na+/K+ ATPase pump

201Tl thallous cation

9. Phagocytosis

99mTc-colloids in RES and lymph nodes

10. Increased vascular permeability and capillary leakage

67Ga-citrate, radiolabeled proteins

11. Cell proliferation

[11C]-thymidine, [124I]-iododeoxyuridine (IudR), 18F-fluorothymidine (FLT)

12. Metabolic trapping

[18F]-FDG, 99mTc-pertechnetate

13. Metabolic substrates

123I and 131I as sodium iodide, 123I-fatty acids

14. Tissue hypoxia and acidic pH

[18F]fluoromisonidazole, 67Ga-citrate

15. Specific receptor binding
 

 Somatostatin receptors

Octreoscan, NeoTect

 VIP receptors

123I-VIP

 Transferrin receptors

67Ga-citrate

 Estrogen receptors

16α-[18F]fluoro-17β-estradiol (FES)

 Dopamine D2 receptors

[123I]-IBZM, 99mTc-TRODAT

 LDL receptors

131I-6β-iodomethyl-19-norcholesterol (NP-59)

 Presynaptic adrenergic reuptake

[131I or 123I]-MIBG

16. Specific binding to tumor antigens
 

17. PSMA

ProstaScint

 CEA

CEA-Scan

 TAG-72

OncoScint

 Cell surface 40-kd glycoprotein

Verluma

 CD22

Bexaar

 CD15

99mTc-fanolesomab

 Antimyosin

111In-antimyosin

The mechanisms of radiopharmaceutical localization may be substrate nonspecific (not participating in any specific biochemical reaction) or substrate specific (participating in a specific biochemical reaction), depending upon the chemistry of the molecule. Many radiopharmaceuticals were designed to take advantage of the pathophysiology in order to increase the specificity of the nuclear medicine imaging techniques. Since some radiopharmaceuticals are not specific for a particular disease, the cellular uptake might include a combination of different mechanisms, as in the case of 67Ga-citrate. However, the unique chemistry of each radiopharmaceutical may determine the manner in which it is transported and retained within a specific tissue or organ. It is very important to recognize that since the radiopharmaceutical may undergo significant metabolism and degradation in vivo, the observed biodistribution and tissue localization may represent the behavior of only radiolabeled metabolic product and not necessarily that of the intact parent radiopharmaceutical as exemplified by 99mTc l,l-ECD. For the radiopharmaceuticals that do not undergo biotransformation the biodistribution and tissue localization represent the behavior of the parent radiopharmaceuticals such as 99mTcMDP, 99mTc colloids, and gaseous radiopharmaceuticals.

In addition, the patient’s medication, physical status, and other factors may significantly alter the biodistribution and tissue localization and retention characteristics of a radiopharmaceutical. The different mechanisms of localization are discussed below, using specific examples of the more common radiopharmaceuticals.


3.2.1 Isotope Dilution


The dilution principle is based on the concept of “diluting” a radiotracer (or tracer) of known activity (or mass) in an unknown volume. By measuring the degree to which the radiotracer was diluted by the unknown volume, one can determine the total volume (or mass) of the unknown volume. The dilution principle is currently used for a quantitative determination of RBC volume (mass), plasma volume, and total blood volume.

It is very important that the radiotracer remain only in the blood volume to be measured. Nondiffusible intravascular agents such as 51Cr-RBCs are used to measure RBC mass, while 125I-HSA is used to measure plasma volume. There is no specific mechanism involved other than simple dilution of the radiotracer.


3.2.2 Capillary Blockade


The technique most commonly used to determine the perfusion to an organ depends on trapping the radiolabeled particles (microembolization) in the capillary bed of an organ such as lung, heart, or brain. Following intravenous injection, 99mTc-MAA particles are physically trapped in the arteriocapillary beds of the lung and block the blood flow to the distal regions. Therefore, the mechanism of localization of particles in lungs is purely a mechanical process, called capillary blockade.


3.2.3 Physicochemical Adsorption and Ion Exchange


Bone scanning with 99mTc-labeled phosphonates (MDP, HDP) is extensively used in nuclear medicine to evaluate benign and malignant bone diseases. The 99mTc-phosphonates accumulate in the hydroxyapatite (HA) crystal (containing Ca2+ and phosphate ions) matrix or in the amorphous (noncrystalline) calcium phosphate (ACP).

The principal uptake mechanism of the radiotracer appears to be simply “physicochemical adsorption.” However, the exact mechanisms involved in the extraction of the radiotracer from the blood through the endothelial cells, extracellular fluid, and finally to HA are not known. In contrast to the P–O–P bond in phosphates, the P–C–P bond in phosphonates is not a substrate for alkaline phosphatase and is very stable in vivo.

Primary bone tumors such as osteogenic sarcomas avidly accumulate bone agents because of the production of bone matrix in extraosseous tissue. Metastatic deposits that produce a vigorous osteoblastic response will appear as hot spots in a bone scan, while the lesions that generate osteolytic reactions may not accumulate the bone agent [3]. The bone scanning agents may also be taken up occasionally in soft tissues. The primary underlying factor responsible for the uptake of these tracers is excess calcium in soft tissue. Cell hypoxia and cell death would lead to increased deposition of calcium phosphates in the extracellular fluid. The uptake of 99mTc-phosphonates in the soft tissues is believed to be due to chemisorption on the surface of calcium salts such as in myocardial infarction.

The localization of bone-seeking radiotracers in increased amounts at the tumor–bone interface provides the basis for the use of radionuclides in the treatment of bone pain. Several radiopharmaceuticals (Table 3.3) are indicated for relief of pain (bone pain palliation) in patients with confirmed osteoblastic bone lesions. The exact mechanism of action of relieving the pain of bone metastases is not known, however.

For the ion exchange mechanism in the use of 18F-NaF, the fluoride ion exchanges with the hydroxyl ion in the hydroxyapatite crystal of bone to form fluorapatite [4]. It is therefore conceivable that in addition to imaging primary and metastatic tumors 18F can be used for studying bone metabolism.


3.2.4 Cellular Migration and Sequestration


111In-oxine- or 99mTc-HMPAO-labeled autologous mixed leukocytes (predominantly neutrophilic polymorphonuclear leukocytes, PMNs) are routinely used to image various inflammatory diseases and infectious processes. The inflammatory reaction is a well-described sequence of events (see Chap.​ 4) in response to an infection.

In an acute infection, the predominant cells infiltrating a site of infection are the PMNs. Following intravenous administration of radiolabeled leukocytes, the labeled cells migrate to the site of infection, similar to the circulating leukocytes because they are attracted by the immediately generated chemotactic factors, such as complement subcomponents.

In a similar manner, 111In-platelet localization at the site of active thrombus formation also involves simple cellular migration, since platelets play a major role in thrombus formation. Accessory splenic tissue can develop after splenectomy. Heat-damaged 99mTc-RBCs are more specific for the detection of accessory splenic tissue. Following intravenous administration, the spleen sequesters the heat-damaged RBCs in the same way that old and damaged circulating RBCs are normally removed. Hence, the heat-damaged 99mTc-RBCs can be used to visualize the spleen when 99mTc colloid fails to do so [5, 6].


3.2.5 Membrane Transport


Transport through the lipid bilayer or through the transport proteins may involve simple diffusion, passive transport (facilitated diffusion), or active transport mechanisms. Certain macromolecules may also be transported by vesicle formation, involving either endocytosis or exocytosis mechanisms.


3.2.5.1 Simple Diffusion


The mechanism of localization of many radiopharmaceuticals in target organs involves a simple diffusion process. The direction of movement of the radiotracers by diffusion is always from a higher to a lower concentration, and the initial rate of diffusion is directly proportional to the concentration of the radiotracer. A net movement of molecules from one side to another will continue until the concentration on each side is at chemical equilibrium. The gases used for ventilation studies, such as 133Xe, 127Xe, and 81mKr, are inert lipophilic gases. Following their administration through inhalation, these gases are distributed within the lung air spaces by diffusion, proportional to ventilation. The distribution, however, is interrupted in obstructive airways. The gases pass from the lungs into the pulmonary venous circulation and are released through the lungs by the mechanism of alveolar capillary diffusion. Similarly, distribution of 99mTc-Technegas within the lung also involves diffusion. By contrast, the irregular distribution of 99mTc-DTPA aerosol preparation within the lung is due mostly to gravity sedimentation depending on particle size.


Simple Diffusion and Intracellular Biotransformation

The blood–brain barrier (BBB) plays an important role in the mechanism of localization of many radiopharmaceuticals in the brain. The endothelial cells of the cerebral vessels form a continuous layer without gap junctions, preventing diffusion of water-soluble molecules.

In certain pathological conditions, the BBB is disrupted, allowing water-soluble molecules to diffuse from the blood into brain tissue. Traditionally, brain scan was performed with such radiopharmaceuticals as 99mTc-pertechnetate and 99mTc-DTPA that diffuse freely in the extracellular fluid and can accumulate in lesions with defects in BBB. The intact BBB does allow the transport of small molecules across the plasma membrane of the neuron by facilitated diffusion. Some small, neutral molecules, however, can cross the BBB depending on their relative lipid solubility. Brain perfusion-imaging agents such as 99mTc-HMPAO and 99mTc-ECD are lipophilic radiotracers that cross the BBB via passive diffusion. The extraction of these tracers by the brain tissue is proportional to regional cerebral blood flow (rCBF). The retention of these tracers within the neuronal tissue following diffusion and extraction is assumed to be due to intracellular biotransformation to polar metabolites or charged complexes that cannot be washed out of the cell by back-diffusion as exemplified by the cellular retention of 99mTc-ECD (Fig. 3.1) and 99mTc HMPAO.

A59117_3_En_3_Fig1_HTML.jpg


Fig. 3.1
With the labeling of red blood cells (RBCs) with 99mTc whether in vitro or in vivo, the 99mTcO4 freely diffuses in and out of the RBCs, but in the presence of stannous ion it is reduced intracellularly, where it reacts with hemoglobin (HB) to form 99mTc-Hb. The 99mTc-Hb does not diffuse out of the RBCs as shown in Fig. 3.2

For 99mTC-ECD the radiotracer freely diffuses into the brain tissue, where it is hydrolyzed by the action of esterase to a carboxylic acid which is trapped in the brain tissue.

For 99mTcHMPAO, it is presumed that the tracer is protonated to form a positively charged molecule (the so-called secondary 99mTc HMPAO) that is trapped in the brain tissue.

Similarly, in vivo labeling of ROCs with 99mTc pertechnetate occurs by independent simple diffusion of 99mTc pertechnetate and stannous ion into the red blood cell where the stannous ion reduces the pertechnetate and the reduced 99mTc binds to Hgb to form 99mTc Hgb that does not diffuse out of the red cell (Fig. 3.2).

A59117_3_En_3_Fig2_HTML.jpg


Fig. 3.2
Intracellular binding of 99mTcO4 to Hgb


Simple Diffusion and Mitochondrial Binding

A number of lipophilic, cationic 99mTc radiopharmaceuticals (sestamibi, tetrofosmin, and furifosmin) have been developed for imaging myocardial perfusion. Although 99mTc-sestamibi is cationic, similar to 201Tl+, the transport of this agent through the cell membrane involves only passive diffusion since the transport process is temperature dependent and nonsaturable [7].

The myocardial cell uptake of 99mTc-sestamibi is due to intracellular binding of 99mTc-sestamibi associated mainly with mitochondria. The cellular entry of 99mTc-sestamibi is related to the mitochondrial metabolism and the negative inner membrane potential of the mitochondria [8]. Hematochondrial retention of 99mTc-sestamibi, however, is not organ or tumor specific, but appears to be a mechanism common to most types of tissue. The intracellular levels of Ca2+ in normal cells are significantly low. However, with irreversible ischemia, extracellular calcium enters the cell and is sequestered in the mitochondria, resulting in mitochondrial destruction. The increased calcium concentration in mitochondria blocks 99mTc-sestamibi binding to mitochondria.

99mTc lipophilic cationic complexes are also used for diagnostic imaging of parathyroid adenomas, osteosarcomas, and tumors of the brain, breast, lung, and thyroid. The mechanisms of uptake of sestamibi and tetrofosmin in tumors are different from that of thallium-201 [9]. While the 99mTc agents are associated with mitochondria, 201Tl remains in the cytoplasmic compartment.

There are significant differences between sestamibi and tetrofosmin regarding intracellular localization based on in vitro studies. While 90 % of total sestamibi was associated with mitochondria, most of the tetrofosmin accumulated in the cytosolic fraction [9].

The transport of the tracer out of the tumor cell is mediated by P-glycoprotein (Pgp), a 17-kd plasma membrane lipoprotein encoded by the human multidrug resistance (MDR) gene. Piwnica-Worms et al. [10, 11] demonstrated that sestamibi is a transport substrate for Pgp and is useful for imaging Pgp expression.


Simple Diffusion and Increased Capillary and Plasma: Membrane Permeability

67Ga-citrate has been shown to localize in a variety of tumors and inflammatory lesions. There is still no general agreement on the exact mechanisms of localization in tumors [12, 13]. Following intravenous administration of carrier-free 67Ga as gallium citrate, 67Ga is bound exclusively to the two specific metal-binding sites of iron transport glycoprotein, transferrin in normal plasma, and is transported to normal tissues and tumor sites predominantly as 67Ga–transferrin complex [14].

The mechanisms involved in the uptake of 67Ga by tumor cells are very complex, since a variety of factors appear to affect transport and retention of 67Ga within the tumor tissue. Based on in vivo studies, Hayes et al. [15] concluded that the initial entry of 67Ga into tumor tissue involves simple diffusion of the unbound or loosely bound form of 67Ga, whereas its uptake by normal soft tissues is strongly promoted by its binding to transferrin. There is increased transferrin concentration within the interstitial fluid of the tumors. The increased permeability of the tumor cell membrane compared with normal cells may also account for increased diffusion of non-transferrin-bound gallium species into cells. The accumulation of 67Ga within tumor cells is very much dependent upon the intracellular binding of 67Ga to iron-binding proteins such as lactoferrin and ferritin or other higher-molecular-weight molecules which can chelate gallium with greater affinity, thereby preventing back-diffusion of free gallium species [13].


3.2.5.2 Facilitated Diffusion


Facilitated diffusion is also called carrier-mediated diffusion because a substance transported in this manner usually cannot pass through the membrane without a specific carrier protein allowing its entry. That is, the carrier facilitates the diffusion of the substance to the other side. However, the carrier protein transports a specific molecule partly but not all the way through the membrane. The molecule to be transported enters the channel and then becomes bound. Then in a fraction of a second a conformational change occurs in the carrier protein so that the channel now opens to the opposite side of the membrane. This mechanism allows the transported molecule to diffuse in either direction through the membrane as shown in Fig. 3.3.

A59117_3_En_3_Fig3_HTML.jpg


Fig. 3.3
A postulated mechanism for facilitated diffusion


18F-fluorodeoxyglucose (FDG)

The glucose analog deoxyglucose, which has one oxygen atom less than the glucose molecule (Fig. 3.4), is transported into the cell in the same way as glucose. The uptake of glucose by human cells can take place however through two mechanisms of transport. The first method involves the facilitative glucose transport (GLUT) and the second method is the active transport.

A59117_3_En_3_Fig4_HTML.jpg


Fig. 3.4
[18F]2-deoxy-2-fluoro-d-glucose (FDG). In FDG the hydroxyl group in the 2-position of d-glucose is replaced by 18F

Six isoforms of facilitative glucose transporters have been identified so far: GLUT-1 to GLUT-5 and GLUT-7 (Table 3.4). These isoforms share the same transmembrane topology, but they differ in kinetic properties, tissue location, sugar specificities, and regulation in states of imbalanced glucose homeostasis [16].
Aug 27, 2016 | Posted by in NUCLEAR MEDICINE | Comments Off on Basis of Radiopharmaceutical Localization

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