Evidence for energy-dependent transport of aluminum out of brain extracellular fluid

Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration

“…Further assessment of Al distribution across the BBB was conducted by microdialysis during steady state Al concentrations, achieved by i.v. Al citrate infusion, over an 8-fold range of infusion rates [142]. As in bolus dose studies, the BBr was ∼ 0.15.…”

“…Assuming 1) transferrin saturation by Al, 2) comparable K in values for Al and Fe by TfR-ME, and 3) the initial confinement of Al to brain ECF, then the maximum brain ECF Al concentration that could be achieved by TfR-ME in 20 minutes would be ∼ 0.15 µM. This is very much lower than the brain ECF Al concentration seen in microdialysis studies (18-245 µM) [142], which was estimated from dialysate Al concentrations and 3.25% relative recovery of Al by microdialysis probes [143]. The marker of BBB integrity (4-trimethylammonium antipyrine) administered in this study showed no significant BBB disruption.…”

Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration

“…Further assessment of Al distribution across the BBB was conducted by microdialysis during steady state Al concentrations, achieved by i.v. Al citrate infusion, over an 8-fold range of infusion rates [142]. As in bolus dose studies, the BBr was ∼ 0.15.…”

“…Assuming 1) transferrin saturation by Al, 2) comparable K in values for Al and Fe by TfR-ME, and 3) the initial confinement of Al to brain ECF, then the maximum brain ECF Al concentration that could be achieved by TfR-ME in 20 minutes would be ∼ 0.15 µM. This is very much lower than the brain ECF Al concentration seen in microdialysis studies (18-245 µM) [142], which was estimated from dialysate Al concentrations and 3.25% relative recovery of Al by microdialysis probes [143]. The marker of BBB integrity (4-trimethylammonium antipyrine) administered in this study showed no significant BBB disruption.…”

In Vivo Evidence for P‐Glycoprotein–Mediated Transport of Phenytoin at the Blood–Brain Barrier of Rats

“…The “metabolic inhibitor” sodium cyanide is often used for inhibition of ATP‐dependent drug transporters such as P‐gp (11,24), but by reacting with the trivalent iron of cytochrome oxidase in mitochondria, cyanide also inhibits cellular respiration, resulting in lactic acidosis and cytotoxic hypoxia (25). In a previous microdialysis study on brain distribution of the chemotherapeutic agent etoposide, sodium cyanide was perfused through the microdialysis probe at either 1 or 100 m M (11).…”

The biological behaviour and bioavailability of aluminium in man, with special reference to studies employing aluminium-26 as a tracer: review and study update

“…It is suggested that the free carboxylate of the aluminium citrate complex provides a binding site for the MCT. The report of Allen et al 115 also suggests that citrate may also facilitate the loss of aluminium from the brain. It is possible that such aluminium is present in extracellular tissue fluids, but not in cells.…”

Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration

“…Further assessment of Al distribution across the BBB was conducted by microdialysis during steady state Al concentrations, achieved by i.v. Al citrate infusion, over an 8-fold range of infusion rates [142]. As in bolus dose studies, the BBr was ∼ 0.15.…”

“…Assuming 1) transferrin saturation by Al, 2) comparable K in values for Al and Fe by TfR-ME, and 3) the initial confinement of Al to brain ECF, then the maximum brain ECF Al concentration that could be achieved by TfR-ME in 20 minutes would be ∼ 0.15 µM. This is very much lower than the brain ECF Al concentration seen in microdialysis studies (18-245 µM) [142], which was estimated from dialysate Al concentrations and 3.25% relative recovery of Al by microdialysis probes [143]. The marker of BBB integrity (4-trimethylammonium antipyrine) administered in this study showed no significant BBB disruption.…”

In Vivo Evidence for P‐Glycoprotein–Mediated Transport of Phenytoin at the Blood–Brain Barrier of Rats

“…The “metabolic inhibitor” sodium cyanide is often used for inhibition of ATP‐dependent drug transporters such as P‐gp (11,24), but by reacting with the trivalent iron of cytochrome oxidase in mitochondria, cyanide also inhibits cellular respiration, resulting in lactic acidosis and cytotoxic hypoxia (25). In a previous microdialysis study on brain distribution of the chemotherapeutic agent etoposide, sodium cyanide was perfused through the microdialysis probe at either 1 or 100 m M (11).…”

The biological behaviour and bioavailability of aluminium in man, with special reference to studies employing aluminium-26 as a tracer: review and study update

“…It is suggested that the free carboxylate of the aluminium citrate complex provides a binding site for the MCT. The report of Allen et al 115 also suggests that citrate may also facilitate the loss of aluminium from the brain. It is possible that such aluminium is present in extracellular tissue fluids, but not in cells.…”

Blood-brain barrier flux of aluminum, manganese, iron and other metals suspected to contribute to metal-induced neurodegeneration

“…Further assessment of Al distribution across the BBB was conducted by microdialysis during steady state Al concentrations, achieved by i.v. Al citrate infusion, over an 8-fold range of infusion rates [142]. As in bolus dose studies, the BBr was ∼ 0.15.…”

“…Assuming 1) transferrin saturation by Al, 2) comparable K in values for Al and Fe by TfR-ME, and 3) the initial confinement of Al to brain ECF, then the maximum brain ECF Al concentration that could be achieved by TfR-ME in 20 minutes would be ∼ 0.15 µM. This is very much lower than the brain ECF Al concentration seen in microdialysis studies (18-245 µM) [142], which was estimated from dialysate Al concentrations and 3.25% relative recovery of Al by microdialysis probes [143]. The marker of BBB integrity (4-trimethylammonium antipyrine) administered in this study showed no significant BBB disruption.…”

In Vivo Evidence for P‐Glycoprotein–Mediated Transport of Phenytoin at the Blood–Brain Barrier of Rats

“…The “metabolic inhibitor” sodium cyanide is often used for inhibition of ATP‐dependent drug transporters such as P‐gp (11,24), but by reacting with the trivalent iron of cytochrome oxidase in mitochondria, cyanide also inhibits cellular respiration, resulting in lactic acidosis and cytotoxic hypoxia (25). In a previous microdialysis study on brain distribution of the chemotherapeutic agent etoposide, sodium cyanide was perfused through the microdialysis probe at either 1 or 100 m M (11).…”

The biological behaviour and bioavailability of aluminium in man, with special reference to studies employing aluminium-26 as a tracer: review and study update

“…It is suggested that the free carboxylate of the aluminium citrate complex provides a binding site for the MCT. The report of Allen et al 115 also suggests that citrate may also facilitate the loss of aluminium from the brain. It is possible that such aluminium is present in extracellular tissue fluids, but not in cells.…”