The role of anion transport in the passive movement of lead across the human red cell membrane.

Simons, T. J. B.

doi:10.1113/jphysiol.1986.sp016220

Cited by 79 publications

(62 citation statements)

References 16 publications

(28 reference statements)

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“…In addition, this transport was dependent upon anion exchange, much like the exchanger. It was concluded, therefore, that the uptake of Pb 2+ into erythrocytes is most likely mediated by an anion exchanger (Simons, 1986b(Simons, , 1993. Subsequent studies in human erythrocytes have provided further support for the findings of Simons (1986bSimons ( , 1993, confirming that that the transport of Pb 2+ into erythrocytes is mediated by an anion exchanger (Bannon et al, 2000).…”

Section: Leadsupporting

confidence: 49%

“…It was concluded, therefore, that the uptake of Pb 2+ into erythrocytes is most likely mediated by an anion exchanger (Simons, 1986b(Simons, , 1993. Subsequent studies in human erythrocytes have provided further support for the findings of Simons (1986bSimons ( , 1993, confirming that that the transport of Pb 2+ into erythrocytes is mediated by an anion exchanger (Bannon et al, 2000). In addition, the uptake of Pb 2+ by immortalized renal distal tubular (MDCK) cells was found to be dependent on time of exposure and temperature.…”

Section: Leadmentioning

confidence: 55%

“…Anion exchangers have also been implicated in the transport of Pb 2+ into erythrocytes (Bannon et al, 2000;Simons, 1986bSimons, , 1993. Using resealed erythrocyte ghosts, Simons (1986b) demonstrated that over 90% of the uptake of Pb 2+ could be attributed to transport via an anion exchanger.…”

Section: Leadmentioning

confidence: 99%

“…Using resealed erythrocyte ghosts, Simons (1986b) demonstrated that over 90% of the uptake of Pb 2+ could be attributed to transport via an anion exchanger. He showed that inhibitors of anion exchangers (DIDS, 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonic acid (SITS), phloretin, furosemide, and bumetanide) blocked nearly all of the Pb 2+ uptake in erythrocyte ghosts.…”

Section: Leadmentioning

confidence: 99%

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Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

665

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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Section: Leadsupporting

confidence: 49%

Section: Leadmentioning

confidence: 55%

Section: Leadmentioning

confidence: 99%

Section: Leadmentioning

confidence: 99%

See 2 more Smart Citations

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

665

460

View full text Add to dashboard Cite

show abstract

“…In addition, Zn (Alda & Garay 1989;Kalfakakou & Simons 1990), Cu (Alda & Garay 1990), and Pb (Simons 1986) were reported to be taken up by red blood cells via the anion exchanger, and Kalfakakou & Sinions (1990) suggested the competitive inhibitory effect of Zn on Pb uptake by the cells. These investigators (Alda & Garay 1989& 1990Lou et al 1991) implied the contribution of the inorganic anion exchanger in the renal reabsorption of these metals, however, this point had not yet been investigated.…”

mentioning

confidence: 99%

Cadmium Uptake from Apical Membrane of LLC–PK Cells via Inorganic Anion Exchanger

Endo

Kimura

Sakata

1998

Pharmacology & Toxicology

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ilbsrrtrci; Effects of Na+, CI-, OH-and HCO,-, and an inorganic tinion exchange inhibitor (HCO, iC1 ), 4,4'-diisothiocyanostilbcne-2,2'-disulfonic acid, on Cd uptake from the apical membrane of LLC-PK I cells were investigated to elucidate the mechanism of Cd uptake by thcsc cells. Furthermore, the initial uptake of Cd incubated at different temperatures was analyLed by using the Arrhcnius plot to tcst if Cd is taken up by the cells via the carrier-mediated process. The cells were incubated with 1 pM CdClz for 30 min. at 37" in phosphate buffer containing NaCl at pH 5.5 or 7.4. Cd accumulation by the cclls at pH 7.4 was about 5 times higher than at pH 5.5. Rcplaccmcnt of NaCl in the phosphate buffer with KCI or niannitol dccrcased the Cd accumulation at pH 7.4 about 80%, but had no effect at pH 5.5. The addition of 2 mM NaHCOl to the pH 7.4 buffer containing NaCl significantly increased the Cd accurnulation, and pretreatment of the cells with the inorganic anion exchange inhibitor abolished this effect of NaHCOl on Cd accumulation. The cells were incubated for 10 min. at different temperatures with 1 pM CdClz in the phosphate buffer containing NaCl at pH 7.4 in the presence or absence of 2 mM NaHCO3 or at pH 5.5 in the absence of NaHCOl. In all cases, the Arrhenius plots of Cd accumulation were nonlinear. The breakpoint was observed at about 30" in thc Cd accumulation at pH 7.4 in the presence of NaIICO,, suggesting the involvement of a carrier-mediated process. This brcakpoirit was not as clear in the Cd accumulation at pH 7.4 in the absence of NaHCO3 and not observed at all at pH 5.5. These findings suggested that Cd is partially taken up from the apical membrane of LLC-PKI cells via the inorganic anion exchanger and the uptake of Cd is more efficient a t alkaline pH and in the presence of Na+, C1-and HCO, .We studied the mechanism of uptake of CdClz by LLC-PKI cells, iin established renal tubular epithelial cell line and brush border metnbranc vesicles isolated from rat renal cortex. Cd appears to be partially taken up from the apical membrane of LLC-PK I cells via a carrier-mediated system involving tcmpcrature-, N a~' -, energy-, and pH-dependent process(es) when the cells were incubated with non

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Role of anion exchange and thiol groups in the regulation of potassium efflux by lead in human erythrocytes

1996

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Pb2+ is thought to enter erythrocytes through anion exchange (AE) and to remain in the cell by binding to thiol groups. To define the role of AE mechanisms and thiol groups in Pb2+ toxicity, we studied the effects of drugs and conditions that modify AE and that modify thiol groups on the ability of Pb2+ to stimulate potassium efflux as measured with 86Rb. The most potent stimulation of 86Rb efflux by Pb2+ occurred when conditions were optimal for the AE mechanism--that is, when bicarbonate was included in the buffer or a buffer made with Nal or NaCl rather than NaClO4 or NaNO3 was used. Furthermore, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfuonic acid, potent inhibitors of the AE mechanism, completely inhibited stimulation of the 86Rb efflux by Pb2+. These conditions or inhibitors did not affect stimulation of the 86Rb efflux by ionomycin plus Ca2+. A role for Ca2+ channels was dismissed because the inorganic Ca2+ channel blockers, Cd2+ or Mn2+, did not prevent stimulation of 86Rb efflux by Pb2+ but did inhibit stimulation by ionomycin plus Ca2+. 86Rb efflux was more sensitive to Pb2+ if erythrocytes were treated for 15 min with thiol-modifying reagents that enter cells, such as iodoacetamide, N-ethylmaleimide, or dithiothreitol, than to reduced glutathione, a thiol-modifying reagent that is not permeable to the cell. Thus, in erythrocytes the AE mechanism and internal thiol groups are critical factors that affect the stimulation of a Ca(2+)-dependent process by Pb2+.

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The role of anion transport in the passive movement of lead across the human red cell membrane.

Cited by 79 publications

References 16 publications

Molecular and ionic mimicry and the transport of toxic metals

Molecular and ionic mimicry and the transport of toxic metals

Cadmium Uptake from Apical Membrane of LLC–PK Cells via Inorganic Anion Exchanger

Role of anion exchange and thiol groups in the regulation of potassium efflux by lead in human erythrocytes

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