Lead transport by renal slices and its inhibition by tin

Vander, Arthur J.; Mouw, David R.; Cox, James R.; Johnson, Brian F. G.

doi:10.1152/ajprenal.1979.236.4.f373

Cited by 8 publications

(6 citation statements)

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“…In conclusion, these experiments along with our previous study (2) suggest that lead accumulation by renal slices (an indication, presumably, of uptake across basolateral cell membranes) is mainly by free-ion transport, cotransport with lowmolecular-weight ligands playing a minor role, if any at all. One question raised by the present data is why the slice-to-medium ratio-5-10-for lead in the presence of protein is still so much above unity.…”

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confidence: 73%

Accumulation of Lead by Renal Slices in the Presence of Organic Anions

Vander

Johnson

1981

Experimental Biology and Medicine

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Abslruct. In vitvo uptake of lead by rabbit renal cortical slices was measured using 20:'Pb. In protein-free medium, steady-state slice-to-medium ratios were 30-70. The addition of protein (2 g/dl) or cysteine (1 1.5 or 23 p M ) markedly reduced this ratio. All other experiments were performed with protein-containing medium. Cysteine or citrate, 113 p M , significantly increased the slice-to-medium ratio by 12-19%, but addition of serum ultrafiltrate had no effect. Metabolic inhibitors significantly reduced the ratio by 12%, but because this figure was similar to the percentage swelling by the slices, there was no effect on the mass of lead accumulated. The inhibitors had no significant effect on the increment in S,'M ratio produced by cysteine or citrate. We conclude that lead cotransport into renal slices with low-molecular-weight organic ligands of plasma is very small compared to the uptake due to active transport of free ionic lead.

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confidence: 73%

Accumulation of Lead by Renal Slices in the Presence of Organic Anions

Vander

Johnson

1981

Experimental Biology and Medicine

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“…An interesting comparison with the behaviour of '03Pb in another organ is that vanadate, stannic chloride, and certain metabolic blockers inhibit active accumulation of lead by kidney slices in vitro (Vander et a]., 1979). Presumably, the same mechanism, a cal-cium pump, is involved in both the latter activity and in pumping lead out of brain.…”

Section: Discussionmentioning

confidence: 98%

“…Carbonyl cyanide 4-(trifluoromethoxy)phenylhy- drazone (FCCP) at 2 pM also markedly increased 203Pb uptake. Tin, as stannic chloride, has been observed to inhibit active accumulation of lead into kidney slices (Vander et al, 1979). Freshly made 2 pM stannic chloride strikingly increased the 203Pb uptake into all brain regions ( p < 0.00 1).…”

Section: Metabolic Inhibitorsmentioning

confidence: 95%

Transport of Lead‐203 at the Blood‐Brain Barrier During Short Cerebrovascular Perfusion with Saline in the Rat

Deane

Bradbury

1990

Journal of Neurochemistry

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Lead transport at the blood-brain barrier has been studied by short (less than 1.5 min) vascular perfusion of one cerebral hemisphere of the rat with a buffered physiological salt solution at pH 7.4 without calcium, magnesium, or bicarbonate and containing 203 Pb-labelled lead chloride. In the absence of complexing agents, 203Pb uptake was rapid, giving a space of 9.7 ml/100 g of wet frontal cortex at 1 min. Lead-203 influx was linear with lead concentration up to 4 microM. Five percent albumin, 200 microM cysteine, or 1 mM EDTA almost abolished 203Pb uptake. Lead-203 entry into brain was uninfluenced by varying the calcium concentration or by magnesium or the calcium blocker methoxyverapamil. Similarly, 1 mM bicarbonate or 50 microM 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid was without effect. Increasing the potassium concentration reduced 203Pb uptake. Vanadate at 2 mM, 2 microM carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (a metabolic uncoupler), or 2 microM stannic chloride all markedly enhanced lead entry into brain, as did a more alkaline pH (7.80). In conclusion, there is a mechanism allowing rapid passive transport of 203Pb at the brain endothelium, perhaps as PbOH+. Lead uptake into brain via this system is probably made less important by active transport of lead back into the capillary lumen by the calcium-ATP-dependent pump.

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“…As reported earlier lead induces oxidative stress in liver and kidney causing pathological changes (Offor et al, 2017; Reddy et al, 2014). Studies on transport of Lead in the kidney have revealed that it is taken up by proximal tubular cells (Vander, Mouw, Cox, & Johnson, 1979). Also exposure to increased levels of lead produces renal tubular damage with vascular congestion, Bowman’s space enlargement and massive infiltration (Ekong, Jaar, & Weaver, 2006).…”

Section: Discussionmentioning

confidence: 99%

Zingerone prevents lead‐induced toxicity in liver and kidney tissues by regulating the oxidative damage in Wistar rats

et al. 2020

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Among the heavy metal poisonings, lead is considered as a major toxic metal causing hematological, neurological, immunological, hepatic, and renal dysfunctions. Lead causes inhibition of ALAD leading to the ALA accumulation inside the cells. Lead also leads to disruption of the anti-oxidative enzyme system, organ function, and lipid membranes of the cell causing oxidative stress. Zingerone, a phenolic alkanone, is an active edible ingredient present in the ginger that possess varied pharmacological properties. The aim of our study was to evaluate the protective effect of zingerone in lead-induced toxicity in wistar rats. ALAD concentration was improved in kidney and liver tissues treated with zingerone. Protective effect of zingerone was observed in terms of significant improvement in kidney and liver histology, anti-oxidant enzyme activity (CAT, SOD, GPx, and GR), organ function parameters, lipid profile, and decreased level of LPO. Therefore, zingerone pretreatment can be a promising agent for alleviation of lead-induced oxidative damage in cells. Practical applications Published reports have revealed that consumption of certain bioactive nutrients for example, flavonoids, mineral elements, and vitamins can offer defense from the environmental lead contamination. Zingerone is a strong anti-oxidant, with very less side effects and has exceptional property of scavenging free radicals, hence reducing the oxidative stresses. This fundamental property of zingerone can alone help in countering the heavy metal toxicity. Different groups have published reported numerous properties of zingerone but as per our understanding till date no study about alleviation of lead toxicity by zingerone in animal model has been undertaken. Hence, we conducted this research to explore the preventive effect of zingerone in lead induced kidney and liver toxicity. The outcome of our study shows potent anti-oxidant effect and ALAD modulatory property of zingerone which makes it suitable edible candidate for use in countering lead toxicity.

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Lead transport by renal slices and its inhibition by tin

Cited by 8 publications

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Accumulation of Lead by Renal Slices in the Presence of Organic Anions

Accumulation of Lead by Renal Slices in the Presence of Organic Anions

Transport of Lead‐203 at the Blood‐Brain Barrier During Short Cerebrovascular Perfusion with Saline in the Rat

Zingerone prevents lead‐induced toxicity in liver and kidney tissues by regulating the oxidative damage in Wistar rats

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