Influence of Dietary Zinc on Lead Toxicity in the Rat

Cerklewski, Florian L.; Forbes, R. M.

doi:10.1093/jn/106.5.689

Cited by 143 publications

(49 citation statements)

References 23 publications

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“…The role of selenium in lead intoxication has rather been controversial. Cerklewski and Forbes investigated the effect of low and high dietary selenium on toxicity of dietary lead in male rats and suggested that low dietary levels mildly protect against toxic effects of lead, but at high levels it exaggerates the lead toxicity 112) . Enzymatic activity of ALAD and Cytochrome P-450 in liver was normal in rats exposed concomitantly to selenium and lead 113) .…”

Section: Seleniummentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

269

161

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Strategies for Safe and Effective Therapeutic Measures for Arsenic and LeadPoisoning: Kiran Kalia, et al. Department of Biosciences, Sardar Patel University, IndiaExposure to toxic metals remains a widespread occupational and environmental problem in world. There have been a number of reports in the recent past suggesting an incidence of childhood lead poisoning and chronic arsenic poisoning due to contaminated drinking water in many areas of West Bengal in India and Bangladesh has become a national calamity. Low level metal exposure in humans is caused by air, food and water intake. Lead and arsenic generally interferes with a number of body functions such as the central nervous system (CNS), the haematopoietic system, liver and kidneys. Over the past few decades there has been growing awareness and concern that the toxic biochemical and functional effects are occurring at a lower level of metal exposure than those that produce overt clinical and pathological signs and symptoms. Despite many years of research, we are still far from an effective treatment of chronic plumbism and arsenicosis. Medical treatment of acute and chronic lead and arsenic toxicity is furnished by chelating agents. Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. They have been used clinically as antidotes for acute and chronic poisoning. 2, 3-dimercaprol (BAL) has long been the mainstay of chelation therapy for lead or arsenic poisoning. Meso 2, 3, -dimercaptosuccinic acid (DMSA) has been tried successfully in animals as well as in a few cases of human lead and arsenic poisoning. DMSA could be a safe and effective method for treating lead or arsenic poisoning, but one of the major disadvantages of chelation with DMSA has been its Review inability to remove lead from the intracellular sites because of its lipophobic nature. Further, it does not provide protection in terms of clinical/ biochemical recovery. A new trend in chelation therapy is to use combined treatment. This includes the use of structurally different chelators or a combination of an adjuvant and a chelator to provide better clinical/ biochemical recovery in addition to lead mobilization. The present review article attempts to provide update information about the current strategies being adopted for a safe, effective and specific treatment for two major toxic metals or metalloid.

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Section: Seleniummentioning

confidence: 99%

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Kalia¹,

Flora²

2005

Journal of Occupational Health

269

161

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“…[20], phosphorus [8,15], and sulfur [21,22]. The disappearance curves for lead excretion in blood, plasma, hematic cells, and some other soft tissues can be expressed as sums of exponential functions.…”

Section: Zincmentioning

confidence: 99%

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Verbeeck

Lassuyt

Heijligers³

et al. 1981

Calcif Tissue Int

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Summary. Solid solutions of calcium hydroxyapatite (CaOHA) and lead hydroxyapatite (PbOHA) of the formula Ca,0.x Pbx (PO4)6 (OH)2 were prepared by coprecipitation followed by heating at 800~ in a stream of CO2-free water vapor of 1 atm. The samples were apatitic in the range 0 < x < 6 and contained lead phosphates as a second phase at higher Pb/Ca ratios. Lattice parameters and cation distribution of the apatitic samples were determined by X-ray diffraction. The lattice parameters varied linearly with x in the range considered, whereas all Pb 2+ were located in the sixfold position for cations. There was a miscibility gap in the apatite series of solid solutions in the range 1 < x < 4, whereas apatites in the range 6 < x < 10 were not stable under the conditions of preparation. It is concluded that apatites in the range 4 < x < 6 represent a minimum in the free energy of solid solutions between CaOHA and PbOHA.

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“…Cerklewski and Forbes (50) showed that increasing dietary zinc from 8 to 200 ppm in lead-poisoned rats decreased lead concentrations in tissues, urinary excretion of 6-aminolevulinic acid, and inhibition of 8-aminolevulinic acid dehydratase activity in the kidney. This antagonistic effect of zinc on lead was thought to be due to its interference in lead absorption since zinc did not affect urinary lead excretion and injected zinc had no effect on lead toxicity.…”

Section: Zinc and Coppermentioning

confidence: 99%

Lead toxicity and nutritional deficiencies.

Levander¹

1979

Environ Health Perspect

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Under appropriate conditions, deficiencies of certain minerals and vitamins as well as high intakes of dietary fat increase the toxicity of a given dose of lead in experimental animals. The severity of lead poisoning can also be increased by the consumption of either deficient or excessive levels of protein. Mineral deficiencies appear to have some of the most profound effects on lead toxicity, since the consequences of plumbism can be exaggerated by feeding diets low in calcium, phosphorus, iron, zinc, and in some cases, copper. Evidence for an antagonism between lead and nutritional levels of selenium is inconclusive. Vitamin E deficiency and lead poisoning interact to produce an anemia in rats that is more severe than that caused by either treatment alone. Lead apparently exerts a pro-oxidant stress on the red cell, thereby causing its accelerated destruction. One of the biochemical mechanisms of lead poisoning may be the disruption of normal membrane architecture, thereby leading to peroxidative damage. Epidemiological surveys have suggested a negative correlation between the poor nutritional status of children with regard to calcium and the concentration of lead in blood. Other examples of potential interactions of mineral status and lead poisoning in humans include the hypothesized hazards of soft water to public health in areas with lead plumbing and the possible role of mineral deficiencies in the etiology of pica. Experimental studies have shown that in some situations combined nutritional deficiencies can have an additive effect in potentiating lead toxicity.

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Influence of Dietary Zinc on Lead Toxicity in the Rat

Cited by 143 publications

References 23 publications

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Strategies for Safe and Effective Therapeutic Measures for Chronic Arsenic and Lead Poisoning

Lattice parameters and cation distribution of solid solutions of calcium and lead hydroxyapatite

Lead toxicity and nutritional deficiencies.

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