Antagonistic Effect In Vivo of Zinc on Inhibition of δ -Aminolevulinic Acid Dehydratase by Lead

Hæger-Aronsen, Birgitta; Schütz, Andrejs; Abdulla, M.

doi:10.1080/00039896.1976.10667222

Cited by 76 publications

(26 citation statements)

References 18 publications

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“…Rather, they hypothesized that zinc and lead competed for similar binding sites on a metallothionein-like protein in the intestine responsible for metal transport. Interactions between zinc and lead are possible beyond the level of the gastrointestinal tract, however, since zinc added in vitro or given in ii'o has been shown to activate the enzyme 8-aminolevulinic acid dehydratase and to prevent the inhibition of this enzyme by lead (51,52). In fact, concern was expressed that in workers exposed to both zinc and lead the zinc might activate the enzyme enough to mask the excessive lead burden of the body (53).…”

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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Section: Zinc and Coppermentioning

confidence: 99%

Lead toxicity and nutritional deficiencies.

Levander¹

1979

Environ Health Perspect

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“…It has been demonstrated that zinc, as well as DL-dithiothreitol (DTT) in vitro, is able to restore the lead-inhibited ALA-D activity in rat and human blood (1, [12][13][14]. In addition, an antagonistic effect of zinc on the inhibition of ALA-D by lead in vivo has been reported (15), as well as the absence of an antagonistic effect (16). However, data are lacking regarding the ability of zinc to restore the normal activity of ALA-D inhibited by lead in vivo during a specific stage of rapid postnatal brain development.…”

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confidence: 99%

Effects of lead and/or zinc exposure during the second stage of rapid postnatal brain growth on delta-aminolevulinate dehydratase and negative geotaxis of suckling rats

Goulart

Pereira

Garcia

et al. 2001

Braz J Med Biol Res

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Lead has been shown to produce cognitive and motor deficits in young rats that could be mediated, at least in part, by inhibition of the zinccontaining heme biosynthetic enzyme d-aminolevulinate dehydratase (ALA-D). In the present study we investigated the effects of lead and/ or zinc treatment during the second stage of rapid postnatal brain development on brain, kidney and blood ALA-D specific activity, as well as the negative geotaxis behavior of rats. Eight-day-old Wistar rats were injected intraperitoneally with saline, lead acetate (8 mg/kg) and/or zinc chloride (2 mg/kg) daily for five consecutive days. Twentyfour hours after treatment, ALA-D activity was determined in the absence and presence of DL-dithiothreitol (DTT). The negative geotaxis behavior was assessed in 9-to 13-day-old rats. Treatment with lead and/or zinc did not affect body, brain or kidney weights or brainor kidney-to-body weight ratios of the animals. In spite of the absence of effect of any treatment on ALA-D specific activity in brain, kidney and blood, the reactivation index with DTT was higher in the groups treated with lead or lead + zinc than in the control group, in brain, kidney and blood (mean ± SEM; brain: 33. 33 ± 4.34, 38.90 ± 8.24, 13.67 ± 3.41; kidney: 33.50 ± 2.97, 37.60 ± 2.67, 15.80 ± 2.66; blood: 63.95 ± 3.73, 56.43 ± 5.93, 31.07 ± 4.61, respectively, N = 9-11). The negative geotaxis response behavior was not affected by lead and/or zinc treatment. The results indicate that lead and/or zinc treatment during the second stage of rapid postnatal brain growth affected ALA-D, but zinc was not sufficient to protect the enzyme from the effects of lead in brain, kidney and blood.

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“…This study suggests that zinc has a protective role in reducing the biological effects of absorbed lead as well as a probable role in altering absorption of lead. The ability of high levels of dietary zinc to play this role has been confirmed by Haeger-Aronsen, Schutz, and Abdulla (16).…”

Section: Lead and Zinc Interrelationshipsmentioning

confidence: 56%

Some observations on the interaction of zinc, copper, and iron metabolism in lead and cadmium toxicity.

Petering¹

1978

Environ Health Perspect

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A brief review of the literature indicates that nutritional deficiencies have been shown to increase the absorption and toxicity of orally ingested lead and cadmium. Results from recent studies indicate that low level oral ingestion of cadmium and lead perturbs the metabolism of zinc, copper, and iron and that these changes may be the earliest manifestation of the toxicity of lead and cadmium. The significance of these rmdings reveals itself in two ways: namely, that toxicologic investigations of lead and cadmium, whether experimental or clinical, must be based on a definitive consideration of the nutritional status of animals or people, and, secondly, that the preventive role of nutrition, especially that of trace metal intakes, must be taken seriously when establishing measures for reducing, eliminating, or combatting the toxic effects of widespread exposure to lead and cadmium in humans.

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Antagonistic Effect In Vivo of Zinc on Inhibition of δ -Aminolevulinic Acid Dehydratase by Lead

Cited by 76 publications

References 18 publications

Lead toxicity and nutritional deficiencies.

Lead toxicity and nutritional deficiencies.

Effects of lead and/or zinc exposure during the second stage of rapid postnatal brain growth on delta-aminolevulinate dehydratase and negative geotaxis of suckling rats

Some observations on the interaction of zinc, copper, and iron metabolism in lead and cadmium toxicity.

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