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Pharmacological prevention of acute lead poisoning in Paramecium

To understand how lead (Pb 2+) and other heavy metals and chelating agents affect living cells, behavioral experiments in the marine ciliate Paramecium calkinsi were carried out. The duration of Backward Swimming Behavior (BSB) of Paramecium was partially reduced when celis were exposed to 100 μM of...

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Bibliographic Details
Published in:Toxicology (Amsterdam) 1996-04, Vol.108 (3), p.165-173
Main Authors: Bernal, Juan, Ruvalcaba, Sergio
Format: Article
Language:English
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Summary:To understand how lead (Pb 2+) and other heavy metals and chelating agents affect living cells, behavioral experiments in the marine ciliate Paramecium calkinsi were carried out. The duration of Backward Swimming Behavior (BSB) of Paramecium was partially reduced when celis were exposed to 100 μM of Ni 2+, Cd 2+ and Co 2+. In contrast, Pb 2+ increased Paramecium BSB in a dose-dependent manner. Thus, 1, 10, 20, 50 and 100 μM of Pb 2+ increased the duration of BSB by 20.4, 83.9, 143.2, 163.2 and 185.2%, respectively. The naphthalenesulphonamide W-7, a calcium channel blocker in lower organisms, abolished the increase of Paramecium BSB initially produced by Pb 2+. Paramecium, poisoned with 10 μM of Pb 2+, were also treated with putative Pb 2+ chelating agents, such as meso-2-3-dimercaptosuccinic acid (DMSA), Ca-Na 2-EDTA and ascorbic acid. These compounds inhibited the increase of the duration of BSB initially produced by Pb 2+ in a dose-dependent manner. The potency of these antidotes in blocking the effects of Pb 2+ was as follows: DMSA ⪢ Ca-Na 2-EDTA > ascorbic acid. These results provide evidence for a membrane-based mechanism of lead poisoning and support the use of DMSA as a lead antidote.
ISSN:0300-483X
1879-3185
DOI:10.1016/0300-483X(95)03272-H