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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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| Published in: | Toxicology (Amsterdam) 1996-04, Vol.108 (3), p.165-173 |
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| Main Authors: | , |
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| Language: | English |
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| container_title | Toxicology (Amsterdam) |
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| creator | Bernal, Juan Ruvalcaba, Sergio |
| description | 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. |
| doi_str_mv | 10.1016/0300-483X(95)03272-H |
| format | article |
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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.</description><identifier>ISSN: 0300-483X</identifier><identifier>EISSN: 1879-3185</identifier><identifier>DOI: 10.1016/0300-483X(95)03272-H</identifier><identifier>PMID: 8658535</identifier><identifier>CODEN: TXICDD</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Animals ; Antidotes - pharmacology ; Ascorbic acid ; Ascorbic Acid - pharmacology ; Biological and medical sciences ; Ca-Na 2-EDTA ; Calcium channels ; Cations, Divalent - pharmacology ; Cell Membrane - drug effects ; Chelating Agents - pharmacology ; Chemical and industrial products toxicology. Toxic occupational diseases ; Cilia - drug effects ; DMSA ; Edetic Acid - pharmacology ; Fundamental and applied biological sciences. Psychology ; Lead - toxicity ; Marine ; Medical sciences ; meso-2,3-Dimercaptosuccinic acid ; Metals and various inorganic compounds ; Paramecium ; Paramecium - drug effects ; Paramecium - physiology ; Pathology ; Pb 2 ; Protozoa ; Succimer - pharmacology ; Sulfonamides - pharmacology ; Swimming - physiology ; Time Factors ; Toxicology</subject><ispartof>Toxicology (Amsterdam), 1996-04, Vol.108 (3), p.165-173</ispartof><rights>1996</rights><rights>1996 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-d1cc7453048b2a34ad7ff799c3db3760f8239d74d0959b316609bab916e2dce53</citedby><cites>FETCH-LOGICAL-c448t-d1cc7453048b2a34ad7ff799c3db3760f8239d74d0959b316609bab916e2dce53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3068954$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8658535$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bernal, Juan</creatorcontrib><creatorcontrib>Ruvalcaba, Sergio</creatorcontrib><title>Pharmacological prevention of acute lead poisoning in Paramecium</title><title>Toxicology (Amsterdam)</title><addtitle>Toxicology</addtitle><description>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.</description><subject>Animals</subject><subject>Antidotes - pharmacology</subject><subject>Ascorbic acid</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Ca-Na 2-EDTA</subject><subject>Calcium channels</subject><subject>Cations, Divalent - pharmacology</subject><subject>Cell Membrane - drug effects</subject><subject>Chelating Agents - pharmacology</subject><subject>Chemical and industrial products toxicology. Toxic occupational diseases</subject><subject>Cilia - drug effects</subject><subject>DMSA</subject><subject>Edetic Acid - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Lead - toxicity</subject><subject>Marine</subject><subject>Medical sciences</subject><subject>meso-2,3-Dimercaptosuccinic acid</subject><subject>Metals and various inorganic compounds</subject><subject>Paramecium</subject><subject>Paramecium - drug effects</subject><subject>Paramecium - physiology</subject><subject>Pathology</subject><subject>Pb 2</subject><subject>Protozoa</subject><subject>Succimer - pharmacology</subject><subject>Sulfonamides - pharmacology</subject><subject>Swimming - physiology</subject><subject>Time Factors</subject><subject>Toxicology</subject><issn>0300-483X</issn><issn>1879-3185</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><recordid>eNqFkE1P3DAURS1UBAPlHxQpi6qCRai_Y28QFQKm0kjMopW6sxz7hRol8WAnSP33ZDrRLGH1Fvfcq6eD0BeCrwgm8jtmGJdcsT8XWlxiRitaLg_QgqhKl4wo8Qkt9sgxOsn5GWNMGZdH6EhJoQQTC3Sz_mtTZ11s41Nwti02CV6hH0Lsi9gU1o0DFC1YX2xiyLEP_VMR-mJtk-3AhbH7jA4b22Y4m-8p-n1_9-t2Wa4eH37e_liVjnM1lJ44V3HBMFc1tYxbXzVNpbVjvmaVxI2iTPuKe6yFrhmREuva1ppIoN6BYKfo2253k-LLCHkwXcgO2tb2EMdsiJBaCq0-BjmnlBI5gXwHuhRzTtCYTQqdTf8MwWZr2Gz1ma0-o4X5b9gsp9r5vD_WHfh9aVY65V_n3OZJaJNs70LeYwxLpQWfsOsdBpO01wDJZBegd-BDAjcYH8P7f7wBfE6W3A</recordid><startdate>19960430</startdate><enddate>19960430</enddate><creator>Bernal, Juan</creator><creator>Ruvalcaba, Sergio</creator><general>Elsevier Ireland Ltd</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7ST</scope><scope>C1K</scope><scope>SOI</scope><scope>7U7</scope><scope>F1W</scope><scope>H97</scope><scope>L.G</scope><scope>M7N</scope></search><sort><creationdate>19960430</creationdate><title>Pharmacological prevention of acute lead poisoning in Paramecium</title><author>Bernal, Juan ; Ruvalcaba, Sergio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-d1cc7453048b2a34ad7ff799c3db3760f8239d74d0959b316609bab916e2dce53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Antidotes - pharmacology</topic><topic>Ascorbic acid</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Ca-Na 2-EDTA</topic><topic>Calcium channels</topic><topic>Cations, Divalent - pharmacology</topic><topic>Cell Membrane - drug effects</topic><topic>Chelating Agents - pharmacology</topic><topic>Chemical and industrial products toxicology. Toxic occupational diseases</topic><topic>Cilia - drug effects</topic><topic>DMSA</topic><topic>Edetic Acid - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Lead - toxicity</topic><topic>Marine</topic><topic>Medical sciences</topic><topic>meso-2,3-Dimercaptosuccinic acid</topic><topic>Metals and various inorganic compounds</topic><topic>Paramecium</topic><topic>Paramecium - drug effects</topic><topic>Paramecium - physiology</topic><topic>Pathology</topic><topic>Pb 2</topic><topic>Protozoa</topic><topic>Succimer - pharmacology</topic><topic>Sulfonamides - pharmacology</topic><topic>Swimming - physiology</topic><topic>Time Factors</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bernal, Juan</creatorcontrib><creatorcontrib>Ruvalcaba, Sergio</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Environment Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Environment Abstracts</collection><collection>Toxicology Abstracts</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 3: Aquatic Pollution & Environmental Quality</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><jtitle>Toxicology (Amsterdam)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bernal, Juan</au><au>Ruvalcaba, Sergio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacological prevention of acute lead poisoning in Paramecium</atitle><jtitle>Toxicology (Amsterdam)</jtitle><addtitle>Toxicology</addtitle><date>1996-04-30</date><risdate>1996</risdate><volume>108</volume><issue>3</issue><spage>165</spage><epage>173</epage><pages>165-173</pages><issn>0300-483X</issn><eissn>1879-3185</eissn><coden>TXICDD</coden><abstract>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.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier Ireland Ltd</pub><pmid>8658535</pmid><doi>10.1016/0300-483X(95)03272-H</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0300-483X |
| ispartof | Toxicology (Amsterdam), 1996-04, Vol.108 (3), p.165-173 |
| issn | 0300-483X 1879-3185 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_15696598 |
| source | ScienceDirect Freedom Collection |
| subjects | Animals Antidotes - pharmacology Ascorbic acid Ascorbic Acid - pharmacology Biological and medical sciences Ca-Na 2-EDTA Calcium channels Cations, Divalent - pharmacology Cell Membrane - drug effects Chelating Agents - pharmacology Chemical and industrial products toxicology. Toxic occupational diseases Cilia - drug effects DMSA Edetic Acid - pharmacology Fundamental and applied biological sciences. Psychology Lead - toxicity Marine Medical sciences meso-2,3-Dimercaptosuccinic acid Metals and various inorganic compounds Paramecium Paramecium - drug effects Paramecium - physiology Pathology Pb 2 Protozoa Succimer - pharmacology Sulfonamides - pharmacology Swimming - physiology Time Factors Toxicology |
| title | Pharmacological prevention of acute lead poisoning in Paramecium |
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