ParkinsonFranceV1, PascalFrancis, Corpus, bibRecord, 001281

In vitro and in vivo studies on chelation of manganese

Identifieur interne : 001281 ( PascalFrancis/Corpus ); précédent : 001280; suivant : 001282

In vitro and in vivo studies on chelation of manganese

Auteurs : P. Missy ; M-C Lanhers ; Y. Grignon ; M. Joyeux ; D. Burnel

Source :

Human & experimental toxicology [ 0960-3271 ] ; 2000.

RBID : Pascal:01-0041987

Descripteurs français

Pascal (Inist)
- Manganèse, Métal lourd, Chélateur, Intoxication, Antidote, Efficacité traitement, Chimiothérapie, In vivo, Rat, Animal, In vitro, Toxicité.

English descriptors

KwdEn :
- Animal, Antidote, Chelating agent, Chemotherapy, Heavy metal, In vitro, In vivo, Manganese, Poisoning, Rat, Toxicity, Treatment efficiency.

Abstract

This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl₂. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn² + and different molecules such as hemoglobin and certain cytochromes, instead of Fe²⁺. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O₂ with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 Hum. exp. toxicol.`
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A06				`@2 8`
A08	`01`	`1`	`ENG`	`@1 In vitro and in vivo studies on chelation of manganese`
A11	`01`	`1`		`@1 MISSY (P.)`
A11	`02`	`1`		`@1 LANHERS (M-C)`
A11	`03`	`1`		`@1 GRIGNON (Y.)`
A11	`04`	`1`		`@1 JOYEUX (M.)`
A11	`05`	`1`		`@1 BURNEL (D.)`
A14	`01`			`@1 Laboratoire de Chimie et de Toxicologie des Métaux, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I @2 Vandoeuvre-lès-Nancy @3 FRA @Z 1 aut. @Z 2 aut. @Z 5 aut.`
A14	`02`			`@1 Laboratoire d'Anatomie Pathologique, Faculté de Médecine, Université Henry Poincaré, Nancy I @2 Vandoeuvre-lès-Nancy @3 FRA @Z 3 aut.`
A14	`03`			`@1 SERES, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I @2 Vandoeuvre-lès-Nancy @3 FRA @Z 4 aut.`
A20				`@1 448-456`
A21				`@1 2000`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 19290 @5 354000093665510040`
A44				`@0 0000 @1 © 2001 INIST-CNRS. All rights reserved.`
A45				`@0 20 ref.`
A47	`01`	`1`		`@0 01-0041987`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Human & experimental toxicology`
A66	`01`			`@0 GBR`
C01	`01`		`ENG`	@0 This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl₂. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn² + and different molecules such as hemoglobin and certain cytochromes, instead of Fe²⁺. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O₂ with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).
C02	`01`	`X`		`@0 002B03L05`
C03	`01`	`X`	`FRE`	`@0 Manganèse @2 NC @5 01`
C03	`01`	`X`	`ENG`	`@0 Manganese @2 NC @5 01`
C03	`01`	`X`	`SPA`	`@0 Manganeso @2 NC @5 01`
C03	`02`	`X`	`FRE`	`@0 Métal lourd @5 04`
C03	`02`	`X`	`ENG`	`@0 Heavy metal @5 04`
C03	`02`	`X`	`SPA`	`@0 Metal pesado @5 04`
C03	`03`	`X`	`FRE`	`@0 Chélateur @5 07`
C03	`03`	`X`	`ENG`	`@0 Chelating agent @5 07`
C03	`03`	`X`	`SPA`	`@0 Quelante @5 07`
C03	`04`	`X`	`FRE`	`@0 Intoxication @5 10`
C03	`04`	`X`	`ENG`	`@0 Poisoning @5 10`
C03	`04`	`X`	`SPA`	`@0 Intoxicación @5 10`
C03	`05`	`X`	`FRE`	`@0 Antidote @5 11`
C03	`05`	`X`	`ENG`	`@0 Antidote @5 11`
C03	`05`	`X`	`SPA`	`@0 Antídoto @5 11`
C03	`06`	`X`	`FRE`	`@0 Efficacité traitement @5 12`
C03	`06`	`X`	`ENG`	`@0 Treatment efficiency @5 12`
C03	`06`	`X`	`SPA`	`@0 Eficacia tratamiento @5 12`
C03	`07`	`X`	`FRE`	`@0 Chimiothérapie @5 13`
C03	`07`	`X`	`ENG`	`@0 Chemotherapy @5 13`
C03	`07`	`X`	`SPA`	`@0 Quimioterapia @5 13`
C03	`08`	`X`	`FRE`	`@0 In vivo @5 14`
C03	`08`	`X`	`ENG`	`@0 In vivo @5 14`
C03	`08`	`X`	`SPA`	`@0 In vivo @5 14`
C03	`09`	`X`	`FRE`	`@0 Rat @5 15`
C03	`09`	`X`	`ENG`	`@0 Rat @5 15`
C03	`09`	`X`	`SPA`	`@0 Rata @5 15`
C03	`10`	`X`	`FRE`	`@0 Animal @5 16`
C03	`10`	`X`	`ENG`	`@0 Animal @5 16`
C03	`10`	`X`	`SPA`	`@0 Animal @5 16`
C03	`11`	`X`	`FRE`	`@0 In vitro @5 17`
C03	`11`	`X`	`ENG`	`@0 In vitro @5 17`
C03	`11`	`X`	`SPA`	`@0 In vitro @5 17`
C03	`12`	`X`	`FRE`	`@0 Toxicité @5 18`
C03	`12`	`X`	`ENG`	`@0 Toxicity @5 18`
C03	`12`	`X`	`SPA`	`@0 Toxicidad @5 18`
C07	`01`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`01`	`X`	`SPA`	`@0 Rodentia @2 NS`
C07	`02`	`X`	`FRE`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`ENG`	`@0 Mammalia @2 NS`
C07	`02`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`03`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`03`	`X`	`SPA`	`@0 Vertebrata @2 NS`
N21				`@1 022`

Format Inist (serveur)

NO :	PASCAL 01-0041987 INIST
ET :	In vitro and in vivo studies on chelation of manganese
AU :	MISSY (P.); LANHERS (M-C); GRIGNON (Y.); JOYEUX (M.); BURNEL (D.)
AF :	Laboratoire de Chimie et de Toxicologie des Métaux, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (1 aut., 2 aut., 5 aut.); Laboratoire d'Anatomie Pathologique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (3 aut.); SERES, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Human & experimental toxicology; ISSN 0960-3271; Royaume-Uni; Da. 2000; Vol. 19; No. 8; Pp. 448-456; Bibl. 20 ref.
LA :	Anglais
EA :	This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl₂. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn² + and different molecules such as hemoglobin and certain cytochromes, instead of Fe²⁺. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O₂ with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).
CC :	002B03L05
FD :	Manganèse; Métal lourd; Chélateur; Intoxication; Antidote; Efficacité traitement; Chimiothérapie; In vivo; Rat; Animal; In vitro; Toxicité
FG :	Rodentia; Mammalia; Vertebrata
ED :	Manganese; Heavy metal; Chelating agent; Poisoning; Antidote; Treatment efficiency; Chemotherapy; In vivo; Rat; Animal; In vitro; Toxicity
EG :	Rodentia; Mammalia; Vertebrata
SD :	Manganeso; Metal pesado; Quelante; Intoxicación; Antídoto; Eficacia tratamiento; Quimioterapia; In vivo; Rata; Animal; In vitro; Toxicidad
LO :	INIST-19290.354000093665510040
ID :	01-0041987

Links to Exploration step

Pascal:01-0041987

Le document en format XML

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<front><div type="abstract" xml:lang="en">This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl<sub>2</sub>
. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn<sup>2</sup>
 + and different molecules such as hemoglobin and certain cytochromes, instead of Fe<sup>2+</sup>
. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O<sub>2</sub>
 with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).</div>
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<fC01 i1="01" l="ENG"><s0>This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl<sub>2</sub>
. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn<sup>2</sup>
 + and different molecules such as hemoglobin and certain cytochromes, instead of Fe<sup>2+</sup>
. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O<sub>2</sub>
 with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).</s0>
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<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Heavy metal</s0>
<s5>04</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Metal pesado</s0>
<s5>04</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Chélateur</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Chelating agent</s0>
<s5>07</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Quelante</s0>
<s5>07</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Intoxication</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Poisoning</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Intoxicación</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Antidote</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Antidote</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Antídoto</s0>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Efficacité traitement</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Treatment efficiency</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Eficacia tratamiento</s0>
<s5>12</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Chimiothérapie</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Chemotherapy</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Quimioterapia</s0>
<s5>13</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>In vivo</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>In vivo</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>In vivo</s0>
<s5>14</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Rat</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Rat</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Rata</s0>
<s5>15</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Animal</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Animal</s0>
<s5>16</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Animal</s0>
<s5>16</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>In vitro</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>In vitro</s0>
<s5>17</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>In vitro</s0>
<s5>17</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Toxicité</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Toxicity</s0>
<s5>18</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Toxicidad</s0>
<s5>18</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>022</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 01-0041987 INIST</NO>
<ET>In vitro and in vivo studies on chelation of manganese</ET>
<AU>MISSY (P.); LANHERS (M-C); GRIGNON (Y.); JOYEUX (M.); BURNEL (D.)</AU>
<AF>Laboratoire de Chimie et de Toxicologie des Métaux, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (1 aut., 2 aut., 5 aut.); Laboratoire d'Anatomie Pathologique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (3 aut.); SERES, Département Environnement et Santé Publique, Faculté de Médecine, Université Henry Poincaré, Nancy I/Vandoeuvre-lès-Nancy/France (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Human & experimental toxicology; ISSN 0960-3271; Royaume-Uni; Da. 2000; Vol. 19; No. 8; Pp. 448-456; Bibl. 20 ref.</SO>
<LA>Anglais</LA>
<EA>This work deals with new chelating agents of manganese (Mn). Out of 24 compounds chosen for their chemical structure supposed to be favorable for Mn complexation, six polyaminopolycarboxylic acids proved to be efficient for displacing Mn bound to serum bovine proteins in vitro: TTHA, DTPA, DPTA, DPTA-OH, HBED, EDTA (mobilization >50%). The first five compounds were then tested in vivo on rats pre treated with MnCl<sub>2</sub>
. They exhibited only slight to moderate efficacy to diminish Mn in tissues and were ineffective on increased Mn concentration in whole blood; in addition, they had different and specific mobilizing effects on other essential elements (Fe, Zn, Cu). Their limited efficacy in vivo could be due to the formation of very stable complexes between Mn<sup>2</sup>
 + and different molecules such as hemoglobin and certain cytochromes, instead of Fe<sup>2+</sup>
. This could disturb the functioning of the cellular respiratory chain, leading to an incomplete reduction of O<sub>2</sub>
 with formation of free oxygenated radicals, reduction in the energy supply, and disturbance of the cytochromes renewal mechanism. All of these phenomena could accelerate cellular aging and explain the lack of efficacy ofthe chelating agents towards Mn neurotoxicity (Parkinson's syndrome).</EA>
<CC>002B03L05</CC>
<FD>Manganèse; Métal lourd; Chélateur; Intoxication; Antidote; Efficacité traitement; Chimiothérapie; In vivo; Rat; Animal; In vitro; Toxicité</FD>
<FG>Rodentia; Mammalia; Vertebrata</FG>
<ED>Manganese; Heavy metal; Chelating agent; Poisoning; Antidote; Treatment efficiency; Chemotherapy; In vivo; Rat; Animal; In vitro; Toxicity</ED>
<EG>Rodentia; Mammalia; Vertebrata</EG>
<SD>Manganeso; Metal pesado; Quelante; Intoxicación; Antídoto; Eficacia tratamiento; Quimioterapia; In vivo; Rata; Animal; In vitro; Toxicidad</SD>
<LO>INIST-19290.354000093665510040</LO>
<ID>01-0041987</ID>
</server>
</inist>
</record>

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La maladie de Parkinson en France (serveur d'exploration)

In vitro and in vivo studies on chelation of manganese

In vitro and in vivo studies on chelation of manganese

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