Plasmodium berghei: Implication of Intracellular Glutathione and Its Related Enzyme in Chloroquine Resistance in Vivo
Identifieur interne : 000774 ( Istex/Corpus ); précédent : 000773; suivant : 000775Plasmodium berghei: Implication of Intracellular Glutathione and Its Related Enzyme in Chloroquine Resistance in Vivo
Auteurs : V. L. Dubois ; D. F. N. Platel ; G. Pauly ; J. TribouleyduretSource :
- Experimental Parasitology [ 0014-4894 ] ; 1995.
Abstract
Abstract: Glutathione (GSH) plays a critical role in the detoxication and the protection of cells against oxidative stress. In the present study we examined the relationship between the intracellular GSH level as well as glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) activities and how they relate to Plasmodium berghei resistance to chloroquine. Resistant strains (CQR30 and CQR60) were selected in vivo from a sensitive strain (NK65). Marked increases in GSH levels and GST activity within resistant parasites were observed, compared to sensitive parasites. On the other hand, GR and GPx activities were similar in sensitive and resistant parasites. Treatment with chloroquine did not influence the intracellular level of GSH, but it was found to significantly decrease GR activity. Intracellular depletion of GSH, by a nontoxic concentration of buthionine sulfoximine (BSO), significantly sensitized the resistant parasites to chloroquine. These results suggest that the P. berghei resistance results from altered GSH and GST levels and activity, respectively, which enable the detoxification of chloroquine in resistant parasites.
Url:
DOI: 10.1006/expr.1995.1099
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Tribouleyduret</name><affiliation><mods:affiliation>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Experimental Parasitology</title><title level="j" type="abbrev">YEXPR</title><idno type="ISSN">0014-4894</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1995">1995</date><biblScope unit="volume">81</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="117">117</biblScope><biblScope unit="page" to="124">124</biblScope></imprint><idno type="ISSN">0014-4894</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-4894</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Glutathione (GSH) plays a critical role in the detoxication and the protection of cells against oxidative stress. In the present study we examined the relationship between the intracellular GSH level as well as glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) activities and how they relate to Plasmodium berghei resistance to chloroquine. Resistant strains (CQR30 and CQR60) were selected in vivo from a sensitive strain (NK65). Marked increases in GSH levels and GST activity within resistant parasites were observed, compared to sensitive parasites. On the other hand, GR and GPx activities were similar in sensitive and resistant parasites. Treatment with chloroquine did not influence the intracellular level of GSH, but it was found to significantly decrease GR activity. Intracellular depletion of GSH, by a nontoxic concentration of buthionine sulfoximine (BSO), significantly sensitized the resistant parasites to chloroquine. These results suggest that the P. berghei resistance results from altered GSH and GST levels and activity, respectively, which enable the detoxification of chloroquine in resistant parasites.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>V.L. Dubois</name><affiliations><json:string>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</json:string></affiliations></json:item><json:item><name>D.F.N. Platel</name><affiliations><json:string>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</json:string></affiliations></json:item><json:item><name>G. Pauly</name><affiliations><json:string>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</json:string></affiliations></json:item><json:item><name>J. 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In the present study we examined the relationship between the intracellular GSH level as well as glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) activities and how they relate to Plasmodium berghei resistance to chloroquine. Resistant strains (CQR30 and CQR60) were selected in vivo from a sensitive strain (NK65). Marked increases in GSH levels and GST activity within resistant parasites were observed, compared to sensitive parasites. On the other hand, GR and GPx activities were similar in sensitive and resistant parasites. Treatment with chloroquine did not influence the intracellular level of GSH, but it was found to significantly decrease GR activity. Intracellular depletion of GSH, by a nontoxic concentration of buthionine sulfoximine (BSO), significantly sensitized the resistant parasites to chloroquine. 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In the present study we examined the relationship between the intracellular GSH level as well as glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) activities and how they relate to <ce:italic>Plasmodium berghei</ce:italic> resistance to chloroquine. Resistant strains (CQR30 and CQR60) were selected <ce:italic>in vivo</ce:italic> from a sensitive strain (NK65). Marked increases in GSH levels and GST activity within resistant parasites were observed, compared to sensitive parasites. On the other hand, GR and GPx activities were similar in sensitive and resistant parasites. Treatment with chloroquine did not influence the intracellular level of GSH, but it was found to significantly decrease GR activity. Intracellular depletion of GSH, by a nontoxic concentration of buthionine sulfoximine (BSO), significantly sensitized the resistant parasites to chloroquine. These results suggest that the <ce:italic>P. berghei</ce:italic> resistance results from altered GSH and GST levels and activity, respectively, which enable the detoxification of chloroquine in resistant parasites.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Plasmodium berghei: Implication of Intracellular Glutathione and Its Related Enzyme in Chloroquine Resistance in Vivo</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Implication of Intracellular Glutathione and Its Related Enzyme in Chloroquine Resistance</title></titleInfo><name type="personal"><namePart type="given">V.L.</namePart><namePart type="family">Dubois</namePart><affiliation>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">D.F.N.</namePart><namePart type="family">Platel</namePart><affiliation>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Pauly</namePart><affiliation>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Tribouleyduret</namePart><affiliation>Univ Bordeaux 2, UFR Sci Pharmaceut, Immunol & Parasitol Lab, 146 Leo Saignat, F 33076 Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1995</dateIssued><copyrightDate encoding="w3cdtf">1995</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: Glutathione (GSH) plays a critical role in the detoxication and the protection of cells against oxidative stress. In the present study we examined the relationship between the intracellular GSH level as well as glutathione S-transferase (GST), glutathione reductase (GR), and glutathione peroxidase (GPx) activities and how they relate to Plasmodium berghei resistance to chloroquine. Resistant strains (CQR30 and CQR60) were selected in vivo from a sensitive strain (NK65). Marked increases in GSH levels and GST activity within resistant parasites were observed, compared to sensitive parasites. On the other hand, GR and GPx activities were similar in sensitive and resistant parasites. Treatment with chloroquine did not influence the intracellular level of GSH, but it was found to significantly decrease GR activity. Intracellular depletion of GSH, by a nontoxic concentration of buthionine sulfoximine (BSO), significantly sensitized the resistant parasites to chloroquine. 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