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Filename: drivers/Session_files_driver.php

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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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File: /home/orthodiedw/nutridatabase/index.php
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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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File: /home/orthodiedw/nutridatabase/index.php
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Filename: drivers/Session_files_driver.php

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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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Filename: drivers/Session_files_driver.php

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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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Filename: drivers/Session_files_driver.php

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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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File: /home/orthodiedw/nutridatabase/index.php
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Filename: drivers/Session_files_driver.php

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File: /home/orthodiedw/nutridatabase/application/controllers/Articles.php
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Line: 7
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File: /home/orthodiedw/nutridatabase/index.php
Line: 315
Function: require_once

La génistéine et l'acide ascorbique réduisent les dommages causés à l'ADN par le stress oxydatif induit par l'antimoniate de méglumine antileishmanien.

L'antimoniate de méglumine (Glucantime) est un antimonial pentavalent utilisé pour traiter la leishmaniose, malgré ses effets toxiques reconnus, tels que son aptitude à causer des dommages oxydatifs aux lipides et aux protéines. Récemment, notre groupe a démontré que l’antimoniate de méglumine provoque des dommages à l’ADN dérivés du stress oxydatif. Sachant que les antioxydants modulent les espèces d'oxygène réactives, nous avons évalué la capacité de la génistéine et de l'acide ascorbique à prévenir la génotoxicité causée par l'antimoniate de méglumine. Pour cela, les souris (n = 5 / groupe) ont reçu de la génistéine (par gavage) à des doses de 5, 10 et 20 mg / kg pendant trois jours consécutifs. Après cette période, ils ont été traités avec 810 mg / kg d'antimoniate de méglumine par voie intraperitoneale (i.p.). En outre, des souris (n = 5 / groupe) ont simultanément reçu de l'acide ascorbique (i.p.) à des doses de 30, 60 et 120 mg / kg et de 810 mg / kg d'antimoniate de méglumine. Nous avons également effectué des tests de post-traitement et de prétraitement, dans lesquels les animaux recevaient de l'acide ascorbique (60 mg / kg) 24 h avant ou après l'administration de l'antimoniate de méglumine. L'instabilité génomique et la mutagénicité ont été analysées par un test conventionnel sur les comètes et un test enzymatique utilisant l'enzyme formamide pyrimidine ADN glycosylase (Fpg), ainsi que le test du micronoyau, respectivement. L’antimoniate de méglumine a entraîné une augmentation des dommages de l’ADN après la digestion avec Fpg, renforçant ainsi son potentiel mutagène en oxydant les bases de l’ADN, ce qui a été empêché par la génistéine. De même, l'acide ascorbique était capable de réduire les effets mutagènes lors du traitement simultané et post-traitement. Par conséquent, nos résultats démontrent que les deux composés sont efficaces pour prévenir les mutations dans les cellules de mammifère traitées avec de l’antimoniate de méglumine.


Source: https://www.ncbi.nlm.nih.gov/pubmed/29941649


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