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Statut en zinc, polymorphisme du gène SOD3 et risque cardiovasculaire

Statut en zinc, polymorphisme du gène SOD3 et risque cardiovasculaire

Camila Revoredo / Dilina Marreiro / Heila Dias

60,13 €
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Editorial:
KS OmniScriptum Publishing
Año de edición:
2025
Materia
Empresa y gestión
ISBN:
9786209127687
60,13 €
IVA incluido
Disponible

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Les interactions entre les facteurs environnementaux et génétiques entraînent une augmentation du risque de maladies cardiovasculaires. À cet égard, des études cliniques et observationnelles ont mis en évidence une relation entre les caractéristiques quantitatives et qualitatives de l’alimentation et la survenue de ces maladies, car certains composants alimentaires peuvent être impliqués dans le métabolisme des lipoprotéines. D’autre part, l’action des nutriments ayant une fonction antioxydante est importante dans la protection vasculaire, comme le zinc minéral. L’enzyme superoxyde dismutase 3 (SOD3) est l’une des enzymes qui ont besoin du zinc comme cofacteur et agit contre la production intracellulaire de radicaux libres. Cependant, un polymorphisme peut se produire dans le gène qui code la SOD3, tel que le polymorphisme Arg213Gly, ce qui entraîne une réduction de l’activité antioxydante de cette enzyme dans la paroi vasculaire, diminuant ainsi sa protection contre les radicaux libres dans les vaisseaux. Par conséquent, tant les modifications des concentrations de zinc que l’existence du polymorphisme Arg213Gly dans le gène de l’enzyme SOD3 peuvent être associées à une réduction de son activité antioxydante et, par conséquent, à un risque accru de développer des maladies cardiovasculaires.

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