摘要
In biological systems there is a balance between the production and neutralization of reactive oxygen species(ROS). This balance is maintained by the presence of natural antioxidants and antioxidant enzymes suchas superoxide dismutase(SOD), catalase and glutathione peroxidase. The enhancement of lipid peroxidation or the decrease of antioxidant protection present in metabolic diseases or bad lifestyle can induce endothelial dysfunction and atherosclerosis.Clinical studies have shown that oxidative stress can increase ROS reducing the formation of antioxidant defences, especially in subjects with coronary artery disease(CAD). Some observation indicated that in the early stages of the disease there is a homeostatic upregulation of the antioxidant enzyme system in response to increased free radicals to prevent vascular damage.As soon as free radicals get to chronically elevated levels, this compensation ceases. Therefore, SOD and the other enzymes may represent a good therapeutic target against ROS, but they are not useful markers for the diagnosis of CAD. In conclusion antioxidant enzymes are reduced in presence of metabolic disease and CAD. However the existence of genes that promote their enzymatic activity could contribute to create new drugs for the treatment of damage caused by metabolic diseases or lifestyle that increases the plasma ROS levels.
In biological systems there is a balance between the production and neutralization of reactive oxygen species(ROS). This balance is maintained by the presence of natural antioxidants and antioxidant enzymes suchas superoxide dismutase(SOD), catalase and glutathione peroxidase. The enhancement of lipid peroxidation or the decrease of antioxidant protection present in metabolic diseases or bad lifestyle can induce endothelial dysfunction and atherosclerosis.Clinical studies have shown that oxidative stress can increase ROS reducing the formation of antioxidant defences, especially in subjects with coronary artery disease(CAD). Some observation indicated that in the early stages of the disease there is a homeostatic upregulation of the antioxidant enzyme system in response to increased free radicals to prevent vascular damage.As soon as free radicals get to chronically elevated levels, this compensation ceases. Therefore, SOD and the other enzymes may represent a good therapeutic target against ROS, but they are not useful markers for the diagnosis of CAD. In conclusion antioxidant enzymes are reduced in presence of metabolic disease and CAD. However the existence of genes that promote their enzymatic activity could contribute to create new drugs for the treatment of damage caused by metabolic diseases or lifestyle that increases the plasma ROS levels.
