The role of oxidative stress in congenital syndromes antioxidants_OA SapienzaRoma stress oxidativestress syndrome congenitalsyndrome
By Dr. Liji Thomas, MDOct 10 2022Reviewed by Benedette Cuffari, M.Sc. Children born with various syndromes caused by genetic or acquired factors have been the focus of many clinical and research studies. It is important to both understand the underlying mechanism and ameliorate the condition when possible.
Oxidizing species ROS mediate a host of useful functions, including killing pathogens during inflammatory responses or regulating cardiovascular function and protein activation. However, when inadequately regulated by cellular antioxidants, ROS can cause tissue damage and organ dysfunction. The effects of ROS production include DNA breaks and other types of damage that can lead to cancer, accelerated aging, neurodegenerative diseases, autoimmune conditions, or cardiovascular disease. Epigenetic changes that alter DNA repair may also occur.
FASD FASD denotes a spectrum of cognitive and behavioral abnormalities in the neonate related to maternal alcohol use during pregnancy. Fetal alcohol syndrome is the major cause of mental retardation worldwide and the primary cause of preventable neurodevelopmental abnormalities. As a result, alcohol at any dose is completely prohibited in pregnancy, pending the establishment of a safe minimum.
AT AT is a purely genetic syndrome with multiple clinical manifestations in the first 20 years of life. Of these, the most disabling are T-cell tumors and cerebellar ataxia. The pathology lies in the Ataxia Telangiectasia Mutated gene, which is key to initiating DNA repair. Several other proteins and transcription factors involved in regulating antioxidant responses have been reported to be affected in DS. The oxidative stress associated with these changes could account for the cognitive and intellectual disabilities associated with DS, as well as the heart anomalies often found in these children.
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