Abstract
Autism is a neurodevelopmental disorder that is characterized by deficits in social interaction, communication and repetitive behaviors. As the prevalence of the disorder increases, the need to understand the cause to account for its treatment increases. Besides the genetic factors that attribute to the cause, studies have examined other environmental factors that may lead to a diagnosis of autism. Children with autism are thought to be more susceptible to oxidative stress, which may contribute to the pathological nature of the disorder. Studies have shown nearly 35% of autistic children have low glutathione levels. Glutathione is an antioxidant that the body creates to reduce oxidative stress; which could lead to oxidative damage to the brain and periphery. The purpose of this study will be to examine whether lymphoblastoid cells(LCLs) from autistic patients are more vulnerable to oxidative stress than cells of neurotypical controls. The study will investigate the effects of 2,3-dimethoxy-1,4- naphthoquinone(DMNQ), a mitochondrial oxidized stressor, on the LCLs. Very few studies have been conducted to understand how DMNQ induces cytotoxicity and its effects. Levels of intracellular reactive oxygen species(ROS) will be quantified via the use of dichlorofluorescein(DCF) assays in LCLs from both autistic and neurotypical children using a plate reader. We hypothesize that children with autism will have higher ROS levels at baseline and after treatment with the DMNQ. The findings of this study will advance our understanding of how LCLs from autistic patients respond to oxidative insult, which will contribute to future studies to reduce oxidative stress-induced cytotoxicity.
Faculty Sponsors
Dr. Ana Castejon
Project Type
Event
Location
Alvin Sherman Library
Start Date
4-8-2016 1:00 PM
End Date
4-8-2016 5:30 PM
Reactive Oxygen Species Production During Oxidative Stress in Lymphoblastoid Cell Lines from Autistic Children
Alvin Sherman Library
Autism is a neurodevelopmental disorder that is characterized by deficits in social interaction, communication and repetitive behaviors. As the prevalence of the disorder increases, the need to understand the cause to account for its treatment increases. Besides the genetic factors that attribute to the cause, studies have examined other environmental factors that may lead to a diagnosis of autism. Children with autism are thought to be more susceptible to oxidative stress, which may contribute to the pathological nature of the disorder. Studies have shown nearly 35% of autistic children have low glutathione levels. Glutathione is an antioxidant that the body creates to reduce oxidative stress; which could lead to oxidative damage to the brain and periphery. The purpose of this study will be to examine whether lymphoblastoid cells(LCLs) from autistic patients are more vulnerable to oxidative stress than cells of neurotypical controls. The study will investigate the effects of 2,3-dimethoxy-1,4- naphthoquinone(DMNQ), a mitochondrial oxidized stressor, on the LCLs. Very few studies have been conducted to understand how DMNQ induces cytotoxicity and its effects. Levels of intracellular reactive oxygen species(ROS) will be quantified via the use of dichlorofluorescein(DCF) assays in LCLs from both autistic and neurotypical children using a plate reader. We hypothesize that children with autism will have higher ROS levels at baseline and after treatment with the DMNQ. The findings of this study will advance our understanding of how LCLs from autistic patients respond to oxidative insult, which will contribute to future studies to reduce oxidative stress-induced cytotoxicity.
