Add like
Add dislike
Add to saved papers

Enhanced activity of superoxide dismutase is a common response to dietary and genetically induced increased cholesterol levels.

OBJECTIVES: Hypercholesterolaemia has been implicated in the pathogenesis of neurodegenerative diseases. In this work, we tested whether cholesterol-mediated neurodegeneration induced either by cholesterol-rich diet or genetic mutation may share a common mechanism involving increased oxidative stress and mitochondria oxidant status. Additionally, we analysed whether upon cholesterol-rich diet, different brain regions (prefrontal cortex, cortex, hippocampus, and cerebellum) show distinct vulnerability to an oxidative stress response.

METHODS: Oxidative stress parameters were measured both in vivo (in the liver and in different brain regions) in cholesterol-fed mice and in vitro in genetically induced cholesterol accumulation in NPC1-null cells.

RESULTS: Increased superoxide dismutase (SOD) activity was a common feature of cholesterol-mediated antioxidant response in both models. Moreover, upon high-cholesterol diet, all four brain regions analysed responded via somewhat different capacity of antioxidant defence, hippocampus showing the highest basal activity of SOD. Increased activity of SOD upon cholesterol accumulation in vitro involves mitochondrial SOD2. We found that SOD/SOD2 activities are modulated by cholesterol levels.

DISCUSSION: Hypercholesterolaemia could potentiate brain dysfunction and neurodegenerative processes via oxidative stress, and activity of mitochondrial SOD2 may play a key role in this process. Our findings suggest that preventing/reducing mitochondrial oxidative stress may represent a common approach against neurodegenerative diseases.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app