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Printable Handouts
Navigable Slide Index
- Introduction
- Outline - ROS production by mitochondria - ageing
- Mitochondrial free radical theory of ageing
- Mitochondria in a rat hepatocyte
- Electron transport chain, oxidative phophorylation
- ROS production is low in long-lived mammals
- Long-lived small mammals and short-lived birds
- ROS production in long-lived mammals and birds
- Outline - topology and sites of ROS production
- Topology of mitochondrial superoxide production
- ROS production in glycerol phosphate oxidation
- Topology of mitochondrial ROS production
- Topology and sites of ROS production
- Outline - regulation of ROS production
- ROS and uncoupling in flies
- ROS and uncoupling in rats
- Outline - ROS activation of UCPs
- Oxidative phosphorylation
- UCP1 structure
- GDP inhibition of UCP1
- Regulation of UCP1
- The UCPs
- Proton conductance in UCP3 knock-out mice
- Superoxide activates UCP3
- Superoxide activates other UCPs
- Activation of UCPs by reactive oxygen species (1)
- AAPH generates carbon-centred free radicals
- Carbon-centred radicals activate UCPs
- Activation of UCPs by reactive oxygen species (2)
- HNE activation of proton leak
- Activation of UCPs by reactive oxygen species (3)
- Time-dependent activation of proton leak
- Time-dependent endogenous activation of UCP3
- Proton leak in thymocytes depends on UCP2
- Activation of UCPs by reactive oxygen species (4)
- Outline - evidence that UCPs attenuate ROS
- Leak inhibition increases superoxide production
- GDP inhibition of UCP3 inactivates aconitase (1)
- GDP inhibition of UCP3 inactivates aconitase (2)
- Oxidative damage in UCP3 KO mice mitochondria
- Fine-tuning the model
- Synergistic activation of UCP1
- Regulation of UCPs
- Conclusion
- Acknowledgments
- Research group - 2005
Topics Covered
- Reactive oxygen species production by mitochondria
- Mitochondrial free radicals and ageing in short-lived and long-lived species
- Topology and sites of ROS production in the electron transport chain
- Regulation of ROS production by mild uncoupling
- Uncoupling of mitochondria by uncoupling proteins
- Superoxide and reactive alkenal activation of UCPs
- A model for UCP activation
- Evidence that UCPs attenuate ROS
Talk Citation
Brand, M. (2016, November 18). Respiration, reactive oxygen species and uncoupling proteins [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/ADWS5272.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Martin Brand has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Cell Biology
Transcript
Please wait while the transcript is being prepared...
0:00
My name is Martin Brand and I'm going to talk about Respiration,
Reactive Oxygen Species and Uncoupling Proteins and I'll do this using examples from
work done on my own laboratory to try and give an impression
of where the field is and perhaps, where it's going.
0:17
I'll divide my talk into two parts.
In the first part,
I'm going talk about Reactive Oxygen Species production by mitochondria.
First of all, I'll talk about ageing,
then I'll talk about the topology and sites
of ROS production in the electron transport chain,
and then move on to look at regulation of ROS production by mild uncoupling.
In the second part,
I will consider uncoupling of mitochondria by uncoupling proteins, UCPs.
First of all, I'll talk about ROS activation of UCPs,
and then I'll say something about the evidence that this activation of UCPs
by ROS acts to attenuate ROS production by mitochondria.
So first of all,
Reactive Oxygen Species production by
mitochondria and what that may have to do with ageing.
0:60
This is a self-portrait of Rembrandt,
painted in 1628, when he was 22 years old.
If he was still alive today,
he'd be just passing his 400th birthday and I think it's a reasonable thing to ask,
why isn't he still here today?
Well, the portrait on the right,
is painted 33 years later,
and you can see that he's aged dramatically and of course,
that's why he's not here today,
because 400 years of ageing would be impossible for any human to take.
So he's aged and we're all aging, and what's going on?
Well, best theory to explain it is the Mitochondrial free radical theory
of ageing which suggests that mitochondrial free radicals,
reactive oxygen species, are being produced
all the time in our bodies and they're killing us,
so we age and die as a result.
The cells in Rembrandt,