Redox biology Flashcards
What does “redox” stand for?
REDuction
OXidation
What is reduction?
gain of electrons
what is oxidation?
loss of electrons
What are the two types pf reactive oxygen species (ROS)?
> free radicals
> not free radical
Describe a free radical and give an example
any species capable of independent existence that contains one or more unpaired electrons
e.g. superoxide or nitric oxide
Give an example of a not free radical reactive oxygen species
hydrogen peroxide
Give some examples of antioxidants
dietary : vitamin C + E
enzymatic : superoxide dismutase
What is oxidative stress?
when the balance of reactive oxygen species and antioxidants falls in favour of the reactive oxygen species
ROS > antioxidant defence
So we want zero reactive oxygen species?
No
some ROS are needed for cell signalling and the body’s immune response
How can too much ROS be harmful?
causes damage and disease
How are ROS concentration and activity levels associated?
ROS conc drops in an arc shape from sedentary to active / v.active.
ROS conc starts to increase again once activity levels are very extreme but not to levels of sedentary
Two ends of activity spectrum = high ROS conc
Outline findings of Michailidis et al (2007) into the exercise induced plasma antioxidant response
Found large lipid damage/lipid peroxidation (peaking at 2 hours) post-exercise.
Slower climb and fall for protein which has less of a response (peaking at 6 hours)
Why should you observe the traces of multiple antioxidants?
They may vary hugely, you could make many conclusions based off the observations of a singular marker.
What is the plasma antioxidant response to exercise?
Exercise = AMP build up
AMP converted into Hypoxanthine, which is converted into Xanthine.
Xanthine is converted into Uric Acid which triggers an antioxidant response
How does the plasma antioxidant response to exercise vary in high and low oxygen conditions?
Vary in terms of what is used and produced to cause the conversions of Hypoxanthine to Xanthine and Xanthine to Uric Acid.
High O2 used NAD+ and converts it to NADH
Low O2 takes O2 and converts it to O2- (superoxide)
What are the results of superoxide production during the plasma antioxidant response to exercise when there is low O2?
Superoxide is a ROS, excess production of it leads to oxidative stress.
What is the name of the system when hypoxanthine is converted to uric acid under low oxygen conditions?
xanthine oxidase system
What is the name of the system when hypoxanthine is converted to uric acid under high oxygen conditions?
xanthine dehydrogenase system
How long does the damage from oxidative stress last?
varying amounts of time
- Tsai et al (2011)
Carbonylated plasma proteins levels remain significantly elevated for up to 28 days post ultra-endurance exercise
- Turner et al (2011)
Cite some research and explain whether it is beneficial or not to try and stop ROS production (xanthine oxidase)
Gomez-Cabrera et al (2005)
Rats divided into 3 groups control, exercise to exhaustion and exercise to exhaustion with allopurinol injection to prevent uric acid build up (stop xanthine oxidase)
> Inhibiting xanthine oxidase prevents exercise-induced oxidative stress, which is critical for exercise adaptations
Should we supplement with dietary antioxidants?
YES or NO?!?
Hold you horses BUSTER!
This is a complex and “hotly debated issue in redox biology”.
I’m going to need a bit more information first
How many antioxidants improve performance?
improving….
recovery
fatigue
muscle damage
What bodily processes may antioxidants impair?
cellular defences
insulin sensitivity
mitochondrial biogenesis
What is mitochondrial biogenesis?
process by where mitochondria increase their individual mitochondrial mass and copy number to generate more ATP in response to greater energy expenditure
Give some evidence of why we CAN take antioxidants for performance
12 week intervention
antioxidants vs control
found no difference between groups in markers of adaptation to exercise
no difference in changes to insulin sensitivity or mitochondrial biogenesis
- Yfanti et al (2011)
Give some evidence of why we should NOT take antioxidants
Paulsen et al (2014)
11 weeks training, control vs antioxidants.
>VO2max and body comp improved similarly.
>antioxidant supplementation led to impairment of signalling and mitochondrial biogenesis markers.
What effect does exercise have on ROS production?
more free radicals post-exercise
Why is it difficult to detect free radicals?
they are highly reactive and extremely short lived
How do we assess for free radical production?
search for end/by products of free radical production
Give examples of by-products of free radical production
malonyldialdehyde (MDA) in tissues as a result of lipid peroxidation (oxidative degeneration of lipids as a result of free radicals stealing electrons)
Alternatively could measure for pentane in exhaled air as an estimate of extent of lipid peroxidation
Also Glutathione disulphide dimer (GSSG), which is the result of glutathione oxidation
- Sachdev & Davies (2008)
Other than xanthine oxidase system, what is a method of free radical production during exercise?
“leak” in the mitochondrial ETC.
molecular oxygen reduced by one electron to form superoxide.
This leak usually actually produces greater levels of superoxide at rest than when VO2 is high.
- Sachdev & Davies (2008)
- Vollaard et al (2005)
