Anti-oxidants, uric acid, and evolution

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Discussion Overview

The discussion centers around the evolutionary aspects of uric acid metabolism in humans and higher apes, particularly why these species do not break down uric acid into allantoin as other animals do. Participants explore the potential evolutionary benefits of uric acid as an antioxidant and the implications of losing the ability to synthesize ascorbate.

Discussion Character

  • Exploratory
  • Technical explanation
  • Conceptual clarification
  • Debate/contested

Main Points Raised

  • Some participants question the evolutionary reasoning behind humans and higher apes retaining uric acid instead of breaking it down, suggesting a possible 'de-evolution' of this function.
  • Others propose that the loss of the ability to synthesize ascorbate necessitated a mutation that allowed uric acid to serve as a reducing agent, which may have been favored by selection pressure.
  • One participant expresses uncertainty about the roles of antioxidants, specifically questioning how they function and their overall significance in biological processes.
  • Another participant explains that reactive oxygen species (ROS) produced during cellular respiration can cause oxidative damage, and antioxidants react with these species to mitigate that damage.
  • There is a mention of programmed cell death in organisms, which involves the release of ROS, indicating a complex relationship between antioxidants and cellular processes.

Areas of Agreement / Disagreement

Participants express varying degrees of understanding and acceptance of the theories presented, with some agreeing on the potential roles of antioxidants while others remain uncertain about their mechanisms and implications. The discussion does not reach a consensus on the evolutionary significance of uric acid in higher apes.

Contextual Notes

Participants reference various articles and sources to support their claims, but the discussion includes unresolved questions about the specific mechanisms of antioxidants and the evolutionary pathways involved in uric acid metabolism.

Who May Find This Useful

Readers interested in evolutionary biology, biochemistry, and the roles of antioxidants in cellular processes may find this discussion relevant.

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TL;DR
Humans and higher apes don't break down uric acid. Why not? Was this 'de-evolved' and if so why?
This might be a 'that's just how it is' sort of question, but are there any theories of how humans and higher apes have evolved so that they don't break down uric acid?

All other animals break this down into allantoin, and fish go one further and break that down into ammonia.

Did 'us apes' end up 'de-evolving' this function, and if so is there any evolutionary benefit to having uric acid as an anti-oxidant present in our blood?

Presumably the ability to break down uric acid to allantoin came about after animals evolved to generate uric acid, so what's with the backward step for apes?
 
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Wikipedia gives a couple of different theories along with links:
https://en.m.wikipedia.org/wiki/Uric_acid
https://www.nature.com/articles/228868a0
https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-2362.1997.1390687.x
According to the articles, you seem to have answered your own question. Since higher primates lost the ability to synthesize ascorbate, another molecule was needed to act as a reducing agent in the body. A mutation that resulted in a loss of functional uricase would have served that function nicely and would therefore have been subjected to selection pressure.
 
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OK, I wasn't aware of the ascorbate-synthesis loss. So if that happened, then that could make sense.

So that was part of what I am interested in; what are the actual roles of anti-oxidants and how do they actually do their 'thing' that makes a difference? What I have read and heard sounds a bit 'hand wavy', TBH. What's the actual thing that they do and why does that help? As far as I understand it, for example, L-ascorbic acid can be both an anti-oxidant and pro-oxidant, depending on the chemistry, and at that point my non-chemistry engineering brain bogs over and I figure that's not something I'm going to get to understand with any degree of conclusive certainty.
 
Cellular respiration produces a lot of reactive oxygen species (ROS) as byproducts, but those species can do a lot of oxidative damage to other important molecules in the cell. Reducing agents (i.e., antioxidants) will react with these ROS and mitigate the damage that they cause. Again, wiki has a decent primer:
https://en.m.wikipedia.org/wiki/Reactive_oxygen_species
 
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There are times in the life of some organisms when certain cells must die for the benefit of the whole organisms. This often done through programmed cell death. In these cases, reactive oxygen species are released to rapidly kill the cell. This usually occurs at mitochondria, where lots of reactive oxygen species are constantly being produced.

That your fingers and toes are not webbed, is the result of cell death in regions that would otherwise form the webbing.
Otherwise, you couldn't do this:
Screen Shot 2021-07-10 at 9.27.40 AM.png
 
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BillTre said:
There are times in the life of some organisms when certain cells must die for the benefit of the whole organisms...
Otherwise, you couldn't do this:
View attachment 285751
Grow pointy ears? :)

Thanks for the responses, I will look through these links.
 
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Thank you all for your great answers. Now it’s time to close this thread before we get inundated with Spockian humor.

Jedi
 

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