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Toxicity and organ targeting freshwater fish
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Toxicity and organ targeting freshwater fish - 06-20-2008, 06:34 PM

I am going to discuss a number of topics in this thread and continue along this same line of discussion.

One thing I've come to realize is that aquarist overall have a very poor understanding of fish biology. Sure, we know how to breed(perhaps plant folks much less so), feed, and keep groups together, but when it comes to envirponmental stresses, much less so.

This is not really our fault.

We have little research in the way of specific species, comparative studies and good understandings about the way dissolve gases influence fish health. I will be referring to Target Organ Toxicity in Marine and Freshwater Telelosts (Vol 1, Schlenk and Benson 2001)

The goal is to better understand the issues in aquariums about adding things like KNO3, CO2, O2 and current.

The Gill represents a multifunctional organ for fish.

Respiration
Ion regulation
Acid base regulation
Nitrogen waste excretion

It accounts for over 50% of the surface area, they provide a very thin layer of exchange between the water and the blood(about 0.5 to 10 um), and they have a massive flow over them, in part due to the low O2 capacity in water. This means that if the fish is exposed to a toxicant, the gills are typically where we will first see the effect/s. If you stop any of the above 4 main physiological processes, you have death, if you have sublethal exposure, then the quantification is much more difficult to access.

CO2 and O2.

These are exchanged at roughly equal molar concentrations at the gills.
with this concept in mind: think about high CO2 and high O2 together.
Now think about what happens if you have low O2 and high CO2.
High O2 and low CO2.

O2 moves through the water into the blood entirely by diffusion, and at least 90% of the CO2 moves via diffusion also in the opposite direction.
Since the partial pressures drives this diffusion, and since O2 is much less soluble than CO2 or NH4, the flow required by the gills is high to maintain enough O2.
This results in extremely low partial pressures of CO2 in the fish's blood(about 30X less than O2 typically).

The so called Borh and Root effects on fish: The addition of CO2 and /or H+ to the blood(like as is the case for us when we add CO2 gas) decreases the O2 affinity/capacity of hemoglobin. This effectively increases mean blood partial pressure of O2. So the fish hyperventilates to reduce and wash out excess CO2 by also increases the rate of O2 exchange across the gills.

So while the resting fish might be okay, when they really start swimming and exercising a lot, they are really in much worse shape. Sort of like us at high altitudes and trying to job or run at 12,000ft without any acclimatization. you suck wind and cannot catch your breath and cannot run.

CO2 excretion is less understood and more complex than O2 uptake in fish.
Buffering capacity(eg the KH) plays a large role here. So in general, without going into enzymatic pathways, the higher KH allows the CO2 to be excreted more rapidly and maintain a low CO2 internal partial pressure.

Who said hard water was bad?





Fish waste: about 70% is NH4 and the rest is urea.
  
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