Nitrate 40 ppm, is this ok

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Bderick67;3622912; said:
If this were the case then most of the captive kept fish in the world would be dead.
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there are varying degrees of toxicity. 25ppm NO3 is sort of like second hand smoke. 40ppm might be like first hand smoking. 75ppm like trying to breath in a house fire. It's not good for the fish, but they can live a long long time with it. Who knows whether or not it actually decreases the life span.
 
kdrun76;3623195; said:
Its not the nitrates themselves that cause the problem. Nitrates greatly impede the production of white blood cell which over time renders the immune system useless. Once the immune system is shut down, its only a matter of time until some germ/parasite/ buggy gets in there and kills the defenseless fish.

Fish can survive a LONG time in nitrates of 200ppm...as long as they don't get exposed to ICH or something worse... they live on. Personally I would rather have my fish a little more capable of fending for themselves. Keep the nitrates under 20.
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I've never heard this before. My understanding was that enterohepatic metabolism reduced the O2 carrying capacity of the heme groups on the RBC (not WBC). This is a syndrome known as methemoglobinemia in humans.

few links:
nitrate toxicosis - University of Illinois
http://www.aces.uiuc.edu/news/stories/news3248.html

spanish research on nitrate toxicity- practical fishkeeping
http://www.practicalfishkeeping.co.uk/pfk/pages/item.php?news=560

according to the spanish study, sensitivity varies from species to species (but I guess we knew that already).

"Just 10ppm of nitrate-nitrogen (that's a mere 3.03 ppm of nitrate) has been shown to have adverse effects on salmonids such as Oncorhynchus mykiss, Oncorhynchus tshawytscha and Salmo clarki, as well as upon a number of freshwater invertebrates and frogs.

Marine organisms, however, are much more tolerant and levels of 20ppm nitrate-nitrogen (that's still just 6ppm nitrate) were required to cause adverse effects. "
 
Diogenes, what you are describing is the result of nitrite poisoning not nitrate. This is a quote from your first link...

"When unconditioned cattle consume plants containing high levels of nitrates, the nitrate to nitrite conversion exceeds the ability of the rumen microbes to convert nitrites to ammonia," said Wallace. "Blood levels of nitrites increase and alter the hemoglobin in red blood cells to produce methemoglobin. Unlike hemoglobin, methemoglobin cannot carry oxygen to the tissues of the body."

I am pulling up the citation for the second paper now. I am quite interested in what it has to say as it indicated the toxicity of nitrites and nitrates work on the same mechanisms.
 
This is from the citation at the bottom of the second link...

"Elevated nitrate concentrations in drinking waters have serious risks for humans. Ingested nitrates may cause methemoglobinemia in infants through their conversion to nitrites (under anaerobic conditions in the gut) and the subsequent blockade of the oxygen-carrying capacity of hemoglobin (Sandstedt, 1990, Amdur et al., 1991 and Wolfe and Patz, 2002). In addition, ingested nitrates have a potential role in developing cancers of the digestive tract through their contribution to the formation of nitrosamines, which are among the most potent of the known carcinogens in mammals (Harte et al., 1991 and Nash, 1993 L. Nash, Water quality and health In: P.H. Gleik, Editors, Water in Crisis: A Guide to the World’s Fresh Water Resources, Oxford University Press, New York (1993), pp. 25–39.Nash, 1993)."

The paper deals exclusively with invertebrates in the research being presented. The abstract (which is what was published in your link) states that there are adverse effects of fish, but doesn't say what they are. The physiology of inverts is so radically different than that of fish that I put little merit in the research having any direct correlation to fish husbandry.

I have too much to do to look further in the primary literature on the topic tonight.
 
well chemistry is chemistry is chemistry and fish have livers just like other organisms. Nitrogenous waste is toxic to all carbon based life forms. It really doesn't matter all that much which species is studied, the mechanism remains the same. The entero hepatic metabolization of nitrates converts NO3 to NO2 (nitrite), so the damage done is from NO3 that has been converted to NO2. One of the posts quoted states as much.

you guys find little merit in the research shown, but I have yet to see one source that supports the assertion that NO3 causes damage to leukocytes as stated in a previous post.

Proof or STFU...
 
Diogenes;3624710; said:
Proof or STFU...
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I had every intention of doing a literature search today, but I honestly feel no need to prove anything to anyone so crude as to make that statement, YOU are not worth my efforts.
 
The nitrate to nitrite conversion in BOTH articles you cited took place in the gut under anerobic conditions. Neither involved a liver or any metabolizing impacts from it. The article you posted involved invertebrates which lack a liver entirely. Hepatic physiology is an area I know very little about, but I really don't understand what liver function has to do with nitrate poisoning. Especially since the toxic build up of nitrates in mammals is dealt with in the renal system!
 
kdrun76;3625626; said:
The nitrate to nitrite conversion in BOTH articles you cited took place in the gut under anerobic conditions. Neither involved a liver or any metabolizing impacts from it. The article you posted involved invertebrates which lack a liver entirely. Hepatic physiology is an area I know very little about, but I really don't understand what liver function has to do with nitrate poisoning. Especially since the toxic build up of nitrates in mammals is dealt with in the renal system!
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entero= gut

hepatic= liver

entero + hepatic = entero hepatic

I still have yet to see any support for any of these claims. Both articles cite entero hepatic metabolization as the mechanism for NO3-> NO2 reduction, as well as others. I could be wrong, I don't know everything, but I do know the liver is responsible for making nitrogenous wastes inert in mammals. Not the kidneys. Your just plain wrong in that regard. The liver converts ammonia into urea which is excreted by the kidneys and the bowels, but the liver makes it safe. Thats why when you have fulminate hepatic failure, you have a large volume of NH3 in blood circulation.

I've provided my sources which you guys wanted to be smart a**es about, i'm just asking that someone actually use facts to prove me wrong. I'm not just making unsubstantiated claims about leukocytes and renal systems. I was trying to contribute to the discussion and rather than participate in a productive way, you guys just want to shoot me down. On top of that, your wrong about half your A+P. How'd you expect me to react?
 
How'd you expect me to react?
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Like a lady or a gentleman. Notice: you are the only one swearing or being rude.

I would also like to point out (again) that the paper you are claiming says the method of NO3 to NO2 reduction involves the liver is about invertebrates that do not have a liver.


I found no mention of liver/ hepatic system use in the first article either.

Here's your source. I hope you have a joyous and pleasant day. It is difficult to find primary literature that is available to the public and can therefore be legally linked to. The vast majority of the sources I found require a paid subscription, or alliance with a university to read. While I have that, I am going to presume that most readers on here do not.


This article shows lymphocyte production as being halved in high nitrate conditions.
http://www.atlantech.ca/public/articles/Water Quality.PDF
Full citation:
Nitrate Toxicity: A Potential Problem of Recirculating Systems. Hrubec, TC; Smith, SA; Robertson, JL. Proceedings of the 1st International Conference on Recirculating Aquaculture. 2002.

This quote is taken from the conclusion.
The data presented here support the theory that prolonged exposure to elevated levels of nitrate may
decrease the immune response, induce hematological and biochemical changes indicative of a
pathologic response, and may increase mortality. If elevated nitrate levels are responsible for the
pathologic changes seen in these fish, then management of recirculating systems must change to lower
nitrate levels. The pathologic changes are sufficient to affect the normal physiology of the fish and
will probably result in decreased growth and increased susceptibility to disease.
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