Question about Nitrates

[MJV Aquatics]

6 minutes ago, Coronal Mass Ejection Carl said:

Growing fish fast and big shortens their chronological lifespans so I don't know if this is really a good measure of success. What fish farms and hobbyists do isn't any different.

Lets get real here....What I said was that fry raised in FRESH, CLEAN water grow faster and larger and are healthier. I bred, raised, and sold over 300 fish last year - how about you?

6 minutes ago, Coronal Mass Ejection Carl said:

The vet at UC Davis told me that <150 ppm was fine but what do they know they only take care of the exhibits in public aquariums and aren't "experts."

Out of context, 150ppm nitrates may be fatal for some fish. I'm not going to continue to debate the merits of fresh, clean water with you. Quibbling over nitrate number values seems pretty pointless to me. 🙂

[Coronal Mass Ejection Carl]

6 minutes ago, MJV Aquatics said:

Lets get real here....What I said was that fry raised in FRESH, CLEAN water grow faster and larger and are healthier. I bred, raised, and sold over 300 fish last year - how about you?

Anybody can do that. It doesn't make you an authority on the subject. Have you kept track of the lifespans of the fish you sold? Do they live longer than breeders who change water less frequently?

6 minutes ago, MJV Aquatics said:

Out of context, 150ppm nitrates may be fatal for some fish. I'm not going to continue to debate the merits of fresh, clean water with you. Quibbling over nitrate number values seems pretty pointless to me. 🙂

Really? Which fish? Scientific evidence required.

I have provided scientific evidence. All you have is an opinion.

You still haven't answered my previous points:

A lot of those studies are for establishing discharge limits in natural waters. Not to mention there are a few on fathead minnows, guppies, and gamefish.

Age in fish isn't just related to years but growth rate and size. A fish that's grown rapidly to market size is chronologically young but biologically older as it's at the point where feed conversion ratio drops and it's no longer economical to keep growing them. Anything that doesn't manifest in those eight months probably isn't ever going to manifest.

Growing fish fast and big shortens their chronological lifespans so I don't know if this is really a good measure of success. What fish farms and hobbyists do isn't any different.

[MJV Aquatics]

1 minute ago, Coronal Mass Ejection Carl said:

Anybody can do that.

Like I said, the debate is over. 🙂

[Sandra the fish rookie]

I am dreaming of the day that I see some Nitrates...one day.. one day.. ugh! 

 

[Socqua]

11 minutes ago, MJV Aquatics said:

Like I said, the debate is over. 🙂

I don't think that's how debates work 🤔

[Coronal Mass Ejection Carl]

2 hours ago, MattyIce said:

Nitrate bonds with Hemoglobin to create Methoglobin which can no longer carry oxygen.   This causes low oxygen concentrations in the fishes blood,(Human Blood, Livestock Blood, ect) requiring the fish to inhale more oxygen.

in the study below, it found at around 100 ppm nitrate, oxygen was consumed at 3 times the rate with water at 0 nitrates.

https://academic.oup.com/conphys/article/8/1/coz092/5658492

While not completely analogous, it seems like climbing mount Everest, where the higher one goes/ the higher the nitrates go, the less oxygen is able to be used.  

Having to take a breath more often than you are used to 24/7/365, the stress of that can't be good.

Ah, yes, the old Isaza article.

That paper states that:

Quote

Nitrate enters the body via passive diffusion across the gills and results in the endogenous conversion of nitrate to nitrite (Camargo et al., 2005; Monsees et al., 2017), which then causes methaemoglobin formation.

Which is interesting because the Monsees paper doesn't say that at all. Monsees is a pivotal paper in nitrate toxicity research because it finally answers the question of how nitrate gets into fish:

Quote

Until today, the uptake of nitrate is still poorly understood, mainly due to the fact that most tissues represent a barrier preventing the passage of the large hydrated nitrate ion. In their study on nitrate toxicity to African catfish (Clarias gariepinus), Schram, Roques, Abbink, et al. (2014) concluded that the integument of the fish forms a significant barrier to waterborne nitrate. As a consequence, alternative routes for nitrate uptake are limited and uptake via the gills seems most plausible with regard to the direct contact with the ambient water as well as the importance in osmoregulation and ion uptake (Hwang 2009). However, a low permeability for nitrate through the gills was discussed in trout (Stormer et al. 1996) and has been reported in freshwater crayfish (Jensen 1996). In contrast, nitrite uptake has been described for the gills as well as the intestinal wall. For example, Grosell and Jensen (2000) documented nitrite passage over the intestinal/stomach wall of the European flounder and nitrite uptake in the stomach is very fast in rats (Bryan, Fernandez, Bauer, Garcia-Saura, Milsom, Rassaf, Maloney, Bharti, Rodriguez & Feelisch 2005). Additionally, nitrite and chloride compete for the active branchial chloride uptake mechanism in freshwater fish (Williams & Eddy 1986), and as the chloride concentration in freshwater is low, the presence of nitrite can lead to massive nitrite accumulation in the plasma (Grosell & Jensen 2000). Furthermore, low stability of nitrite suggests rather acetic conditions to prevent fast oxidation.

Consequently, we hypothesized that uptake involves a reduction of nitrate to nitrite in the stomach, prior to the actual passage of the intestinal wall. Such route would result in high plasma nitrite, similar to those observed here. Therefore, we assessed the reduction of nitrate to nitrite in stomach juice in an in vitro experiment. We demonstrate that nitrate is rapidly converted into nitrite reaching a maximum of 74 lMNO?2 after 90 min. Our findings strongly indicate that conversion of nitrate to nitrite in the gastrointestinal system of tilapia represents the most probable uptake route. As a consequence, nitrate toxicity in tilapia is mainly a result of nitrate reduction to nitrite and irreversible oxidation of haemoglobin to methaemoglobin.

 

In the early days, scientists thought it could be through the gills since a lot of ions pass or are transported through them. But later studies found that gills were fairly impermeable to nitrate which left them wondering what alternative routes could there be.

Isaza also cites Camargo which is just a review paper that I don't believe performed any experiments. It mentions branchial permeability twice:

Quote

The main toxic action of nitrate on aquatic animals is due to the conversion of oxygen-carrying pigments (e.g., hemoglobin, hemocyanin) to forms that are incapable of carrying oxygen (e.g., methemoglobin) (Grabda ct al., 1974; Conrad, 1990; Jensen, 1996; Scott and Crunkilton, 2000; Cheng and Chen, 2002). Nevertheless, owing to the low branchial permeability to nitrate, the NO3 uptake in aquatic animals seems to be more limited than the uptake of NHt and NO2, contributing to the relatively low toxicity of nitrate (Russo, 1985; Meade and Watts, 1995; Jensen, 1996; Stormer et al., 1996; Cheng and Chen, 2002; Alonso and Camargo, 2003).

Quote

Jensen (1996) studied the uptake and physiological effects of nitrate ions (from NaNO3) in the freshwater crayfish Astacus astacus. The nitrate uptake was minor in crayfish exposed to a nitrate concentration of 14 mg NO3-N/l for seven days, indicating a low branchial permeability to nitrate (Table I). This minor uptake of nitrate appeared to be passive, the haemolymph nitrate concentration staying far below the ambient nitrate concentration. In addition, nitrate exposure did not induce significant changes in haemolymph chloride, sodium or potassium concentrations, nor in divalent cations and anions, extracellular osmolality and amino acid concentrations (Table 1).

Both of those studies are pre-Monsees so it likely never occurred to them to consider incidental ingestion. Regardless, they failed to control for it so they can't legitimately conclude that any nitrate uptake, however minor, was via the gills.

So, basically, Isaza cites Monsees as support for branchial uptake when in fact Monsees concludes it's not branchial uptake. Then it indirectly references two old studies that didn't consider and prevent incidental ingestion.

And in its own experiments, Isaza makes the same mistake. This is on top of the fact that the alleged branchial uptake only occurred when the fish were exposed to extreme pH levels.

Edited February 15, 2021 by Coronal Mass Ejection Carl

[Coronal Mass Ejection Carl]

13 minutes ago, MJV Aquatics said:

Like I said, the debate is over. 🙂

I accept your concession.

[MattyIce]

39 minutes ago, Coronal Mass Ejection Carl said:

Ah, yes, the old Isaza article.

That paper states that:

Which is interesting because the Monsees paper doesn't say that at all. Monsees is a pivotal paper in nitrate toxicity research because it finally answers the question of how nitrate gets into fish:

In the early days, scientists thought it could be through the gills since a lot of ions pass or are transported through them. But later studies found that gills were fairly impermeable to nitrate which left them wondering what alternative routes could there be.

Isaza also cites Camargo which is just a review paper that I don't believe performed any experiments. It mentions branchial permeability twice:

Both of those studies are pre-Monsees so it likely never occurred to them to consider incidental ingestion. Regardless, they failed to control for it so they can't legitimately conclude that any nitrate uptake, however minor, was via the gills.

So, basically, Isaza cites Monsees as support for branchial uptake when in fact Monsees concludes it's not branchial uptake. Then it indirectly references two old studies that didn't consider and prevent incidental ingestion.

And in its own experiments, Isaza makes the same mistake. This is on top of the fact that the alleged branchial uptake only occurred when the fish were exposed to extreme pH levels.

There is a lot there, not sure if I am understanding it all correctly.

It seems the low oxygen is still an issue with the conversion of hemoglobin to methoglobin.

Only that their exposure to it is not proportional to the speed of their breathing, and while they may need to breath more to consume more oxygen, it does not make the situation exponentially worse.

Across the studies it seems the main thing that is happening is hemoglobin is being made incapable of carrying oxygen.

 

 Hypothetically, if there are 200 parts of oxygen every time water passes the gills and the fish typically needs 50, going up to needing 150 at 100ppm nitrates wouldn’t make a noticeable difference.

I’d imagine it is more of an issue in nature with run off creating algae blooms and anoxic environments.

I think in truly determining the toxicity of nitrates in a body of water, oxygen levels and labyrinth organs need to be considered.

 

Also, what you quote notes only trout and some cray fish, I’d imagine that nitrate uptake through both gills and through stomach tissue can vary greatly across all fish and invertebrates, with some being more resistant than trout and some being less.

Edited February 15, 2021 by MattyIce

[Connor Elliott]

I just wanted to know how to read a test kit 😂

[MJV Aquatics]

24 minutes ago, Connor Elliott said:

I just wanted to know how to read a test kit 😂

yellow = great, orange = okay, red = bad 🙂

[Celly Rasbora]

@Connor Elliott, I share your frustration. I decided to buy a 25 pack of the Tetra test strips on Amazon, so I can compare the two. I almost bought the 100 pack, but then saw where the strips can go bad if you forget to seal them properly. I know myself well enough to know I could easily forget.

 

[MJV Aquatics]

1 hour ago, Socqua said:

I don't think that's how debates work 🤔

I dunno, opposing arguments in a public forum would seem to meet the definition. Then again. there's no point in beating a dead horse...but you gotta ask why anyone defends pollution?

 

[Frank]

59 minutes ago, Connor Elliott said:

I just wanted to know how to read a test kit 😂

There is a post, somewhere, where the poster recommends taking the cap off and looking through the full height of the solution.

[Coronal Mass Ejection Carl]

 

1 hour ago, Connor Elliott said:

I just wanted to know how to read a test kit 😂

The good news is that you basically don't have to test nitrate. And you don't have to worry about 20 vs. 40 or even 80 ppm. They are all equally non-toxic.

You know who Diana Walstad is? Well...

And this was before even better studies came out.

 

Edited February 15, 2021 by Coronal Mass Ejection Carl

[Coronal Mass Ejection Carl]

30 minutes ago, MJV Aquatics said:

I dunno, opposing arguments in a public forum would seem to meet the definition. Then again. there's no point in beating a dead horse...but you gotta ask why anyone defends pollution?

Why doesn't everyone do two 90% water changes per day like some discus keepers?

You don't do two 90% water changes per day? You're defending pollution.

Did you not put on sunscreen to get the mail? You're defending skin cancer.

[MattyIce]

9 minutes ago, Coronal Mass Ejection Carl said:

The good news is that you basically don't have to test nitrate. And you don't have to worry about 20 vs. 40 or even 80 ppm. They are all equally non-toxic.

You know who Diana Walstad is? Well...

 

7 out of the 10 are 50% dead in 3 days.   Is this supposed to be  how much nitrates fish can get before a 50% mortality rate? 

Guppy - 836 ppm - 50% dead in 3 days

I wonder if those are fancy inbred 5 times over guppies, feeder guppies, or the cold water tolerant hearty guppies of the 60's and 70's.

Edited February 15, 2021 by MattyIce

[Coronal Mass Ejection Carl]

5 minutes ago, MattyIce said:

7 out of the 10 are 50% dead in 3 days.   Is this supposed to be  how much nitrates fish can get before a 50% mortality rate?

3 out of 8 in the 1,000 mg/L nitrate-N group in the Monsees study died. That's 37.5% in ~30 days.

96-hour LC50 where half die after 4 days is probably going to be higher. One way to determine what chronic exposure level would be tolerable is to take 10% of that value.

[MattyIce]

Just now, Coronal Mass Ejection Carl said:

3 out of 8 in the 1,000 mg/L nitrate-N group in the Monsees study died. That's 37.5% in ~30 days.

96-hour LC50 where half die after 4 days is probably going to be higher. One way to determine what chronic exposure level would be tolerable is to take 10% of that value.

80 for guppies seems reasonable.

[Coronal Mass Ejection Carl]

13 minutes ago, MattyIce said:

Guppy - 836 ppm - 50% dead in 3 days

I wonder if those are fancy inbred 5 times over guppies, feeder guppies, or the cold water tolerant hearty guppies of the 60's and 70's.

This is probably the guppy study she was referencing:

Pretty high numbers that would probably be even higher for older life stages.

[MJV Aquatics]

27 minutes ago, MattyIce said:

The good news is that you basically don't have to test nitrate.

AGREED...if/when like nature, you do routine periodic partial water changes, nitrates and other pollution remains under control... Testing becomes unimportant.

[Coronal Mass Ejection Carl]

23 minutes ago, MattyIce said:

80 for guppies seems reasonable.

Needs to be adjusted upwards for life stages older than fry and also because the Rubin 1977 study used potassium nitrate which is more toxic than sodium nitrate. Later papers put an asterisk by the KNO3 studies because they now know KNO3 is more toxic.

[Coronal Mass Ejection Carl]

Other weirdness in the Rubin study:

Their ammonia LC50s are quite high. It's total ammonia but the pH isn't that low. I wouldn't expect ammonia and nitrate LC50s to be that close.

[MattyIce]

22 minutes ago, Coronal Mass Ejection Carl said:

Needs to be adjusted upwards for life stages older than fry and also because the Rubin 1977 study used potassium nitrate which is more toxic than sodium nitrate. Later papers put an asterisk by the KNO3 studies because they now know KNO3 is more toxic.

With 1977 guppies and no specification on the type of guppies it is hard to make general conclusions on even specifically guppies as a whole. is there anything that explains the strain or source of the guppies?

If it didn't result in the deaths of half the guppies, I'd be interested in a mondern study on different strains of guppies along with Abino guppies, feeder guppies to see if the perceived drop in heartiness in modern guppies is also an actual tolerance drop specific to nitrates.

Id also be interested in how the guppies were sourced and if there was prepwork done prior to testing to ensure the guppies were healthy prior to exposure.

Concerning the use of a chemical,  in this study they do a high nitrate test through build up by lessened "water changes" and a test through chemically increasing the nitrates: ( both against controls)

https://www.sciencedirect.com/science/article/pii/S0144860914000041

from my understanding of it, the test where the nitrates built up naturally showed greater impact on the fish growth.  where with chemically increasing nitrates but keeping "water changes" the same showed almost no difference in growth.

So while it might appear a hearty adult guppy can handle 100+ ppm nitrates long term, in a situation where nitrates have naturally gotten to 100+ ppm in a tank, there is a better chance the fish are facing other stressors than they are with clean water and the nitrates chemically jacked up. 

Edited February 15, 2021 by MattyIce

[Celly Rasbora]

1 hour ago, Frank said:

There is a post, somewhere, where the poster recommends taking the cap off and looking through the full height of the solution.

I've read that somewhere in one of the API test manuals. The problem with the nitrate test is the surface of the solution is so foamy with all that shaking you have to do to get it to make you can't see past it.

[MattyIce]

32 minutes ago, Coronal Mass Ejection Carl said:

Other weirdness in the Rubin study:

Their ammonia LC50s are quite high. It's total ammonia but the pH isn't that low. I wouldn't expect ammonia and nitrate LC50s to be that close.

I am not sure I understand what you are saying, perhaps I need additional info from the study, but recently I found that PH greatly impacts Ammonia/Ammonium ratio, where I can have a tank at PH 6.2 and 6 ppm nh3/nh4 with out issues because it is almost all non toxic Ammonium 

That might be why the PH is only down to 6.95 in the testing, any lower and it wouldn't be deadly.

Edited February 15, 2021 by MattyIce