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Nitrate toxicity and the metabolic traffic jam

Woody Lane, Ph.D., for Progressive Cattle Published on 24 December 2021
Rumen traffic

Young cattle can jump fences. There’s nothing new about that. We usually blame the fence – for being old and in the way – or the heifers and steers, for being … well … heifers and steers.

But did you know the rumen of these cattle contains hydrogen – the same hydrogen that once filled dirigibles – and this hydrogen is related to nitrate toxicity? You might say this gives a whole new, uh, lift to this month’s topic.

Hydrogen? This will require a little chemistry, so please bear with me.

A main feature of a healthy rumen is: It contains very little free oxygen. The technical term for a no-oxygen environment is “anaerobic.” Rumen microbes (bacteria, protozoa and other microscopic organisms) function quite vigorously in this anaerobic environment. Most rumen microbes, in fact, absolutely require a lifestyle without oxygen. They use metabolic processes that don’t need much oxygen, and they produce all sorts of interesting products, like volatile fatty acids (VFAs), carbon dioxide and hydrogen ions (H+). By dirigible standards, the normal level of hydrogen in a rumen may be fairly low, but these rumen H+ ions are chemically very active. They will replace oxygen atoms in any vulnerable molecule.

Now things get interesting. If we make hay from some heavily fertilized grass at the end of a particularly cool and cloudy month, we may be suddenly faced with a serious nutritional problem – nitrate toxicity – in part due to this hydrogen in the rumen.

Nitrates 101

Let’s review some background about nitrates. Nitrates are very soluble in water. In general, plants absorb nitrogen into their roots in the form of nitrates and then transport these nitrates upward through the stem to the leaves. Leaf cells spend their days performing photosynthesis, which uses sunlight and carbon dioxide and water to create sugars (carbohydrates). When nitrates arrive in a leaf cell from the basement, enzymes in these leaf cells link the nitrogen in these nitrates with carbohydrates to form amino acids, which are then combined to form true proteins. The plant then uses these proteins for all sorts of important metabolic functions. It’s a clever system, and it usually works quite smoothly.

But photosynthesis requires sunlight. What happens if there is a lengthy period like a couple of weeks when the sky is heavily overcast day after day, so the plant leaves do not see much sun (for example, in Oregon’s Willamette Valley in March)? Simple – without sunlight, leaf photosynthesis slows down. Which, in turn, restricts the manufacture of protein. But down in the plant basement, the roots don’t get the memo. Since the roots are still bathed in a rich nitrate solution in the soil, they continue to absorb the nitrates and dutifully pump them upward into the plant. But because of the shortage of carbohydrates in the leaves, the leaf cells can’t incorporate all those nitrates quickly, and leaf nitrate levels start to build.

The standard laboratory analysis for crude protein (CP) does not detect this problem because this assay only analyzes for nitrogen, not true protein. Since nitrates and all proteins contain some nitrogen, the CP assay just detects the total amount of nitrogen. It does not differentiate between the different forms of nitrogen, and therefore it cannot identify plants that may contain toxic levels of nitrates. Only a specialized test for nitrate can monitor the nitrate levels in plants. Typically, nitrate levels in plant leaves are lower than 0.44% (dry matter basis). We begin to worry when nitrate levels rise much above this.

Interestingly, high nitrate levels actually don’t harm plants, and anyway, the nitrate surplus is only temporary. As soon as the sun reappears, the leaves kick into high gear with photosynthesis. They will quickly synthesize a new batch of carbohydrates and use up the backlog of nitrates, and all is well.

But timing is critical. If we make hay at the tail end of one of those cloudy periods, we may harvest plants at the wrong end of the cycle. The plants may still contain high levels of nitrates because they hadn’t had enough quality time in the sunlight to convert those nitrates into carbohydrates. Then, if we feed this high-nitrate hay to our livestock, well …

Even though the problem is called “nitrate toxicity,” the reality is: Nitrates themselves are not very toxic. So what’s the problem?

The hydrogen in the rumen.

Enter the hydrogen

Let’s back up and look at the anaerobic environment in the rumen. Nitrates contain three oxygen atoms (NO3). Nitrates don’t have a promising future in the rumen because in that highly reduced, low-oxygen environment, the pesky hydrogen ions will quickly try to replace the oxygen atoms through a series of chemical reactions. Nitrate (NO3) is reduced to nitrite (NO2), which is then further reduced to ammonia (NH3). This is the standard sequence of events. The rumen bacteria then use that ammonia in a similar way that plant cells use nitrate – they combine the nitrogen in the ammonia with carbohydrates to produce true bacterial protein. Under normal conditions, all these steps proceed smoothly without a hitch, and all is well.

But high nitrate conditions in the rumen can present a problem. If for any reason the rumen doesn’t contain enough soluble carbohydrates – for example, if animals are fed mediocre hay containing lots of fiber and no supplemental grain or molasses – the situation becomes analogous to those green leaves I described above: The rumen bacterial cells become metabolically stymied. Without enough soluble carbohydrates to combine with all that ammonia, the rumen bacteria cannot manufacture bacterial protein. Then, just like a traffic jam, the entire series of reactions backs up. The rumen level of ammonia builds up, and so does the product of the preceding step: the nitrites.

Unlike nitrates, nitrites are toxic. As the nitrite levels begin to rise in the rumen, some nitrite molecules will cross the rumen wall into the blood. Nitrites then wreak havoc in red blood cells because they alter the hemoglobin molecules. Normally, hemoglobin combines readily with oxygen, but nitrite converts hemoglobin into an abnormal molecule called “methemoglobin.” This molecule is brown and does not combine with oxygen at all. Essentially, nitrite poisons the red blood cells so they cannot carry oxygen. If enough blood cells are affected, the animal’s blood turns brown, and it begins to suffer from oxygen deprivation. In short, the animal begins to suffocate.

But all is not lost. One method of coping with nitrate toxicity is to dump enough soluble carbohydrates into the rumen to feed the bacteria, which can then combine those carbohydrates with the ammonia. Therefore, when faced with nitrate toxicity, we can feed corn, barley, oats or any grain or molasses – nearly anything that contains lots of soluble carbohydrates. This will take the pressure off the metabolic traffic jam. The bacteria will begin using the nitrate nitrogen to make proteins again, and nitrite levels in the rumen will quickly decline.

Rumen hydrogen is a basic feature of ruminant life. But recently, I was daydreaming about rumen hydrogen, as nutritionists are apt to do. I visualized some potential reactions that could cause hydrogen levels to build up in the rumen. Then I thought: high levels of hydrogen in the rumen? Wouldn’t this lead to the notorious “dirigible effect?” Then in my dream, I had a vision of cloudlike cattle floating over the fences … end mark

ILLUSTRATION: Illustration by Corey Lewis.

Woody Lane, Ph.D., is a livestock nutritionist and forage specialist in Roseburg, Oregon. He operates an independent consulting business and teaches workshops across the U.S. and Canada. His book, From The Feed Trough: Essays and Insights on Livestock Nutrition in a Complex World, is available through Woody Lane.

Woody Lane, Ph.D.
  • Woody Lane, Ph.D.

  • Lane Livestock Services
  • Roseburg, Oregon
  • Email Woody Lane, Ph.D.

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