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Hyperammonemia, or high ammonia levels, is a metabolic disturbance characterised by an excess of ammonia in the blood. Severe hyperammonemia is a dangerous condition that may lead to brain injury and death. It may be primary or secondary. Ammonia is a substance that contains nitrogen. It is a product of the catabolism of protein.
Ammonia is an inorganic ... Temperature and salinity also affect the ... Excess ammonia may accumulate and cause alteration of metabolism or increases in the body pH ...
Ammonia is toxic to aquatic life which leads to increased amounts of fish deaths. [6] Ammonia pollution also leads to eutrophication. Eutrophication is the growth of algae that kills other aquatic life and creates dead zones. Ammonia pollution affects freshwater and salt water ecosystems differently due to physical and chemical differences.
Protein toxicity is the effect of the buildup of protein metabolic waste compounds, like urea, uric acid, ammonia, and creatinine.Protein toxicity has many causes, including urea cycle disorders, genetic mutations, excessive protein intake, and insufficient kidney function, such as chronic kidney disease and acute kidney injury.
A lot of water is needed for the excretion of ammonia, about 0.5 L of water is needed per 1 g of nitrogen to maintain ammonia levels in the excretory fluid below the level in body fluids to prevent toxicity. [citation needed] Thus, the marine organisms excrete ammonia directly into the water and are called ammonotelic. [2]
The resultant effect of this toxicity can be reduced brain energy metabolism and function. Importantly, the toxic effects of ammonia on astrocyte remodeling can be reduced through administration of L-carnitine. [89] This astrocyte remodeling appears to be mediated through ammonia-induced mitochondrial permeability transition.
Some patients may also have an elevation of ammonia, a toxic chemical, which can affect the nervous system. Argininosuccinic aciduria may become evident in the first few days of life because of high blood ammonia, or later in life presenting with "sparse" or "brittle" hair, developmental delay, and tremors.
Spontaneous deamination of 5-methylcytosine results in thymine and ammonia. This is the most common single nucleotide mutation. In DNA, this reaction, if detected prior to passage of the replication fork, can be corrected by the enzyme thymine-DNA glycosylase, which removes the thymine base in a G/T mismatch. This leaves an abasic site that is ...