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Hypervitaminosis A refers to the toxic effects of ingesting too much preformed vitamin A (retinyl esters, retinol, and retinal). Symptoms arise as a result of altered bone metabolism and altered metabolism of other fat-soluble vitamins. Hypervitaminosis A is believed to have occurred in early humans, and the problem has persisted throughout ...
Urolithin A is not known to be found in any food but rather forms as the result of transformation of ellagic acids and ellagitannins by the gut microflora in humans. [ citation needed ] Sources of ellagitannins are: pomegranates, nuts, some berries (raspberries, strawberries, blackberries, cloudberries), tea, muscadine grapes, many tropical ...
Hypervitaminosis is a condition of abnormally high storage levels of vitamins, which can lead to various symptoms as over excitement, irritability, or even toxicity. Specific medical names of the different conditions are derived from the given vitamin involved: an excess of vitamin A, for example, is called hypervitaminosis A.
Chemical structure of urolithin A.. Urolithins are microflora metabolites of dietary ellagic acid derivatives, such as ellagitannins. [1] They are produced in the gut, and found in the urine in the form of urolithin B glucuronide after absorption of ellagitannins-containing foods, such as pomegranate. [2]
Alimentary toxic aleukia is a mycotoxin-induced condition characterized by nausea, vomiting, diarrhea, leukopenia (aleukia), hemorrhaging, skin inflammation, and sometimes death. [1] Alimentary toxic aleukia almost always refers to the human condition associated with presence of T-2 Toxin .
Vitamin D compounds, specifically cholecalciferol (D3) and ergocalciferol (D2) are used in rodenticides due to their ability to induce hypercalcemia, a condition characterized by elevated calcium levels in the blood. This overdose leads to organ failure and is pharmacologically similar to vitamin D's toxic effects in humans.
Orotic aciduria (AKA hereditary orotic aciduria) is a disease caused by an enzyme deficiency, resulting in a decreased ability to synthesize pyrimidines.It was the first described enzyme deficiency of the de novo pyrimidine synthesis pathway.
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.