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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 ...
Early symptoms include intoxication, vomiting and abdominal pain. [1] Later symptoms may include a decreased level of consciousness, headache, and seizures. [1] Long term outcomes may include kidney failure and brain damage. [1] Toxicity and death may occur after drinking even in a small amount [1] as ethylene glycol is more toxic than other diols.
It is the signs, symptoms and results from laboratory tests which result from inadequate excretory, regulatory, and endocrine function of the kidneys. [2] Both uremia and uremic syndrome have been used interchangeably to denote a very high plasma urea concentration that is the result of renal failure. [ 1 ]
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]
Acute toxicity describes the adverse effects of a substance that result either from a single exposure [1] or from multiple exposures in a short period of time (usually less than 24 hours). [ 2 ] To be described as acute toxicity, the adverse effects should occur within 14 days of the administration of the substance.
Hypervalinemia has an autosomal recessive pattern of inheritance.. Hypervalinemia is inherited in an autosomal recessive manner. [1] This means the defective gene responsible for the disorder is located on an autosome, and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder.
Toxic and nutritional optic neuropathy is a group of medical disorders defined by visual impairment due to optic nerve damage secondary to a toxic substance and/or nutritional deficiency. The causes of these disorders are various, but they are linked by shared signs and symptoms.