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Homocysteine thiolactone (HTL) is an organosulfur compound with the formula H 2 NCHC(O)SCH 2 CH 2. It is the thiolactone (intramolecular thioester ) of homocysteine . It is produced by methionyl-tRNA synthetase in an error-editing reaction that prevents translational incorporation of homocysteine into proteins .
As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B 6, folic acid (vitamin B 9), and vitamin B 12 can lead to high homocysteine levels. [2] Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases.
In the body, homocysteine can be recycled into methionine or converted into cysteine with the aid of vitamin B 6, B 9, and B 12. [3] High levels of homocysteine in the blood (hyperhomocysteinemia) is regarded as a marker of cardiovascular disease, likely working through atherogenesis, which can result in ischemic injury.
The activation of the drug clopidogrel (top left) gives a thiolactone, which ring-opens. [3] Thiolactones are intermediates in the activation of some drugs. [4] In nature, the most common thiolactone is homocysteine thiolactone. It is produced from homocysteine. It may play a role in protein damage. [5]
Alcohol depresses the central nervous system, slowing cerebral messaging and altering the way signals are sent and received. Progressively larger amounts of alcohol are needed to achieve the same physical and emotional results. The drinker eventually must consume alcohol just to avoid the physical cravings and withdrawal symptoms.
Continuation of alcohol use will result in a higher risk of progression of liver disease and cirrhosis. In patients with acute alcoholic hepatitis, clinical manifestations include fever, jaundice, hepatomegaly, and possible hepatic decompensation with hepatic encephalopathy, variceal bleeding, and ascites accumulation. Tender hepatomegaly may ...
Zieve's syndrome is an acute metabolic condition that can occur during withdrawal from prolonged heavy alcohol use. It is defined by hemolytic anemia (with spur cells and acanthocytes), hyperlipoproteinemia (excessive blood lipoprotein), jaundice (elevation of unconjugated bilirubin), and abdominal pain. [1]
Alcohol-related brain damage can have drastic effects on the individuals affected and their loved ones. The options for treatment are very limited compared to other disorders. Although limited, most patients with alcohol-related cognitive deficits experienced slight improvement of their symptoms over the first two to three months of treatment. [8]