Adenosine triphosphate degradation in specific disease.
Two hypotheses concerning adenosine triphosphate (ATP) degradation are examined: The metabolic basis of specific disorders involves ATP degradation, and uric acid and its precursors are measurable body fluid markers of ATP degradation. These hypotheses are examined by discussing human models of ATP degradation, methods for measurement of ATP degradation, and disorders of ATP degradation.
D000225:Adenine / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000096:biosynthesis / Q000378:metabolism*; D001711:Biotransformation; D002334:Carnitine O-Palmitoyltransferase / Q000172:deficiency; D000431:Ethanol / Q000494:pharmacology; D005632:Fructose; D005953:Glycogen Storage Disease Type I / Q000097:blood; D006012:Glycogen Storage Disease Type V / Q000378:metabolism; D006073:Gout / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D008659:Metabolic Diseases / Q000378:metabolism*; D008954:Models, Biological; D009135:Muscular Diseases / Q000378:metabolism; D005082:Physical Exertion; D011688:Purinones / Q000378:metabolism; D014527:Uric Acid / Q000097:blood / Q000378:metabolism
D011688:Purinones; D014527:Uric Acid; D005632:Fructose; D000431:Ethanol; D000255:Adenosine Triphosphate; D002334:Carnitine O-Palmitoyltransferase; D000225:Adenine