Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since red cells transport and metabolize acetaldehyde in vivo, the effects of acetaldehyde on human red cell enzyme activities were studied. Incubation of intact red cells or undiluted red cell lysates at 37 degrees C for 4 h with 1-10 mmol/l acetaldehyde decreased only GOT, GPT and aldolase activities among the 26 enzymes tested. No inhibition occurred at 4 degrees C or when acetaldehyde was incubated with dilute hemolysates. Incubation of lysates with other reducing substrates or with acetate inhibited aldolase but not GOT or GPT. Preincubation of lysates with cyanate or fluoride markedly decreased acetaldehyde-mediated transaminase inhibition but not aldolase inhibition. Addition of pyridoxal phosphate, the vitamin B6 transaminase coenzyme, to GOT and GPT assay mixes did not reverse acetaldehyde-mediated transaminase inhibition. These findings suggest that acetaldehyde-mediated aldolase inhibition results from oxidation of acetaldehyde while transaminase inhibition results from nonoxidative acetaldehyde metabolism. When 100-200 mumol/l acetaldehyde is added to lysates at 2-h intervals and when lysates are incubated with ethanol, alcohol dehydrogenase and an NAD-regenerating system, enzyme inhibition occurs at acetaldehyde levels approaching those seen in vivo. Thus, the role of acetaldehyde-mediated enzyme inhibition in the toxicity of alcohol abuse warrants further study.
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PMID:Effects of acetaldehyde on human red cell metabolism: evidence for the formation of enzyme inhibitors. 341 86

History A 43-year-old right-handed man presented with a history of progressive mild left-sided weakness and slowness of movements. Symptoms began 4 years earlier, and the patient noticed a progressive decline in his daily routine due to gait difficulties in the past year. There was no history of head trauma, surgery, drug therapy, smoking, or alcohol abuse, nor was there any relevant family history. Examination revealed normal cognition (29 of 30 points on the Mini-Mental State Examination and 27 of 30 points on the Montreal Cognitive Assessment) and normal cerebellar, sensory, cranial nerve, and autonomic function. There was mild left-sided weakness involving the upper and lower limbs (medical research council graded muscle strength as 4+ out of 5) that was associated with facial hypomimia and a rigid akinetic syndrome only in the patient's left hemibody (Unified Parkinson's Disease Rating Scale [UPDRS] part III [motor examination], 23 out of 52 points). Mild atrophy in the left upper and lower limbs without pain, swelling, or skin lesions was noted at physical examination. Routine blood chemistry was normal, as were serum creatine kinase and aldolase levels and thyroid, hepatic, and renal function. T1- and T2-weighted, fluid-attenuated inversion recovery, diffusion- and perfusion-weighted, and contrast material-enhanced brain magnetic resonance (MR) imaging results were normal, without basal ganglia hyperintensity, lacunae, calcification, or heavy metal deposits. Muscle MR imaging and single photon emission computed tomography (SPECT) with technetium 99m (99mTc) tropane dopamine transporter (TRODAT)-1 were performed for further evaluation. This patient received levodopa and benserazide (200 and 50 mg, respectively) four times a day and amantadine (100 mg) three times a day without adequate improvement (UPDRS score decreased from 23 to 20 points).
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PMID:Case 241: Hemiparkinsonism- Hemiatrophy-SPECT with 99mTc TRODAT-1 and Muscle MR Imaging Abnormalities. 2841 20