lipoamide


Also found in: Dictionary, Encyclopedia, Wikipedia.

li·po·ic ac·id

(li-pō'ik as'id),
A bacterial growth factor present in yeast and liver extracts; may be useful in the treatment of mushroom poisoning. Functions as the amide (lipoamide) cofactor in the disulfide (-S-S-) form in the transfer of "active aldehyde" (acetyl), the two-carbon fragment resulting from decarboxylation of pyruvate from α-hydroxyethylthiamin pyrophosphate to acetyl-CoA, itself being reduced to the dithiol form (that is, dihydrolipoic acid) in the process. Lipoic acid is also an essential component of other α-keto acid dehydrogenase complexes.
References in periodicals archive ?
LDHA, lactate dehydrogenase A; LDHB, lactate dehydrogenase B; PDHA1, pyruvate dehydrogenase (lipoamide) alpha 1; DLAT, dihydrolipoamide S-cetyltransferase; DLD, dihydrolipoamide dehydrogenase; GK, glycerol kinase; GPD1, glycerol-3-phosphate dehydrogenase 1; GPD2, glycerol -3-phosphate dehydrogenase 2; ACSS3, acyl CoA synthetase short chain family member 3; PCCA, propionyl CoA carboxylase alpha; PCCB, propionyl CoA carboxylase beta; MCEE, methylmalonyl CoA epimerase; MUT, methylmalonyl CoA mutase.
Nitrofuran drugs as common subversive substrates of Trypanosoma cruzi lipoamide dehydrogenase and trypanothione reductase.
The result was supported by Reed (1973), who thought that lipoamide dehydrogenase was the flavoprotein component of the a-keto acid, and which was involved in Krebs cycle promoting energy metabolism.
falciparum Thioredoxin reductase (PfTrxR) , belonging to the family of dimeric flavoenzymes, which includes lipoamide dehydrogenase, glutathione reductase, and mercuric ion reductase, is a high molecular weight enzyme that reduces Thioredoxin (Trx) (7).
Sirt4 regulates the pyruvate dehydrogenase complex via enzymatic hydrolysis of the lipoamide cofactor, thus modulating acetyl coenzyme A production, Krebs cycle activity, and ROS generation [12].
The result was supported by Reed (1973), who thought that lipoamide dehydrogenase was the flavoprotein component of the [alpha]-keto acid, and which was involved in Krebs cycle promoting energy metabolism.
This negative effect of HIF-1[alpha] on glucose tolerance is mediated by the attenuation of adipogenic factors such as peroxisome proliferator-activated receptor [gamma] (PPAR[gamma]), glucose transporter type 4 (GLUT4), and pyruvate dehydrogenase lipoamide kinase isozyme 1 (PDK1) and is associated with the metabolic deprivation of adipocytes together with fatty acid accumulation [46].
SIRT4 is also a lipoamidase that hydrolyzes the lipoamide cofactors from the E2 component of the pyruvate dehydrogenase (PDH) complex, which reduces the activity of the complex [142].
Firstly, ROS directly modulate mPTP opening by oxidizing four different sites: [Cys.sup.160] of ANT, regulated by glutathione oxidation and protected by low concentration of N-ethylmaleimide (NEM) or monobromobimane [128]; Cys56 of ANT, sensitive to the redox state of the matricial pyridine nucleotides perhaps with the mediation of thioredoxin or lipoamide and also protected by NEM, not by monobromobimane [129]; external thiol groups (SH), promoting PTP opening by reaction with NEM or copper-orthophenanthroline; and [Cys.sup.203] of Cyp-D, Sglutathionylation of which prevents Cyp-D binding to ANT which blocks MPT [130].
Adam-Vizi, "Stimulation of reactive oxygen species generation by disease-causing mutations of lipoamide dehydrogenase," Human Molecular Genetics, vol.