Bacterial Krebs cycle enzyme

Bacterial Krebs cycle enzymes are central metabolic enzymes that catalyze the sequential reactions of the tricarboxylic acid (TCA) cycle, also known as the citric acid cycle or Krebs cycle, which is a universal pathway for oxidative energy production in aerobic organisms. The main enzymes include citrate synthase, aconitase, isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinyl-CoA synthetase, succinate dehydrogenase, fumarase, and malate dehydrogenase[1][3]. In bacteria, these enzymes operate in the cytoplasm and are essential for cellular respiration, enabling the efficient extraction of energy from organic substrates via NADH and FADH₂ production, feeding electrons to the electron transport chain for ATP synthesis[3][9]. Because of their essentiality, several bacterial Krebs cycle enzymes have been proposed as antibacterial drug targets, particularly in pathogens where TCA cycle activity is linked to antibiotic susceptibility and virulence[2][6]. However, the target as stated ("Bacterial Krebs cycle enzymes") is not a single molecule but a plural, functionally related enzyme family. Specific enzymes (like isocitrate dehydrogenase or succinate dehydrogenase) are more suitable as canonical singular targets for structured information. Note: - The provided name is not a specific molecular target, but rather describes a **class** of enzymes. For best practices in drug discovery or database structuring, each enzyme (e.g., "Bacterial succinate dehydrogenase") should be considered individually for canonical naming. - Enzyme inhibitors must be selective for the bacterial form to minimize eukaryotic toxicity. - TCA cycle modulation is under investigation as a strategy for potentiating antibiotics and attenuating bacterial pathogenicity[2][6]. This entry is **non-canonical** as written ("Bacterial Krebs cycle enzymes" is a class, not a molecule) and should be subdivided for database use.

Other names

Krebs cycle enzyme (bacterial)Tricarboxylic acid (TCA) cycle enzyme (bacterial)Citric acid cycle enzyme (bacterial)

Enzyme inhibition (e.g., succinate dehydrogenase inhibition by malonate). Metabolic modulation (metabolite supplementation increases respiration and potentiates antibiotics). Indirect bactericidal enhancement (augmenting TCA cycle activity to increase sensitivity to antibiotics via altered redox status and membrane potential).