(+/-)-Carnitine (chloride)

461-05-2

C7H16ClNO3

H2O : >= 33 mg/mL (166.95 mM)

Metabolic Enzyme/Protease; NF-kappaB; Immunology/Inflammation

(+/-)-Carnitine chloride exists in two isomers, known as D and L. L-carnitine plays an essential role in the beta-oxidation of fatty acids and also shows antioxidant, and anti-inflammatory activities. In Vitro: The main role of L-carnitine is to shuttle long-chain fatty acids across the inner mitochondrial membrane. After L-carnitine and acyl-CoA become acyl-carnitine by activation of carnitine palmitoyl transferase (CPT)-I, the transported acyl-carnitine is changed into acyl-CoA by CPT-II in the mitochondria matrix. Palmitoyl-CoA-induced mitochondrial respiration is increased by L-carnitine treatment, and then is accelerated by the presence of ADP. This acceleration is induced by treatment with L-carnitine in a concentration-dependent manner, and is saturated at 5 mM L-carnitine^[1]. Pretreatment with L-carnitine augments Nrf2 nuclear translocation, DNA binding activity and heme oxygenase-1 (HO-1) expression in H₂O₂-treated HL7702 cells. L-carnitine protects HL7702 cells against H₂O₂-induced cell damage through Akt-mediated activation of Nrf2 signaling pathway^[2]. In Vivo: L-carnitine is found to down-regulate the ubiquitin proteasome pathway and increase IGF-1 concentrations in animal models. L-carnitine administration for 2 weeks of hindlimb suspension alleviates the decrease in weight and fiber size in the soleus muscle. In addition, L-carnitine suppresses atrogin-1 mRNA expression, which has been reported to play a pivotal role in muscle atrophy^[3]. Simultaneous treatment with L-carnitine attenuates the renal fibrosis (which correlated with a reduction of plasma TGF-beta1 levels) and the pro-oxidative and proinflammatory status reported in L-NAME groups, with a concomitant increase in the expression of PPAR-gamma^[4].