title: Alpha-lipoic acid ameliorates oxidative stress by increasing aldehyde dehydrogenase-2 activity in patients with acute coronary syndrome.
abstract: Aldehyde dehydrogenase-2 (ALDH2) is the main enzyme responsible for acetaldehyde oxidation in ethanol metabolism and also provides protection against oxidative stress.  Alpha-lipoic acid (α-LA), a natural dithiol compound with antioxidant properties, has been reported to increase ALDH2 activity in cultured cells.  We analyzed the therapeutic efficacy of α-LA in 63 patients with confirmed acute coronary syndrome (ACS).  These patients (52 men and 11 women, with age range 49-72 years) were randomized into two groups: untreated group (n = 30) and α-LA group (n = 33).  Patients in the α-LA group were given an intravenous injection of 600 mg α-LA every day for 5 days while the patients in the untreated group were given saline.  An isoprostane, 8-iso-prostaglandin F2α (8-iso-PGF2α), one product of arachidonic acid metabolism, was measured as a marker for oxidative stress.  The serum levels of 8-iso-PGF2α and ALDH2 activity were determined at admission to the hospital (time 0), and at 24 hours and 1 week after treatment.  At 24 hours and 1 week after treatment, ALDH2 activity was significantly higher in the α-LA group than in the untreated group (P < 0.05), whereas the levels of 8-iso-PGF2α were significantly lower in the α-LA group than in the untreated group (all P < 0.05).  Importantly, the decrease of 8-iso-PGF2α levels correlated with the increased ALDH2 activity at both 24 hours (r = 0.6234, P < 0.001) and 1 week after treatment (r = -0.3941, P = 0.0014).  α-LA may ameliorate oxidative stress through up-regulating ALDH2 activity in patients with ACS.
authors.affiliation: Department of Emergency, Qilu Hospital of Shandong University, Jinan, Shangdong, PR China.
authors.forename: Rui-Jian
authors.initials: RJ
authors.lastname: Li
authors.forename: Wen-Qing
authors.initials: WQ
authors.lastname: Ji
authors.forename: Jiao-Jiao
authors.initials: JJ
authors.lastname: Pang
authors.forename: Jia-Li
authors.initials: JL
authors.lastname: Wang
authors.forename: Yu-Guo
authors.initials: YG
authors.lastname: Chen
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D054058:Acute Coronary Syndrome / Q000188:drug therapy* / Q000201:enzymology*; D000368:Aged; D000444:Aldehyde Dehydrogenase / Q000378:metabolism*; D000071396:Aldehyde Dehydrogenase, Mitochondrial; D015415:Biomarkers / Q000097:blood; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D006801:Humans; D007275:Injections, Intravenous; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D008063:Thioctic Acid / Q000008:administration & dosage / Q000494:pharmacology*; D013997:Time Factors
chemical_list: D015415:Biomarkers; C075750:8-epi-prostaglandin F2alpha; D008063:Thioctic Acid; D015237:Dinoprost; C096127:ALDH2 protein, human; D000444:Aldehyde Dehydrogenase; D000071396:Aldehyde Dehydrogenase, Mitochondrial