Effects of coenzyme Q[10] on LDL oxidation in vitro

Coenzyme Q[10], a lipid soluble benzoquinone, has excellent antioxidant and membrane stabilizing properties in the cardiac tissue. The present study investigated the effects of coenzyme Q[10] on in vitro LDL oxidation quantitavely. The formation of conjugated dienes, malondialdehyde [MDA] and electrophoretic mobility were monitored as markers of the oxidation of LDL, respectively. Coenzyme Q[10] showed a decrease the formation of conjugated dienes and MDA, respectively, against oxidation in vitro. Coenzyme Q[10] also reduced electrophoretic mobility of the oxidized human LDL. Thus, results showed that the coenzyme Q10 exhibits strong antioxidant activity in CuSO[4]-mediated oxidation of LDL [P<0.05] in vitro. The inhibitory effects of the coenzyme Q[10] on LDL oxidation were dose-dependent at concentrations ranging from 20 nM to 300 nM. Moreover, the effects of coenzyme Q[10] on LDL oxidation were compared with vitamin E and vitamin C. This study showed that coenzyme Q[10] is a potent antioxidant to protect LDL against oxidation in vitro and may be a good alternative to reduce the risk of atherosclerosis and coronary heart disease and other free radical associated health problems

Analysis of ankyrin-B gene mutations in patients with long QT syndrome / 南方医科大学学报

<p><b>OBJECTIVE</b>To identify the ankyrin-B gene mutations that cause long QT syndrome (LQTS) and determine the prevalence of such mutations in Japanese patients with LQTS.</p><p><b>METHODS</b>We conducted a search for ankyrin-B gene mutation in 78 unrelated patients with LQTS (28 males and 50 females, aged 2 to 89 years). With informed consent from all the subjects and/or their parents, genomic DNA was purified from the white blood cells of the patients and amplified using polymerase chain reaction (PCR). Single-strand conformational polymorphism (SSCP) analysis of the amplified DNA was performed to screen for mutations and aberrant SSCP products were isolated and sequenced by dye terminator cycle sequencing method using an automated fluorescent sequencer. PCR and restriction fragment length polymorphism (PCR-RFLP) analysis was carried out to further confirm the missense mutations by comparison with samples from 150 normal healthy individuals.</p><p><b>RESULTS</b>We identified a T to A transition mutation at position 4,603 in exon 40, resulting in the substitution of arginine for a tryptophan at amino acid residue 1,535 (W1535R) in the regulatory domain of 220-kD ankyrin-B, which is a highly conserved domain shared by different species.</p><p><b>CONCLUSION</b>This novel missense mutation in the ankyrin-B gene may be a cause of type 4 LQTS. Ankyrin-B gene mutation might not play the major role in LQTS in Japanese.</p>

CETP(Cholesteryl Ester Transfer Protein) Deficiency Caused by Genetic Mutation in the CETP Gene in Normal Korean Population

BACKGROUND: CETP(Cholesteryl ester transfer Protein) is the essential protein for 'reverse cholesterol transport' which transfers cholesteryl ester from HDL particles to other lipoproteins. The subjects with CETP deficiency caused by genetic mutation in the CETP gene have very high HDL levels that CETP deficiency implies anti-atherogenic effect. A missense mutation in the exon 15(D442G) and a splicing defect in the intron 14(Int 14A) in the CETP gene are reported to be popular among Japanese population which overall prevalence of both mutations is up to 10%. METHODS: To identify the CETP mutaion such as D442G or Int 14A among Koreans, seven subjects who have high HDL level above 80mg/dl and 14 first-degree relatives of them were included in this study. RESULTS: Of 21 subjects in 7 familes, 5 subjects in 2 families were confirmed as D442G mutation of CETP gene, but Int 14A mutation is not found. Subjects with D442G mutation have high apo A-I levels as well as HDL levels. CONCLUSION: The D442G mutation of CETP gene is firstly confirmed in Koreans. The CETP deficiency caused by genetic mutation in the CETP gene seems to be prevalent among Korean population.