• Nutrition Research and Practice
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• v.6 no.3
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• pp.195-200
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• 2012

The purpose of this study was to investigate the effects of ${\alpha}$-lipoic acid on body weight and lipid profiles in Sprague-Dawley rats fed a high fat diet (HFD). After 4 weeks of feeding, rats on the HFD were divided into three groups by randomized block design; the first group received the high-fat-diet (n = 10), and the second group received the HFD administered with 0.25% ${\alpha}$-lipoic acid (0.25LA), and the third group received the high-fat diet with 0.5% ${\alpha}$-lipoic acid (0.5LA). The high fat diet with ${\alpha}$-lipoic acid supplemented groups had significantly inhibited body weight gain, compared to that in the HFD group (P < 0.05). Organ weights of rats were also significantly reduced in liver, kidney, spleen, and visible fat tissues in rats supplemented with ${\alpha}$-lipoic acid (P < 0.05). Significant differences in plasma lipid profiles, such as total lipids, total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein, were observed between the HFD and 0.5LA groups. The atherogenic index and the plasma high density lipoprotein-cholesterol/total cholesterol ratio improved significantly with ${\alpha}$-lipoic acid supplementation in a dose-dependent manner (P < 0.05). Total hepatic cholesterol and total lipid concentration decreased significantly in high fat fed rats supplemented with ${\alpha}$-lipoic acid in a dose-dependent manner (P < 0.05), whereas liver triglyceride content was not affected. In conclusion, ${\alpha}$-lipoic acid supplementation had a positive effect on weight gain and plasma and liver lipid profiles in rats.

• Asian-Australasian Journal of Animal Sciences
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• v.27 no.7
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• pp.996-1002
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• 2014

An experiment was conducted to evaluate the effects of dietary alpha-lipoic acid (LA) and acetyl-L-carnitine (ALC) on growth performance, carcass characteristics and meat quality in Arbor Acres broilers. A total of 486 1-d-old male Arbor Acres broilers were randomly allocated to 9 dietary treatments, 9 treatments were group A (0 mg/kg LA and 0 mg/kg ALC), group B (50 mg/kg LA and 0 mg/kg ALC), group C (100 mg/kg LA and 0 mg/kg ALC), group D (0 mg/kg LA and 50 mg/kg ALC), group E (50 mg/kg LA and 50 mg/kg ALC), group F (100 mg/kg LA and 50 mg/kg ALC), group G (0 mg/kg LA and 100 mg/kg ALC), group H (50 mg/kg LA and 100 mg/kg ALC), group I (100 mg/kg LA and 100 mg/kg ALC). Birds were slaughtered at 42 days old. Average daily gain (ADG), average feed intake (AFI), feed conversion rate (FCR), eviscerated rate, breast muscle percentage, thigh muscle percentage, abdominal fat percentage, liver weight, muscle color ($L^*$ value, $a^*$ value, $b^*$ value), pH values at 45 min and 24 h postmortem were measured. Results showed that there existed an interaction between LA and ALC in growth performance of broilers, carcass traits and meat quality. The overall result is that high level of LA and ALC led to lower AFI, ADG (p<0.01), lower abdominal fat percentage, liver weight (p<0.01), lower $L^*$ value, $a^*$ value, and $b^*$ value of breast muscle, $L^*$ value of thigh muscle (p<0.05), and higher FCR (p<0.01), eviscerated rate (p<0.01), breast muscle percentage, thigh muscle percentage (p<0.05), $a^*$ value, pH 45 min and pH 24 h of thigh muscle (p<0.01). These results suggested that dietary LA and ALC contributed to the improvement of meat quality in broilers.

• BMB Reports
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• v.43 no.5
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• pp.325-329
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• 2010

Protein kinase CKII (CKII), a heterotetramer composed of two catalytic ($\alpha$ or $\alpha$') subunits and two regulatory ($\beta$) subunits, plays a critical role in cell proliferation and anti-apoptosis. Recently, capsaicin was shown to trigger apoptosis. Therefore, we examined the effect of capsaicin on CKII activity. Although capsaicin induced apoptotic death in HeLa cells, CKII activity was increased in the cytosolic fraction of HeLa cells after treatment. Capsaicin did not change the expression of the $CKII{\alpha}$ and $CKII{\beta}$ proteins. Capsaicin stimulated the catalytic activity of recombinant CKII tetramer, but not the $CKII{\alpha}$ subunit. Moreover, capsaicin enhanced the autophosphorylation of $CKII{\alpha}$ and $CKII{\beta}$. Taken together, our data suggest that capsaicin stimulates the phosphotransferase activity of CKII holoenzyme by interacting with the $CKII{\beta}$ subunit.

• Journal of the Korean Ceramic Society
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• v.31 no.5
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• pp.513-519
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• 1994

Alumina composite was fabricated by introducing tetragonal ZrO2 in alumina composite of $\alpha$-alumina reinforced with in-situ formed La-$\beta$-aluminate (LaAl11O18). The powder mixture of composition (100-x)[88 Al2O3+(La2O3+11 Al2O3)]+x vol% ZrO2 was prepared with x from 0 to 40. Dense composites fabricated by hot-pressing exhibited bending strength up to 1200 MPa. The gain growth inhibiting effect of ZrO2 grains and La-$\beta$-aluminate platelets, and possibly the stress-induced phase transformation of ZrO2 have resulted in the high bending strength. The fracture toughness of the composite also increased up to 8.5 MPa.m1/2. The enhancement in toughness can be explained by transformation and microcrack toughening of ZrO2 and by crack deflection and bridging of La-$\beta$-aluminate platelets and ZrO2.

• The Korean Journal of Zoology
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• v.11 no.3
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• pp.75-82
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• 1968

The effects of x-irradiation on the utilization of glucose, succinate, citrate and $\\alpha$-ketoglutarate, on the response of the cell metabolism to $NaN_3$ and DNP, and on the uptake of lysine in the presence or absence of the metabolitesor the inhibitors were studied using HeLa cells and the results are summarized as follows: 1. 200r of x-irradiation had no immediate effect on the oxygen consumption of cells. 2. The oxygen consumption was greatly stimulated by succinate, $\\alpha$-ketoglutarate and citraed and in decreasing order and x-irradiation caused no remarkable change in this order. 3. The respiratory response of the cell to the metabolic inhibitors seems to be altered by x-irradiation. 4. The initial rate of the uptake of lysine was markedly retarded and the accumulation of lysine in the cell was decreased by irradiation. 5. Glucose increased the lysine uptake whereas succinate had no effect and citrate and $\\alpha$-ketoglutarate reduced the absorption. X-irradiation did not alter this tendency. 6. The inhibitory effects of $NaN_3$ and DNP on the lysine uptake were quite different from those seen in the oxygen consumption.

• Journal of Nutrition and Health
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• v.24 no.5
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• pp.420-430
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• 1991

To compare the hypolipidemic effects of n6 linoleic acid. n3 $\alpha$-linolenic acid and n3 eicosapentaenoic acid in rats fed high carbohydrate(70% Cal) diet. male Sprague Dawley rats were fed different experimental diets for 6 weeks. which were different only in fatty acid composition. The dietary fats were beer tallow(BT) as a source of saturated fatty acid (SFA), corn oil(CO) for n6 linoleic acid(LA), perilla oil(PO) for n3 $\alpha$-linolenic acid(LL) and fish oil(FO) for n3 eicosapentaenoic acid(EPA) and docosahexaenoic acid (DHA) Plasma total cholesterol(Chol) level was increased by n6 LA but decreased by n3 LL and n3 EPA and most effectively reduced by n3 EPA. HDL-Chol level was raised by n6 LA, but there was no significant change in HDL-Chol levels by n3 LL and was lowered by n3 EPA. Plasma TG level was reduced by n6 LA, but lipogenesis in liver was not affected by n6 LA. However, plasma TG level was lowered by n3 LL and EPA. Both lipogenic enzyme activity and liver TC level were also decreased by n3 PUFA. The relative proportions of TG in VLDL was significantly lowered by n3 EPA. but the proportions of Apo B in VLDL was not changed by n3 EPA. Overall. the hypolipidemic effect was in the order of EPA+ DHA(n3) >LL(n3) >LA(n6) and fish oil and perilla oil rich in n3 PUFA may have important nutritional applications in the prevention and treatment of hypertriglyceridemia.

• Biomolecules & Therapeutics
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• v.18 no.2
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• pp.145-151
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• 2010

Oxygen supply into inside solid tumor is often diminished, which is called hypoxia. Many gene transcriptions were activated by hypoxia-inducible factor (HIF)-$1{\alpha}$. Here, we investigated the effect of hypoxia on paclitaxel-resistance induction in HeLa cervical tumor cells. When HeLa cells were incubated under hypoxia condition, HIF-$1{\alpha}$ level was increased. In contrast, paclitaxel-mediated tumor cell death was reduced by the incubation under hypoxia condition. Paclitaxel-mediated tumor cell death was also inhibited by treatment with DMOG, chemical HIF-$1{\alpha}$ stabilizer, in a dose-dependent manner. A significant increase in intracellular ROS level was detected by the incubation under hypoxia condition. A basal level of cell density was increased in response to 10 nM $H_2O_2$. HIF-$1{\alpha}$ level was increased by treatment with various concentration of $H_2O_2$. The increased level of HIF-$1{\alpha}$ by hypoxia was reduced by the treatment with N-acetylcysteine (NAC), a well-known ROS scavenger. Paclitaxel-mediated tumor cell death was increased by treatment with NAC. Taken together, these findings demonstrate that hypoxia could play a role in paclitaxel-resistance induction through ROS-mediated HIF-$1{\alpha}$ stabilization. These results suggest that hypoxia-induced ROS could, in part, control tumor cell death through an increase in HIF-$1{\alpha}$ level.

• BMB Reports
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• v.29 no.1
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• pp.27-31
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• 1996

Using topoisomerase II (topo II) isozyme-specific antibodies, we investigated the phosphorylation of topo $II{\alpha}$ in mitotic HeLa cells. Topo $II{\alpha}$ was specifically modified in the mitotic cells, resulting in slow migration on SDS-polyacrylamide gel electrophoresis. To characterize the nature of this modification, we treated the nuclear extracts prepared from the mitotic cells with alkaline phosphatase. After the treatment with alkaline phosphatase, the slowly migrated band disappeared and instead a normal (170 kDa) topo $II{\alpha}$ band appeared. These results indicate that human topo $II{\alpha}$ is modified at a specific site(s) in M phase by phosphorylation, supporting the possibility that M phase-specific phosphorylation of topo II is critical for mitotic chromosome condensation and segregation.

• Transactions of the Korean hydrogen and new energy society
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• v.1 no.1
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• pp.15-23
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• 1989

The selective separation of hydrogen from gas mixture containing hydrogen was experimentally studied using $LaNi_5$. The capacity and the rate of hydrogen separation, the purity of recovered hydrogen and the optimum condition of the regeneration of deactivated $LaNi_5$ were investigated. The separation rate and the recovery ratio of hydrogen were slowly decreased with the increase of the number of hydrogen absorption cycle. It was found that this result comes from the deactivation of $LaNi_5$ partly because of the blocking of hydrocarbon compounds in the $LaNi_5$ lattice and partly because of the poisoning of $LaNi_5$ surface by carbon monoxide contained in the gas mixture. The optimum condition for the regeneration of deactivated $LaNi_5$ was obtained by heating in a vacuum to about 637 K. The recovery ratio of hydrogen at the optimum condition was observed to be about 80%. The rates of hydrogen separation were measured in the ${\alpha}$-phase and two phase regions. The rate equations could be expressed as follows ; ${\alpha}$ - phase : $$-\frac{dP{_{H_2}}}{dt}=9.836{\times}10^{-3}(P{_{H_2}}_{-P_{eq}})$$ two phase region : $$-\frac{dP_{H{_2}}}{dt}=1.6909{\times}10^2\exp(-17560/RT)(P{_{H_2}}_{-P_{eq}})$$.

• Molecules and Cells
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• v.28 no.6
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• pp.509-513
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• 2009

Here, we show that JNK1 and JNK3 have different roles in ${\alpha}-$ or etoposide-induced apoptosis in HeLa cells. Dominant negative JNK1 inhibited $TNF-{\alpha}-$ or etoposide-induced apoptosis, while dominant negative JNK3 promoted $TNF-{\alpha}-$ or etoposide-induced apoptosis. During $TNF-{\alpha}$-induced apoptosis, JNK1 was activated in a biphasic manner, exhibiting both transient and sustained activity, whereas JNK3 was activated early and in a transient manner. The role of JNK3 activation was an anti-apoptotic effect, while the role of JNK1 activation was a pro-apoptotic effect. These results suggest that the anti-apoptotic mechanism of JNK3 in $TNF-{\alpha}$-induced apoptosis originates before the apoptotic machinery is triggered.