• BMB Reports
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• v.37 no.4
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• pp.416-421
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• 2004

The antioxidant activities of NADH and of its analogue, 1,4-dihydro-2,6-dimethyl-3,5-dicarbethoxy-pyridine ($PyH_2$), were evaluated in vitro. NADH was found to be oxidized by the peroxyl radical derived from 2,2-azobis-(2-amidinopropane) dihydrochloride (AAPH) decomposition, in a pH-dependent manner. Both NADH and $PyH_2$ inhibited the peroxidation of egg yolk lecithin (EYL) liposomes, although $PyH_2$ was more effective than NADH when 2,2'-azobis-4-methoxy-2,4-dimethyl-valeronitrile (methoxy-AMVN) was employed to induce EYL liposome peroxidation. The antioxidant activities of NADH and $PyH_2$ were also evaluated by measuring their influences on 1,3-diphenylisobenzofuran (DPBF) fluorescence decay in the presence of peroxyl radicals. NADH and $PyH_2$ were much more effective at inhibiting DPBF quenching in Triton X-100 micelles than in liposomes. These results indicate that NADH can inhibit lipid peroxidation despite being hydrophilic. Nevertheless, membrane penetration is an important factor and limits its antioxidant activity.

• BMB Reports
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• v.47 no.3
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• pp.158-166
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• 2014

Cell proliferation is a delicately regulated process that couples growth signals and metabolic demands to produce daughter cells. Interestingly, the proliferation of tumor cells immensely depends on glycolysis, the Warburg effect, to ensure a sufficient amount of metabolic flux and bioenergetics for macromolecule synthesis and cell division. This unique metabolic derangement would provide an opportunity for developing cancer therapeutic strategy, particularly when other diverse anti-cancer treatments have been proved ineffective in achieving durable response, largely due to the emergence of resistance. Recent advances in deeper understanding of cancer metabolism usher in new horizons of the next generation strategy for cancer therapy. Here, we discuss the focused review of cancer energy metabolism, and the therapeutic exploitation of glycolysis and OXPHOS as a novel anti-cancer strategy, with particular emphasis on the promise of this approach, among other cancer metabolism targeted therapies that reveal unexpected complexity and context-dependent metabolic adaptability, complicating the development of effective strategies.

• International Journal of Industrial Entomology and Biomaterials
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• v.9 no.2
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• pp.249-254
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• 2004

Dietary supplementation of sodium nitrate with different concentrations 50, 100, 200, 500, 700 and 1000 $\mu\textrm{g}$/ml of single, two, three and four feeds to fifth instar larvae of biovoltine NB$_4$D$_2$ race of the silkworm, B. mori resulted in significant increase in the food conversion, conversion rate and conversion efficiency $K_1$ and $K_2$. However, there were significant decrease in the food assimilation, assimilation rate and assimilation efficiency in the sodium nitrate treated groups as compared with that of the corresponding parameters of the carrier control. This indicates that the administration of sodium nitrate may stimulate metabolic activities, thereby influencing conversion of food into body weight in the bivoltine silkworm, B. mori.

• Toxicological Research
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• v.30 no.4
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• pp.221-234
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• 2014

Mitochondria dysfunction was first described in the 1960s. However, the extent and mechanisms of mitochondria dysfunction's role in cellular physiology and pathology has only recently begun to be appreciated. To adequately evaluate mitochondria-mediated toxicity, it is not only necessary to understand mitochondria biology, but discerning mitochondrial redox biology is also essential. The latter is intricately tied to mitochondrial bioenergetics. Mitochondrial free radicals, antioxidants, and antioxidant enzymes are players in mitochondrial redox biology. This review will provide an across-the-board, albeit not in-depth, overview of mitochondria biology and mitochondrial redox biology. With accumulating knowledge on mitochondria biology and mitochondrial redox biology, we may devise experimental methods with adequate sensitivity and specificity to evaluate mitochondrial toxicity, especially in vivo in living organisms, in the near future.

• Proceedings of the Korean Society of Fisheries Technology Conference
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• 1995.06a
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• pp.169-170
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• 1995

• Journal of Ginseng Research
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• v.45 no.4
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• pp.473-481
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• 2021

Background: Mitochondrial dysfunction is one of the significant reasons for Alzheimer's disease (AD). Ginsenosides, natural molecules extracted from Panax ginseng, have been demonstrated to exert essential neuroprotective functions, which can ascribe to its anti-oxidative effect, enhancing central metabolism and improving mitochondrial function. However, a comprehensive analysis of cellular mitochondrial bioenergetics after ginsenoside treatment under Aβ-oxidative stress is missing. Methods: The antioxidant activities of ginsenoside Rb₁, Rd, Re, Rg₁ were compared by measuring the cell survival and reactive oxygen species (ROS) formation. Next, the protective effects of ginsenosides of mitochondrial bioenergetics were examined by measuring oxygen consumption rate (OCR) in PC12 cells under Aβ-oxidative stress with an extracellular flux analyzer. Meanwhile, mitochondrial membrane potential (MMP) and mitochondrial dynamics were evaluated by confocal laser scanning microscopy. Results: Ginsenoside Rg₁ possessed the strongest anti-oxidative property, and which therefore provided the best protective function to PC12 cells under the Aβ oxidative stress by increasing ATP production to 3 folds, spare capacity to 2 folds, maximal respiration to 2 folds and non-mitochondrial respiration to 1.5 folds, as compared to Aβ cell model. Furthermore, ginsenoside Rg1 enhanced MMP and mitochondrial interconnectivity, and simultaneously reduced mitochondrial circularity. Conclusion: In the present study, these results demonstrated that ginsenoside Rg₁ could be the best natural compound, as compared with other ginsenosides, by modulating the OCR of cultured PC12 cells during oxidative phosphorylation, in regulating MMP and in improving mitochondria dynamics under Aβ-induced oxidative stress.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.12
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• pp.1755-1760
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• 2006

Studies were carried out at the National Institute of Animal Nutrition and Physiology, India to determine the effect of feeding chopped paddy straw (Oryza sativa) on the energy expenditure in crossbred cattle. Four crossbred cattle male, aged 5-6 years and weighing about 450 kg were used for this study. Three experimental trials, one each for the feeding of un-chopped paddy straw offered ad libitum (UCA), chopped paddy straw fed at restricted level (CR) and chopped paddy straw offered ad libitum (CA) were conducted. The quantity of un-chopped paddy straw consumed during UCA was assumed as the voluntary intake by the cattle and the same quantity was offered after chopping during CR. Each trial comprised of 21 d preliminary feeding period and 5 d of observation recording period. Expired gas was collected in Douglas bags using a face-mask and three-way valve at 6 hourly intervals i.e., at 09.30, 15.30, 21.30, and 03.30 h throughout the observation period. Expired gas and ambient air inspired by the animals were analyzed for the oxygen content through paramagnetic oxygen analyzer. Energy expenditure (EE) by the animals was calculated by determining the volume of oxygen consumed per minute (STP) and multiplying by 4.825. Paddy straw used in all the three trials contained (g/kg DM) 90.0 CP, 786 OM, 700 NDF, 489 ADF, 357 Cellulose and 60.0 ADL. Metabolizable energy (ME) was 6.9 MJ/kg DM. Dry matter intake (DMI) both in UCA and CR was about 6.8 kg, except that it was chopped in CR. Chopping has resulted in 32% improvement (9 kg) in DMI of CA as compared to that of UCA. Although ME intake was similar in UCA and CR (47.2 MJ/day), energy expenditure (EE) was higher in UCA (23.3 MJ) when compared to that of CR (19.5 MJ). The ME intake (63.3 MJ) as well as EE (27.1 MJ) was highest in CA. Energy expenditure when expressed as MJ/kg DMI was 3.48, 2.90 and 3.12; whereas as per cent of ME intake it was 50, 41 and 44 in UCA, CR and CA respectively. Our study has unequivocally confirmed that chopping of poor quality roughages like paddy straw has definite advantages not only in terms of improving the intake by decreasing the time taken for ingestion but also in reducing the energy cost of eating.

• Asian-Australasian Journal of Animal Sciences
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• v.15 no.2
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• pp.195-204
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• 2002

The objective of this study was to examine the impact of three categories of supplements on intake and diet induced difference on degradation of straw substrates. Sixteen crossbred cattle fitted with rumen cannula were randomly divided into 4 equal groups. Animals were fed on wheat straw ad libitum without any supplement except mineral mixture (control; $T_1$) or supplemented with concentrate mixture (CS; $T_2$) or green Lucerne (GLS; $T_3$) or urea-molasses block lick (ULS; $T_4$). Total dry matter intake in $T_2$, $T_3$ and $T_4$ was increased by 70, 54 and 49%, respectively compared to $T_1$ which was only 1.55 kg/100 kg B.Wt. Other than control animals, straw intake was less on $T_3$ than $T_2$ or $T_4$. In Sacco degradation of untreated and urea treated wheat or paddy straw in different treatments indicated that the supplements had a significant (p<0.01) impact on rapidly soluble (A) and insoluble but potentially degradable (B) fractions of straw. Urea treatment increased fraction-A but, provision of supplement improved fraction-B also. Effective degradation (ED) of OM was better on $T_2$. Rate of degradation (C) of OM and CWC was dependent on diet and type of straw but hemicellulose and cellulose were related to latter factor only. ED of cell wall carbohydrates (CWC) was similar in $T_2$ and $T_4$ but higher than $T_3$. CS was more effective in improving the degradation of both untreated and urea treated straw while ULS was effective on the former only. CS had more impact on superior quality straw while contrary was true with ULS. Although GLS improved intake and degradability of untreated and urea treated straws, its bulkiness affected the straw intake compared to other supplements.

• Journal of Ginseng Research
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• v.43 no.4
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• pp.517-526
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• 2019

Background: The root of Panax ginseng, a member of Araliaceae family, has been used as herbal medicine and functional food in Asia for thousands of years. According to Traditional Chinese medicine, ginseng is the most widely used "Qi-invigorating" herbs, which provides tonic and preventive effects by resisting oxidative stress, influencing energy metabolism, and improving mitochondrial function. Very few reports have systematically measured cell mitochondrial bioenergetics after ginseng treatment. Methods: Here, H9C2 cell line, a rat cardiomyoblast, was treated with ginseng extracts having extracted using solvents of different polarity, i.e., water, 50% ethanol, and 90% ethanol, and subsequently, the oxygen consumption rate in healthy and tert-butyl hydroperoxideetreated live cultures was determined by Seahorse extracellular flux analyzer. Results: The 90% ethanol extracts of ginseng possessed the strongest antioxidative and tonic activities to mitochondrial respiration and therefore provided the best protective effects to H9C2 cardiomyocytes. By increasing the spare respiratory capacity of stressed H9C2 cells up to three-folds of that of healthy cells, the 90% ethanol extracts of ginseng greatly improved the tolerance of myocardial cells to oxidative damage. Conclusion: These results demonstrated that the low polarity extracts of ginseng could be the best extract, as compared with others, in regulating the oxygen consumption rate of cultured cardiomyocytes during mitochondrial respiration.

• Animal cells and systems
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• v.16 no.4
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• pp.269-273
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• 2012

Controlling metabolism throughout life is a necessity for living creatures, and perturbation of energy balance elicits disorders such as type-2 diabetes mellitus and cardiovascular disease. $Ca^{2+}$ plays a key role in regulating energy generation. $Ca^{2+}$ homeostasis of the endoplasmic reticulum (ER) lumen is maintained through the action of $Ca^{2+}$ channels and the $Ca^{2+}$ ATPase pump. Once released from the ER, $Ca^{2+}$ is taken up by mitochondria where it facilitates energy metabolism. Mitochondrial $Ca^{2+}$ serves as a key metabolic regulator and determinant of cell fate, necrosis, and/or apoptosis. Here, we focus on $Ca^{2+}$ transport from the ER to mitochondria, and $Ca^{2+}$-dependent regulation of mitochondrial energy metabolism.