• Asian-Australasian Journal of Animal Sciences
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• 제33권7호
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• pp.1096-1102
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• 2020

Objective: An experiment was conducted to evaluate the effects of Lonicera japonica extract (LJE) on milk production, rumen fermentation and blood biomarkers of energy metabolism, inflammation and oxidative stress during the perinatal period of Holstein dairy cows. Methods: Eighteen Holstein dairy cows were used in a complete randomized design experiment with 3 dietary treatments and 6 cows per treatment. All cows received the same basal total mixed ration (TMR) including a prepartal diet (1.35 Mcal of net energy for lactation [NE_L]/kg of dry matter [DM], 13.23% crude protein [CP]) from -60 d to calving and a postpartal diet (1.61 Mcal of NE_L/kg of DM, 17.39% CP) from calving to 30 days in milk (DIM). The 3 dietary treatments were TMR supplemented with LJE at 0 (control), 1 and 2 g/kg DM, respectively. LJE was offered from 21 d before calving to 30 DIM. Dry matter intake (DMI) and milk production were measured daily after calving. Milk and rumen fluid samples were collected on 29 and 30 d after calving. On -10, 4, 14, and 30 d relative to calving, blood samples were collected to analyze the biomarkers of energy metabolism, inflammation and oxidative stress. Results: Compared with control diet, LJE supplementation at 1 and 2 g/kg DM increased DMI, milk yield and reduced milk somatic cell count. LJE supplementation also decreased the concentrations of blood biomarkers of pro-inflammation (interleukin-1β [IL-1β], IL-6, and haptoglobin), energy metabolism (nonesterified fatty acid and β-hydroxybutyric acid) and oxidative stress (reactive oxygen metabolites), meanwhile increased the total antioxidant capacity and superoxide dismutase concentrations in blood. No differences were observed in rumen pH, volatile fatty acid, and ammonia-N (NH₃-N) concentrations between LJE supplemented diets and the control diet. Conclusion: Supplementation with 1 and 2 g LJE/kg DM could increase DMI, improve lactation performance, and enhance anti-inflammatory and antioxidant capacities of dairy cows during perinatal period.

• Toxicological Research
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• 제32권3호
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• pp.177-193
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• 2016

After more than half of century since the Warburg effect was described, this atypical metabolism has been standing true for almost every type of cancer, exhibiting higher glycolysis and lactate metabolism and defective mitochondrial ATP production. This phenomenon had attracted many scientists to the problem of elucidating the mechanism of, and reason for, this effect. Several models based on oncogenic studies have been proposed, such as the accumulation of mitochondrial gene mutations, the switch from oxidative phosphorylation respiration to glycolysis, the enhancement of lactate metabolism, and the alteration of glycolytic genes. Whether the Warburg phenomenon is the consequence of genetic dysregulation in cancer or the cause of cancer remains unknown. Moreover, the exact reasons and physiological values of this peculiar metabolism in cancer remain unclear. Although there are some pharmacological compounds, such as 2-deoxy-D-glucose, dichloroacetic acid, and 3-bromopyruvate, therapeutic strategies, including diet, have been developed based on targeting the Warburg effect. In this review, we will revisit the Warburg effect to determine how much scientists currently understand about this phenomenon and how we can treat the cancer based on targeting metabolism.

• Journal of Ginseng Research
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• 제47권4호
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• pp.524-533
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• 2023

Background: Obesity is a risk factor for aging and many diseases, and the disorder of lipid metabolism makes it prominent. This study aims to investigate the effect of ginsenoside Rg1 on aging, lipid metabolism and stress resistance Methods: Rg1 was administered to Caenorhabditis elegans (C. elegans) cultured in NGM or GNGM. The lifespan, locomotory activity, lipid accumulation, cold and heat stress resistance and related mRNA expression of the worms were examined. Gene knockout mutants were used to clarify the effect on lipid metabolism of Rg1. GFP-binding mutants were used to observe the changes in protein expression Results: We reported that Rg1 reduced lipid accumulation and improved stress resistance in C. elegans. Rg1 significantly reduced the expression of fatty acid synthesis-related genes and lipid metabolism-related genes in C. elegans. However, Rg1 did not affect the fat storage in fat-5/fat-6 double mutant or nhr-49 mutant. Combined with network pharmacology, we clarified the possible pathways and targets of Rg1 in lipid metabolism. In addition, Rg1-treated C. elegans showed a higher expression of anti-oxidative genes and heat shock proteins, which might contribute to stress resistance Conclusion: Rg1 reduced fat accumulation by regulating lipid metabolism via nhr-49 and enhanced stress resistance by its antioxidant effect in C. elegans.

• 한국응용약물학회:학술대회논문집
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• 한국응용약물학회 1994년도 춘계학술대회 and 제3회 신약개발 연구발표회
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• pp.336-336
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• 1994

In order to develope the in vitro short term screen-ing method for carcinogen, we studied a purification method for thymine glycol in oxidaized DNA. Thymine glycol (5,6-dihydroxy-5, 6-dihydrothymine) is the major stable radiolysis poduct in thymine by chemical oxidants and ionzing radiation and it is a useful biomarker among oxidized DNA adducts, related with carcinogenests. Standard thymine glycol was prepared by oxidation of 〔$^3$H〕 thymine with KMnO$_4$ followed by purification with HPLC-LSC system and it was assayed by TLC and gas chromatography-MSD. 〔$^3$H〕 DMA adducts was isolated from E. coli (wild type ) treated with oxidative agents such as benzo(a)pyrene, adriamycin, aflatoxin B$_1$ and KBrO$_3$. These oxidative agents generated free radicals in cells by oxidative metabolism. As a result, thymine glycol was produced in cultured E. coli by four chemicals. This result shows that this methodology should be useful tool in screening oxidative carcinogen.

• BMB Reports
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• 제45권2호
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• pp.114-119
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• 2012

Salsolinol (1-methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline) is a compound derived from dopamine metabolism and is capable of causing dopaminergic neurodegeneration. Oxidative modification of neurofilament proteins has been implicated in the pathogenesis of neurodegenerative disorders. In this study, oxidative modification of neurofilament-L (NF-L) by salsolinol and the inhibitory effects of histidyl dipeptides on NF-L modification were investigated. When NF-L was incubated with 0.5 mM salsolinol, the aggregation of protein was increased in a time-dependent manner. We also found that the generation of hydroxyl radicals (${\bullet}OH$) was linear with respect to the concentrations of salsolinol as a function of incubation time. NF-L exposure to salsolinol produced losses of glutamate, lysine and proline residues. These results suggest that the aggregation of NF-L by salsolinol may be due to oxidative damage resulting from free radicals. Carnosine, histidyl dipeptide, is involved in many cellular defense processes, including free radical detoxification. Carnosine, and anserine were shown to significantly prevent salsolinol-mediated NF-L aggregation. Both compounds also inhibited the generation of ${\bullet}OH$ induced by salsolinol. The results indicated that carnosine and related compounds may prevent salsolinol-mediated NF-L modification via free radical scavenging.

• Journal of Microbiology and Biotechnology
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• 제16권11호
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• pp.1819-1825
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• 2006

Four naphthalene-degrading bacteria (Pseudomonas sp. strains O1, W1, As1, and G1) were isolated feom pollutant-contaminated sites. Examination of their substrate utilization and analyses of key naphthalene-catabolic regulatory genes revealed that the pathway and regulation of naphthalene-degradation in all four strains resemble those of NAH7 from P. putida G7. Superoxide anion production, superoxide dismutase activity, and catalase activity during their growth on naphthalene-amended medium increased significantly, compared with those with glucose-amended medium. Addition of ascorbate, an antioxidant, or ferrous iron ($Fe^{2+}$) increased the growth rates of all tested microorganisms on naphthalene. Northern blot and HPLC analyses showed that both nahA gene expression and naphthalene degradation increased under those conditions. Our data suggest that naphthalene degradation can impose severe oxidative stress, and defenses against oxidative stress would play an important role in the metabolism of naphthalene.

• 약학회지
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• 제55권3호
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• pp.251-259
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• 2011

Cigarette smoke condensate (CSC) is known to be carcinogenic compound. CSC contains many organic compounds such as polycyclic aromatic hydrocarbons (PAHs), and heterocyclic amine compounds (HCAs). Reactive oxygen species (ROS) are also generated and induce oxidative DNA damage during the metabolism of CSC. The rat microsome mediated and DNA repair enzyme treated comet assays together with conventional comet assay were performed to evaluate the mechanisms of CSC genotoxicity. The organic extract of CSC induced oxidative and microsome mediated DNA damage. Vitamin C as a model antioxidant reduced DNA damage in endonuclease III treated comet assay. One of flavonoid, galangin as a CYP1A1 inhibitor, reduced DNA damage in the presence of S-9 mixture. The ethanol extracts of the mixed vegetables (BV) or the mixed fruits (BF) showed potent inhibitory effects against CSC induced DNA damage with oxidative DNA lesions and in the prescence of S-9 mixture. These results indicate that BV and BF could prevent CSC-induced cellular DNA damage by inhibiting oxidative stress and suppressing cytochrome P450 in mammalian cells.

• The Korean Journal of Physiology and Pharmacology
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• 제5권3호
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• pp.271-278
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• 2001

Oxidative stress and methylglyoxal (MG), a reactive dicarbonyl metabolites produced by enzymatic and non-enzymatic reaction of normal metabolism, induced aldose reductase (AR) expression in rat aortic smooth muscle cells (SMC). AR expression was induced in a time-dependent manner and reached at a maximum of 4.5-fold in 12 h of MG treatment. This effect of MG was completely abolished by cyclohemide and actinomycin D treatment suggesting AR was synthesized by de novo pathway. Pretreatment of the SMC with N-acetyl-L-cysteine significantly down-regulated the MG-induced AR mRNA. Furthermore, DL-Buthionine-(S,R)-sulfoximine, a reagent which depletes intracellular glutathione levels, increased the levels of MG-induced AR mRNA. These results indicated that MG induces AR mRNA by increasing the intracellular peroxide levels. Aminoguanidine, a scanvenger of dicarbonyl, significantly down-regulated the MG-induced AR mRNA. In addition, the inhibition of AR activities with statil, an AR inhibitor, enhanced the cytotoxic effect of MG on SMC under normal glucose, suggesting a protective role of AR against MG-induced cell damages. These results imply that the induction of AR by MG may contribute to an important cellular detoxification of reactive aldehyde compounds generated under oxidative stress in extrahepatic tissues.

• Toxicological Research
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• 제14권4호
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• pp.577-585
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• 1998

Cadmium is an important industrial and environmental pollutant and has adverse effects on cell growth and metabolism, although the mechanisms of its cellular toxicity are still unclear. This study was performed to elucidate the cytotoxic mechanism of cadmium in the viewpoint of oxidative stress and cytoskeleton alterations in WB-F344 rat liver epithelial cells. 200 $\mu\textrm{M}$ $CdCl_2$ caused a severe disassembling of microtubule and micro filament and an apparent cell retraction under an observation with fluorescence micoscope. (equation omitted)-tubulin and F-actin protein were highly thiolated at 20 min and then disappeared from 1 hour after the treatment of 200 $\mu$M CdCl$_2$in the immunoblot analysis. Intracellular GSH was decreased from 1hr to 24 hrs by 66.6 or 200 $\mu\textrm{M}$ of $CdCl_2$. Intracellular protein thiol was also decreased by 22.2, 66.6 and 200 $\mu\textrm{M}$ of $CdCl_2$ at 1 hour after its treatment. The product of lipid peroxidation (malondialdehyde) was increased from 4 hrs by 66.6 and 200$\mu\textrm{M}$ of $CdCl_2$. These data indicate that cadmium induces oxidative stress involving disassembling of microtubule and micro filament, thiolation of (equation omitted)-tubulin and actin protein, depletion of GSH and protein thiol, and increase of lipid peroxidation.

• Asian Pacific Journal of Cancer Prevention
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• 제15권11호
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• pp.4405-4409
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• 2014

Reactive oxygen species (ROS), highly reactive molecules, are produced by living organisms as a result of normal cellular metabolism and environmental factors, and can damage nucleic acids and proteins, thereby altering their functions. The human body has several mechanisms to counteract oxidative stress by producing antioxidants. A shift in the balance between oxidants and antioxidants in favor of oxidants is termed as "oxidative stress". Paradoxically, there is a large body of research demonstrating the general effect of oxidative stress on signaling pathways, less is known about the initial and direct regulation of signaling molecules by ROS, or what we term the "oxidative interface." This review focuses on the molecular mechanisms through which ROS directly interact with critical signaling molecules to initiate signaling in a broad variety of cellular processes, such as proliferation and survival (MAP kinases and PI3 kinase), ROS homeostasis, and antioxidant gene regulation (Ref-1 and Nrf-2). This review also deals with classification as well as mechanisms of formation of free radicals, examining their beneficial and deleterious effects on cellular activities and focusing on the potential role of antioxidants in preventing and repairing damage caused by oxidative stress. A discussion of the role of phytochemical antioxidants in oxidative stress, disease and the epigenome is included.