• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.631-640
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• 1999

The present study investigated the stimulatory effects of iron (or ascorbate) on cyclosporine-induced kidney mitochondrial damage. Damaging effect of $50\;{\mu}M$ cyclosporine plus $20\;{\mu}M\;Fe^{2+}$ on mitochondrial lipids and proteins of rat kidney and hyaluronic acid was greater than the summation of oxidizing action of each compound alone, except sulfhydryl oxidation. Cyclosporine and $100\;{\mu}M$ ascorbate showed an enhanced damaging effect on lipids but not on proteins. The peroxidative action of cyclosporine on lipids was enhanced with increasing concentrations of $Fe^{2+}.$ Ferric ion $(20\;{\mu}M)$ also interacted with cyclosporine to stimulate lipid peroxidation. Damaging action of cyclosporine on mitochondrial lipids was enhanced by ascorbate $(100\;{\mu}M\;and\;1\;mM)$. Iron chelators, DTPA and EDTA, attenuated carbonyl formation induced by cyclosporine plus ascorbate. Cyclosporine $(100\;{\mu}M)$ and $50\;{\mu}M\;Fe^{2+}$ $(or\;100\;{\mu}M\;ascorbate)$ synergistically stimulated degradation of $2-{\alpha}$ deoxyribose. Cyclosporine $(1\;to\;100\;{\mu}M)$ reduced ferric ion in a dose dependent manner, which is much less than ascorbate action. Addition of $Fe^{2+}$ caused a change in absorbance spectrum of cyclosporine in $230{\sim}350$ nm of wavelengths. The results show that cyclosporine plus iron (or ascorbate) exerts an enhanced damaging effect on kidney mitochondria. Iron and ascorbate appear to promote the nephrotoxicity induced by cyclosporine.

• Journal of Nutrition and Health
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• v.26 no.5
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• pp.547-557
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• 1993

This study was done to investigate whether dietary fats differing in their fatty acid compositions change hepatic mitochondrial lipid composition and thereby change adenine nucleotide translocase activity. Male Sprague-Dawley rats were fed 5 different wxperimental diets for 6 weeks, which were different in their fatty acid compositions. The dietary fats were beef tallow(BT), olive oil(OO), corn oil(CO), perilla oil(PO) and sardine oil(SO) as a source of saturated fatty acid, oleic acid, n-6 linoleic acid, n-3 $\alpha$-linolenic acid and n-3 eiocosapentaenoic acid+docosahexaenoic acid respectively. Body weight of PO group was significantly higher than that of either BT or SO group. This increase in body weight of PO group was due to the increase of food intake. Although there was no difference in liver weight, % liver weight per body weight of SO group was significantly higher than BT and OO groups. Analysis of mitochondrial lipid composition showed that dietary oils differing their fatty acid compositions altered mitochondrial fatty acid patterns, especially n-6/n-3 ratio, cholesterol/phospholipid ratio and phopsholipid composition. The n-6/n-3 ratio was highest in CO group but lowest in SO group whereas the ratio of Chol/PL was highest in SO group but lowest in CO group. Such changes in mitochondrial lipids did not lead to a significant alteration in the activities of adenine nucleotide translocase, which is embedded in mitochodrial inner membrane.

• Molecules and Cells
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• v.38 no.12
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• pp.1054-1063
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• 2015

Mitochondria play a crucial role in eukaryotic cells; the mitochondrial electron transport chain (ETC) generates adenosine triphosphate (ATP), which serves as an energy source for numerous critical cellular activities. However, the ETC also generates deleterious reactive oxygen species (ROS) as a natural byproduct of oxidative phosphorylation. ROS are considered the major cause of aging because they damage proteins, lipids, and DNA by oxidation. We analyzed the chronological life span, growth phenotype, mitochondrial membrane potential (MMP), and intracellular ATP and mitochondrial superoxide levels of 33 single ETC component-deleted strains during the chronological aging process. Among the ETC mutant strains, 14 ($sdh1{\Delta}$, $sdh2{\Delta}$, $sdh4{\Delta}$, $cor1{\Delta}$, $cyt1{\Delta}$, $qcr7{\Delta}$, $qcr8{\Delta}$, $rip1{\Delta}$, $cox6{\Delta}$, $cox7{\Delta}$, $cox9{\Delta}$, $atp4{\Delta}$, $atp7{\Delta}$, and $atp17{\Delta}$) showed a significantly shorter life span. The deleted genes encode important elements of the ETC components succinate dehydrogenase (complex II) and cytochrome c oxidase (complex IV), and some of the deletions lead to structural instability of the membrane-$F_1F_0$-ATP synthase due to mutations in the stator stalk (complex V). These short-lived strains generated higher superoxide levels and produced lower ATP levels without alteration of MMP. In summary, ETC mutations decreased the life span of yeast due to impaired mitochondrial efficiency.

• Journal of Nutrition and Health
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• v.26 no.5
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• pp.532-546
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• 1993

This study was done to investigate the effects of different dietary oils on hepatic mitochondrial lipid compositon, adenine nucleotide translocase(AdNT) and ATPase activities in carcinogen treated rats. Sixty male Sprague-Dawley rats, weighing 50∼60g, were fed three different types of dietary oil, beef tallow(BT), corn oil(CO) and sardine oil(SO) at 15% by weight for 14 weeks. Three weeks after feeding rats were intraperitoneally injected with a single dose of diethylnitrosamine(200mg/Kg BW). After five weeks rate fed 0.02% acetylaminofluorene contating diet for 6 weeks, and after seven weeks 0.05% phenobarbital containing diet for 7 weeks. At 14th week, rats were sacrificed and hepatic mitochondrial lipid composition, AdNT and ATPase activities were determined. Percent liver weight per body weight was significantly by carcinogen treatment. Analysis of mitochondrial lipid composition showed that body cholesterol and phospholipid contents were not affected by dietary oils but significantly increased by carcinogen treatment. Individual phospholipid composition as well as phosphatidyl ethanolamine/phosphatidyl choline ratio were altered by either dietary oils or carcinogen treatment. Fatty acid composition was changed by dietary oils but not much by carcinogen treatment. AdNT activity was affected by dietary oils in only carcinogen treated groups. ATPase activity was affected by dietary oils in only carcinogen nontreated groups. These data indicate that both dietary oils and caricinogen treatment can change mitochondrial lipid composition and thereby change AdNT and ATPase activities. Particularly effects of carcinogen treatment on cholesterol/phopholipid ratio, phospholipid compositon and ATPase activity were different among dietary oil groups. Therefore it is suggested that different dietary oils can somewhat modulate the changes of mitochnodrial lipid composition and membrane bound enzyme activites during hepatocarcinogenesis.

• Journal of the Korean Chemical Society
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• v.63 no.4
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• pp.253-259
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• 2019

5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR), a structural analog of adenosine monophosphate (AMP), promotes oxidative remodeling in muscle cells. AICAR activates AMP-dependent protein kinase (AMPK), thus increasing lipid metabolism, respiration, and mitochondrial counts. This process is called oxidative remodeling, which enhances the physical endurance of mice. To test this drug on an invertebrate that is genetically similar to humans, we used the small water crustacean Daphnia magna, which is sensitive to changes in water conditions. We tested the effects of pH on the efficacy of AICAR using two methods. One method measured oxygen consumption of Daphnia in oxygen chambers. The other method determined lipid levels of Daphnia through fluorescent tagging of lipids. The results showed that when exposed to AICAR at pH 6.58, D. magna consumed more oxygen and had lower overall levels of lipids, which is consistent with the expected effects of AICAR, such as increased respiration and lipid metabolism.

• Korean Journal of Veterinary Research
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• v.34 no.2
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• pp.249-258
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• 1994

This study was carried out to investigate the inhibitory effects of vitamin E on the oxidative damage of cellular lipids and proteins in free radical reaction induced by $FeCl_3$, and ascorbic acid. In this experiment, a vitamin E treated rat group was administered with 100mg/kg body weight of $dl-{\alpha}-tocophery$ 1 acetate and an untreated rat group was administered with the same volume of corn oil. And then assays of malondialdehyde and carbonyl group in total homogenate, mitochondrial and microsomal fraction of rat liver were carried out at the scheduled time. The results obtained from this study were summarized as follows; 1. Lipid peroxidation levels in vitamin E administered rat liver cells were significantly (p<0.05) decreased at the intervals between 1 hour and 4 hours in liver homogenate, at all times except for 1 hour point in mitochondrial fraction, and also at the intervals between 0.5 hour and 3 hours in microsomal fraction compared with those of the control rat liver cell. 2. Protein oxidation levels in vitamin E administered rat liver cell were also significantly (p<0.05) decreased at the intervals between 1.5 hours and 4 hours in liver homogenate, at over 4 hours in liver mitochondrial fraction, and at the intervals between 0.5 hour and 3 hours in liver microsomal fraction compared with those of the control rat liver cells.

• Journal of Integrative Natural Science
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• v.15 no.4
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• pp.137-144
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• 2022

This paper presents the effect of the supramolecular complex of GA (Glycyrrhizic acid) and Mt(menthol) and GA: Mt (4: 1) obtained on their basis can restore functional dysfunction of the liver mitochondria in alloxan diabetes, ie, inhibit lipid peroxidation. The hypoglycemic activity and mitochondrial membrane stabilizing properties of the supramolecular compound GA: Mt (4: 1) in alloxan diabetes were more pronounced than those of menthol, GA and its GK: Mt (2: 1) and GA: Mt (9: 1) compounds. According to the results obtained, the concentration of GA did not affect the peroxidation of lipid membranes of the liver mitochondria. However, a concentration of 15 μM of GA was found to reduce LPO (lipid peroxidation) formed by the effect of Fe²+ / ascorbate on the mitochondrial membrane by 58.0 ± 5.0% relative to control. The inhibitory effect of GA and its supramolecular compounds in different proportions with menthol on the peroxidation of lipids in rat heart and brain tissue has been studied

• Food Engineering Progress
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• v.22 no.4
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• pp.353-357
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• 2018

Previous studies have suggested that rice bran oil (RBO), an edible oil from the byproducts of rice milling, has anti-inflammatory effects in inflammation inducing macrophages, known as M1 subsets. Yet the effects of RBO on the counterpart M2 subsets, the "healing" macrophages, were poorly investigated to date. In this regard, recent studies on the molecular/cellular anti-inflammatory mechanisms of dietary components have demonstrated that mitochondrial respiration contributes to macrophage functioning. Therefore, the current study examined whether RBO regulates cytokine secretion by modulating mitochondrial metabolism in wound healing M2 subsets. Palm oil (PO), enriched with medium-chain fatty acids, served as a positive control. C57BL/6 mice were fed a diet containing either corn oil (CO), PO or RBO for 4 weeks, followed by purification of bone marrow-derived macrophages (BMDM) from their tibias and femurs. Cells were further polarized to M2-BMDM, and the expression of M2 marker (CD206) on cellular surfaces were not affected by dietary intervention. In addition, the secretion of anti-inflammatory cytokine (IL-10) in the culture supernatant was not affected by dietary lipids. Oxygen consumption rate, the indicator of mitochondrial respiration in M2-BMDM was not regulated by RBO intervention and PO treatment. Taken together, this study imply that RBO did not intervene both the regulation of inflammatory responses and mitochondrial respiration in M2 macrophages.

• Journal of Nutrition and Health
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• v.39 no.4
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• pp.323-330
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• 2006

Peripheral insulin resistance in obese/type II diabetes animals results from an impairment of insulin-stimulated glucose uptake into skeletal muscle. Insulin stimulate the translocation of GLUT4 from intracellular location to the plasma membrane. Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) is implicated in mediation of fusion of GLUT4-containing vesicle with the plasma membrane. Present study investigated regulatory effects of Rhodiola sachalinensis administration and exercise training on the expression of GLUT4 protein and SNAREs protein in skeletal muscles of obese Zucker rats. Experimental animals were randomly assigned into one of five groups ; lean control(LN), obese control(OB), exercise-treated(EXE), Rhodiola sachalinensis-treated(Rho), combine of Rho & EXE (Rho-EXE). All animals of exercise training (EXE, Rho-EXE) performed treadmill running for 8 weeks, and animals of Rho groups (Rho, Rho-EXE) were dosed daily by gastric gavage during the same period. After experiment, blood were taken for analyses of glucose, insulin, and lipids levels. Mitochondrial oxidative enzyme (citrate synthase, CS ; $\beta$-hydroxyacyl-CoA dehydrogenase, $\beta$-HAD) activity were analysed. Skeletal muscles were dissected out for analyses of proteins (GLUT4, VAMP2, syntaxin4, SNAP23). Results are as follows. Exercise and/or Rhodiola sachalinensis administration significantly reduced body weight and improved blood lipids (TG, FFA), and increased insulin sensitivity. Endurance exercise significantly increased the activity of mitochondrial enzymes and the expression of GLUT4 protein, however, administration of Rhodiola sachalinensis did not affect them. The effect of exercise and/or Rhodiola sachalinensis administration on the expression of SNARE proteins was unclear. Our study suggested that improvement insulin sensitivity by exercise and/or Rhodiola sachalinensis administration in obese Zucker rats is independent of expression of SNARE proteins.

• Journal of Microbiology and Biotechnology
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• v.33 no.2
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• pp.242-250
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• 2023

Comparative gene identification-58 (CGI-58) is an activating protein of triacylglycerol (TAG) lipase. It has a variety of catalytic activities whereby it may play different roles in diverse organisms. In this study, a homolog of CGI-58 in Phaeodactylum tricornutum (PtCGI-58) was identified. PtCGI-58 was localized in mitochondria by GFP fusion protein analysis, which is different from the reported subcellular localization of CGI-58 in animals and plants. Respectively, PtCGI-58 overexpression resulted in increased neutral lipid content and TAG accumulation by 42-46% and 21-32%. Likewise, it also increased the relative content of eicosapentaenoic acid (EPA), and in particular, the EPA content in TAGs almost doubled. Transcript levels of genes involved in de novo fatty acid synthesis and mitochondrial β-oxidation were significantly upregulated in PtCGI-58 overexpression strains compared with wild-type cells. Our findings suggest that PtCGI-58 may mediate the breakdown of lipids in mitochondria and the recycling of acyl chains derived from mitochondrial β-oxidation into TAG biosynthesis. Moreover, this study potentially illuminates new functions for CGI-58 in lipid homeostasis and provides a strategy to enrich EPA in algal TAGs.