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Junichi Mano - One of the best experts on this subject based on the ideXlab platform.

  • high level of reduced glutathione contributes to detoxification of Lipid Peroxide derived reactive carbonyl species in transgenic arabidopsis overexpressing glutathione reductase under aluminum stress
    Physiologia Plantarum, 2017
    Co-Authors: Junichi Mano, Lina Yin, Shiwen Wang, Kiyoshi Tanaka, Meijuan Zhang, Xiping Deng
    Abstract:

    Lipid Peroxide-derived reactive carbonyl species (RCS), generated downstream of reactive oxygen species (ROS), are critical damage-inducing species in plant aluminum (Al) toxicity. In mammals, RCS are scavenged primarily by glutathione (reduced form of glutathione, GSH), but in plant Al stress, contribution of GSH to RCS detoxification has not been evaluated. In this study, Arabidopsis plants overexpressing the gene AtGR1 (accession code At3g24170), encoding glutathione reductase (GR), were generated, and their performance under Al stress was examined. These transgenic plants (GR-OE plants) showed higher GSH levels and GSH/GSSG (oxidized form of GSH) ratio, and an improved Al tolerance as they suffered less inhibition of root growth than wild-type under Al stress. Exogenous application of 4-hydroxy-2-nonenal, an RCS responsible for Al toxicity in roots, markedly inhibited root growth in wild-type plants. GR-OE plants suffered significantly smaller inhibition, indicating that the enhanced GSH level increased the capacity of RCS detoxification. The generation of H2 O2 due to Al stress in GR-OE plants was lower by 26% than in wild-type. Levels of various RCS, such as malondialdehyde, butyraldehyde, phenylacetaldehyde, (E)-2-heptenal and n-octanal, were suppressed by more than 50%. These results indicate that high levels of GSH and GSH/GSSG ratio by GR overexpression contributed to the suppression of not only ROS, but also RCS. Thus, the maintenance of GSH level by overexpressing GR reinforces dual detoxification functions in plants and is an efficient approach to enhance Al tolerance.

  • accumulation of Lipid Peroxide derived toxic α β unsaturated aldehydes e 2 pentenal acrolein and e 2 hexenal in leaves under photoinhibitory illumination
    Plant Biotechnology, 2010
    Co-Authors: Junichi Mano, Kenji Tokushige, Hirotoshi Mizoguchi, Hiroyuki Fujii, Sergey Khorobrykh
    Abstract:

    Lipid Peroxide-derived α,β-unsaturated aldehydes (2-alkenals) are potent toxins that inhibit enzymes in the Calvin cycle and in the mitochondrial photorespiratory pathway. Production of 2-alkenals in illuminated leaves and their participation in cellular damages have been suggested from the observation that the transgenic tobaccos overexpressing 2-alkenal reductase (AER), a 2-alkenal-detoxifying enzyme, showed tolerance to strong light. In order to identify the involved 2-alkenal species, we here analyzed the leaf aldehyde compositions in the AER-overproducing tobaccos and wild type (SR1), and compared their changes under photoinhibitory light. Aldehydes were extracted from the leaves at an early stage of photoinhibition, derivatized with 2,4-dinitrophenylhydrazine and analyzed on reversed-phase HPLC. In dark-adapted leaves of these tobacco lines, more than 40 carbonyl species were found, of which 17 were identified. In SR1 leaves, 2-alkenals such as (E)-2-pentenal, acrolein, and (E)-2-hexenal were increased by 70–290% after 30 min-illumination. In the leaves of AER-tobaccos, light-dependent increase of these 2-alkenals was apparently lower. Thus the production of highly reactive 2-alkenals in leaves was enhanced under photooxidative stress. The tolerance to strong light due to the overexpression of AER can be explained by the scavenging of these species.

  • the involvement of Lipid Peroxide derived aldehydes in aluminum toxicity of tobacco roots
    Plant Physiology, 2010
    Co-Authors: Lina Yin, Junichi Mano, Shiwen Wang, Wataru Tsuji, Kiyoshi Tanaka
    Abstract:

    Oxidative injury of the root elongation zone is a primary event in aluminum (Al) toxicity in plants, but the injuring species remain unidentified. We verified the hypothesis that Lipid Peroxide-derived aldehydes, especially highly electrophilic α,β-unsaturated aldehydes (2-alkenals), participate in Al toxicity. Transgenic tobacco (Nicotiana tabacum) overexpressing Arabidopsis (Arabidopsis thaliana) 2-alkenal reductase (AER-OE plants), wild-type SR1, and an empty vector-transformed control line (SR-Vec) were exposed to AlCl3 on their roots. Compared with the two controls, AER-OE plants suffered less retardation of root elongation under AlCl3 treatment and showed more rapid regrowth of roots upon Al removal. Under AlCl3 treatment, the roots of AER-OE plants accumulated Al and H2O2 to the same levels as did the sensitive controls, while they accumulated lower levels of aldehydes and suffered less cell death than SR1 and SR-Vec roots. In SR1 roots, AlCl3 treatment markedly increased the contents of the highly reactive 2-alkenals acrolein, 4-hydroxy-(E)-2-hexenal, and 4-hydroxy-(E)-2-nonenal and other aldehydes such as malondialdehyde and formaldehyde. In AER-OE roots, accumulation of these aldehydes was significantly less. Growth of the roots exposed to 4-hydroxy-(E)-2-nonenal and (E)-2-hexenal were retarded more in SR1 than in AER-OE plants. Thus, the Lipid Peroxide-derived aldehydes, formed downstream of reactive oxygen species, injured root cells directly. Their suppression by AER provides a new defense mechanism against Al toxicity.

  • protection against photooxidative injury of tobacco leaves by 2 alkenal reductase detoxication of Lipid Peroxide derived reactive carbonyls
    Plant Physiology, 2005
    Co-Authors: Junichi Mano, Yoshimitsu Torii, Koichi Takimoto, Dirk Inze, Elena Babiychuk, Kozi Asada, Enric Bellesboix, Eiji Hiraoka, Luit Slooten, Sergei Kushnir
    Abstract:

    Degradation of Lipid Peroxides leads to the formation of cytotoxic 2-alkenals and oxenes (collectively designated reactive carbonyls). The novel NADPH-dependent oxidoreductase 2-alkenal reductase (AER; EC 1.3.1.74) from Arabidopsis (Arabidopsis thaliana), which is encoded by the gene At5g16970, catalyzes the reduction of the α,β-unsaturated bond of reactive carbonyls, and hence is presumed to function in antioxidative defense in plants. Here we show that Arabidopsis AER (At-AER) has a broad substrate spectrum to biologically relevant reactive carbonyls. Besides 2-alkenals, the enzyme recognized as substrates the Lipid Peroxide-derived oxenes 9-oxo-octadeca-(10E),(12Z)-dienoic acid and 13-oxo-octadeca-(9E),(11Z)-dienoic acid, as well as the potent genotoxin 4-oxo-(2E)-nonenal, altogether suggesting AER has a key role in the detoxification of reactive carbonyls. To validate this conclusion by in vivo studies, transgenic tobacco (Nicotiana tabacum) plants that had 100- to 250-fold higher AER activity levels than control plants were generated. The engineered plants exhibited significantly less damage from either (1) the exogenously administered 4-hydroxy-(2E)-nonenal, (2) treatment with methyl viologen plus light, or (3) intense light. We further show that the At-AER protein fused with the Aequorea victoria green fluorescent protein localizes in cytosol and the nucleus in Bright-Yellow 2 cells. These results indicate that reactive carbonyls mediate photooxidative injury in leaf cells, and At-AER in the cytosol protects the cells by reducing the α,β-unsaturated bond of the photoproduced reactive carbonyls.

  • the nadph quinone oxidoreductase p1 ζ crystallin in arabidopsis catalyzes the α β hydrogenation of 2 alkenals detoxication of the Lipid Peroxide derived reactive aldehydes
    Plant and Cell Physiology, 2002
    Co-Authors: Junichi Mano, Yoshimitsu Torii, Shunichiro Hayashi, Koichi Takimoto, Kenji Matsui, Kaoru Nakamura, Dirk Inze, Elena Babiychuk, Sergei Kushnir, Kozi Asada
    Abstract:

    P1-zeta-crystallin (P1-ZCr) is an oxidative stress-induced NADPH:quinone oxidoreductase in Arabidopsis thaliana, but its physiological electron acceptors have not been identified. We found that recombinant P1-ZCr catalyzed the reduction of 2-alkenals of carbon chain C-3-C-9 with NADPH. Among these 2-alkenals, the highest specificity was observed for 4-hydroxy-(2E)-nonenal (HNE), one of the major toxic products generated from Lipid Peroxides. (3Z)-Hexenal and aldehydes without alpha,beta-unsaturated bonds did not serve as electron acceptors. In the 2-alkenal molecules, P1-ZCr catalyzed the hydrogenation of alpha,beta-unsaturated bonds, but not the reduction of the aldehyde moiety, to produce saturated aldehydes, as determined by gas chromatography/mass spectrometry. We propose the enzyme name NADPH:2-alkenal alpha,beta-hydrogenase (ALH). A major portion of the NADPH-dependent HNE-reducing activity in A. thaliana leaves was inhibited by the specific antiserum against P1-ZCr, indicating that the endogenous P1-ZCr protein has ALH activity. Because expression of the P1-ZCr gene in A. thaliana is induced by oxidative stress treatments, we conclude that P1-ZCr functions as a defense against oxidative stress by scavenging the highly toxic, Lipid Peroxide-derived alpha,beta-unsaturated aldehydes.

Amal Ahmed Abd Elfattah - One of the best experts on this subject based on the ideXlab platform.

  • the effect of meclofenoxate with ginkgo biloba extract or zinc on Lipid Peroxide some free radical scavengers and the cardiovascular system of aged rats
    Pharmacological Research, 1998
    Co-Authors: Hana Alzuhair, Amal Ahmed Abd Elfattah, Moushira Ibrahim Elsayed
    Abstract:

    Aged rats are highly prone to many physiological changes such as blood pressure and heart rate. These changes could be due to modification in membrane phosphoLipid composition of their blood vessels. Lipid Peroxide in vivo has been identified as a basic deteriorative reaction in cellular mechanisms of aging in human. The effect of a nootropic drug, meclofenoxate (MF) or its combination with extract of ginkgo biloba (EGb-761) or zinc (Zn) on malondialdehyde (MDA) product as an index of endogenous Lipid peroxidation; phosphoLipid; glutathione (GSH) and protein thiols (PrSHs) contents as well as suPeroxide dismutase (SOD) activity in blood, brain, heart and liver of 24-month-old male rats was investigated. Aged rats were treated with MF once daily at oral doses of 100 mg kg-1 body wt. alone or with either EGb at a dose of 150 mg kg-1 body wt. or Zn at 10.5 mg kg-1 body wt. for 4 weeks. This study showed that aging caused a higher increment in MDA level of brain and heart than liver and plasma accompanied with reduction in brain and heart phosphoLipid contents as well as alteration of the antioxidant systems as compared to 4-month-old rats. Treatment of aged rats with MF alone or combined with either EGb or Zn caused improvement in the measured free radical scavengers especially in brain and heart tissues. Our results also showed that both EGb and Zn induced a significant potential effect of MF action on blood pressure and heart rate. The results were explained in the light of the antioxidant properties of EGb and Zn. Thus it is concluded that EGb and Zn have a beneficial role with MF in diminishing cumulative oxidative changes in aging.

  • Lipid Peroxide phosphoLipids glutathione levels and suPeroxide dismutase activity in rat brain after ischaemia effect of ginkgo biloba extract
    Pharmacological Research, 1995
    Co-Authors: Mona Seifelnasr, Amal Ahmed Abd Elfattah
    Abstract:

    The influence of ginkgo biloba extract on the Lipid Peroxide product (malondialdehyde, MDA), glutathione (GSH) and phosphoLipids levels as well as suPeroxide dismutase (SOD, 1.15.1.1) and lactate dehydrogenase (LDH, 1.1.1.27) activities in rat brain after occlusion of common carotid arteries was investigated. Two experimental models were studied: 60 min ischaemia without reperfusion and 60 min ischaemia followed by 60 min reperfusion. Compared to sham-operated animals, ischaemia followed by reperfusion increased cytosolic LDH activity and mitochondrial Lipid Peroxide content and decreased the suPeroxide dismutase activity and mitochondrial total phosphoLipids level. Preischaemic administration of ginkgo biloba extract (150 mg kg-1, p.o.) could normalize the SOD activity of the rat brain. The extract was also able to reduce the Lipid Peroxide and phosphoLipids contents of the mitochondrial rat brain. These effects could be explained on the basis of the antioxidant property of ginkgo biloba extract and suggests its beneficial role in the protection against post-ischaemic injury.

Kunio Yagi - One of the best experts on this subject based on the ideXlab platform.

  • difference in effects of classic and phosphoLipid hydroPeroxide glutathione peroxidases on liver Lipid Peroxide level in selenium deficient rats
    Iubmb Life, 1995
    Co-Authors: Jinyang Guan, Nobuko Ohishi, Sadaaki Komura, Kunio Yagi
    Abstract:

    When weanling male rats of the Wistar strain were fed a selenium-deficient diet, the activity of classic glutathione peroxidase (GPx) in liver cytosol decreased rapidly. In contrast, the activity of phosphoLipid hydroPeroxide GPx (PHGPx) in the cytosol decreased only slowly. Despite the marked decrease in classic GPx activity, the Lipid Peroxide level in the liver did not change until 6 weeks after the start of the feeding, whereas the level was significantly increased by 9 weeks, by which time PHGPx activity and its protein level had markedly diminished. These data indicate that PHGPx is much more crucial than classic GPx in preventing the elevation of liver Lipid Peroxide level in selenium-deficient rats.

  • effect of catecholestrogens on mortality and liver Lipid Peroxide level of mice irradiated with 60co γ ray
    Journal of Clinical Biochemistry and Nutrition, 1993
    Co-Authors: Akira Tomatsu, Nobuko Ohishi, Sadaaki Komura, M Nakanishi, Kunio Yagi
    Abstract:

    When 10 weeks old male BALB/c mice received whole-body irradiation with an 8-Gy single dose of 60Co γ-ray, the survival rate 30 days after the irradiation was only 5%, while the survival rate was increased to 70% when the mice were subcutaneously injected with catecholestrogen 2-hydroxyestradiol (2-OHE2) 3h before and 3h after the irradiation. The survival rates of the mice given other test compounds were as follows: 2-hydroxyestrone, 20%; 2-hydroxyestriol, 20%; 4-hydroxyestradiol, 0%; 2-methoxyestrone, 0%; 2-methoxyestradiol, 0%; 2-methoxyestriol, 0%; estrone, 0%; estradiol, 5%; and estriol, 20%. Upon the irradiation, Lipid Peroxide levels in the liver of the animals markedly increased 4 days after the irradiation. This increase in the level was significantly suppressed by the subcutaneous injection of 2-OHE2. These results indicate that 2-OHE2 has a protective effect against radiation injury.

M Hiramatsu - One of the best experts on this subject based on the ideXlab platform.

  • the efficacy of an antioxidant cocktail on Lipid Peroxide level and suPeroxide dismutase activity in aged rat brain and dna damage in iron induced epileptogenic foci
    Toxicology, 2000
    Co-Authors: M Komatsu, M Hiramatsu
    Abstract:

    Mixed natural antioxidants can be combined in a prophylactic food against age related disease involving reactive oxygen species. β-Catechin is an antioxidant drink, having free radical scavenging activities. It contains green tea extract as a main component as well as ascorbic acid, sunflower seed extract, dunaliella carotene and natural vitamin E. In the present study, we examined the effect of β-catechin on Lipid Peroxide formation and suPeroxide dismutase (SOD) activity in aged rat brain and the effect on 8-hydroxy-2′-deoxyguanosine (8-OHdG) in ipsilateral cortex, 30 min after ferric chloride solution was injected into the left cortex of rats. β-Catechin solution was orally administered to aged rats and normal rats for 1 month. One-month administration of β-catechin solution increased SOD activity in the mitochondria fraction of striatum and midbrain and decreased thiobarbiturate reactive substance formation in the cortex and cerebellum of aged rats. It also inhibited 8-OHdG formation in the ipsilateral cortex 30 min after injection of ferric chloride solution. These results suggest that β-catechin is a suitable prophylactic beverage against age-related neurological diseases associated with reactive oxygen species.

  • free radical scavenging activity of fermented papaya preparation and its effect on Lipid Peroxide level and suPeroxide dismutase activity in iron induced epileptic foci of rats
    Iubmb Life, 1998
    Co-Authors: Katsuki Imao, M Komatsu, H Wang, M Hiramatsu
    Abstract:

    Fermented papaya preparation is a natural health food that has been commercially sold in Japan for 2 years. It is made by yeast fermentation of Carica Papaya Linn. We examined the antioxidant action of the fermented papaya preparation on free radicals and Lipid peroxidation. Free radicals have been related with aging and diseases, such as cancer, diabetes and especially in neurological disorders, for example, Parkinson's disease or Alzheimer's disease. A diet including variable antioxidant foods may therefore help to prevent these illnesses. The free radical scavenging activity of the fermented papaya preparation was examined using an electron spin resonance (ESR) spectrometer. Fermented papaya preparation (50 mg/ml) scavenged 80% of hydroxyl radicals (.OH) as spin adducts of spin trap, 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) (5.27 x 10(15)spins/ml) generated by Fenton reagents. The value of IC50 was 12.5 mg/ml. The oral administration of the fermented papaya preparation for 4 weeks decreased the elevated of Lipid Peroxide levels in the ipsilateral 30 min after injection of iron solution by iron into the left cortex of rats. The fermented papaya preparation also increased suPeroxide dismutase activity in the cortex and hippocampus of them. These results suggest that the fermented papaya preparation has antioxidant actions and that it may be prophylactic food against the age related and neurological diseases associated with free radicals.

Joachim G Liehr - One of the best experts on this subject based on the ideXlab platform.

  • induction by estrogens of Lipid peroxidation and Lipid Peroxide derived malonaldehyde dna adducts in male syrian hamsters role of Lipid peroxidation in estrogen induced kidney carcinogenesis
    Carcinogenesis, 1995
    Co-Authors: Mian Ying Wang, Joachim G Liehr
    Abstract:

    Estrogen-induced kidney carcinogenesis in male Syrian hamsters has previously been postulated to be mediated by free radicals generated by redox cycling of catecholestrogen metabolites. As part of our examination of this hypothesis, we have studied the induction of Lipid peroxidation and Lipid Peroxide-derived malondialdehyde (MDA)-DNA adducts in kidney and liver of hamsters treated with single injections of diethylstilbestrol (DES) or with estradiol (E 2 ) implants for various lengths of time. Treatment of hamsters with 50 and 100 mg/kg DES increased concentrations of both Lipid hydroPeroxides and of MDA-DNA adducts. In hamsters treated with E 2 implants for up to 50 days, Lipid Peroxide levels in liver were double control values 3 h after hormone implantation, and then decreased to plateau values of 30% over controls. Those in kidney rose to 2- to 3-fold above controls 3 days after hormone implantation and then decreased to plateau values of 51% above controls. MDA-DNA adduct levels were two or three times higher than those of controls in liver and kidney of hamsters treated with hormone implants for 3 and 7 days. Renal Lipid Peroxide concentrations were raised by chronic treatment with E 2 , but not by weakly carcinogenic estrogens ethinylestradiol or 2-fluoroestradiol. In contrast, MDA-DNA adduct levels were raised by all three steroidal estrogens 3 days after estrogen implantation. The increases in Lipid Peroxides and in MDA-DNA adducts in estrogen-treated hamsters support a mechanism of carcinogenesis by free radical generation via redox cycling of catcholestrogen metabolites. Lipid Peroxides are postulated to play a dual role in estrogen-induced carcinogenesis, (i) as cofactors for cytochrome P450-mediated formation of catecholestrogen metabolites and their redox cycling, and (ii) as precursors of MDA, a DNA adduct-forming endogenous electrophile.

  • Lipid hydroPeroxide induced endogenous dna adducts in hamsters possible mechanism of Lipid hydroPeroxide mediated carcinogenesis
    Archives of Biochemistry and Biophysics, 1995
    Co-Authors: Mian Ying Wang, Joachim G Liehr
    Abstract:

    DNA of livers or kidneys of rodents contain endogenously modified nucleotides of as yet unknown structure or function. As part of our examination of the origin of endogenous DNA modifications, we examined polar adducts of hamster liver and kidney DNA by 32P-postlabeling analysis (central and upper cuts) and compared them to adducts generated by incubation of DNA with [9Z,11E,(13S)]-13-hydroperoxyoctadecadienoic acid or with malondialdehyde. The central and upper cuts of DNA adduct maps of intact female retired breeder hamsters contained one and three adducts called C1, U1, U2, and U3, respectively, which cochromatographed with similar adducts in DNA incubated with the hydroPeroxide or with malondialdehyde. Concentrations of adducts C1, U1, and U2 in organs of 1-month-old hamsters were lower than those in the 5-month-old female retired breeder hamsters. Adduct concentrations increased in tandem with Lipid Peroxide concentrations in livers and kidneys of hamsters treated with carbon tetrachloride compared to controls. A linear dependence of the concentrations of adducts on those of Lipid Peroxides was demonstrated independent of the treatment conditions or the organ examined. The polar endogenous adducts U1, U2, and U3 were identified by cochromatography in five different chromatographic systems with adducts induced by linoleic hydroPeroxide or malondialdehyde. Adducts U1, U2, or U3 were also formed by incubating malondialdehyde with dAMP or with dGMP, respectively. The dependence of adduct concentrations in vivo on Lipid Peroxide levels are taken as evidence that decomposition products of Lipid Peroxides such as malondialdehyde induced endogenous DNA adducts in intact animals. Moreover, these adducts may mediate carcinogenic processes induced by chemicals which raise Lipid Peroxide levels.