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A series of studies were conducted to examine the antioxidant status, drought and disease tolerance, and growth response to foliar application of soluble seaweed (Ascophyllum nodosum) extracts (SE) and humic acid (HA; 25% active HA or 2.9% active HA) in tall fescue (Festuca arundinacea Schreb), Kentucky bluegrass (Poa pratensis L.) and creeping bentgrass (Agrostis palusttis Huds.) grown under low (-0.5 MPa) and high (-0.03 MPa) soil moisture environments. Foliar application of humic acid (2.9 % active HA) at 23.7 and 47.4 l/ha improved leaf water status, shoot and root development in tall fescue, Kentucky bluegrass and creeping bentgrass grown under drought. Humic acid (2.9% active HA) at 15.5 l/ha or SE at 326 g/ha significantly reduced dollarspot incidence and improved turf quality in creeping bentgrass. Drought stress induced an increase of antioxidants alpha-tocopherol and ascorbic acid concentrations in the three turfgrass species. In the experiment with Kentucky bluegrass, drought stress increased beta-carotene concentration, but did not significantly influence superoxide dismutase (SOD) activity. Foliar application of humic acid (25% active HA) at 5 l/ha and/or SE at 326 g/ha consistently enhanced alpha-tocopherol and ascorbic acid concentrations, leaf water status, and growth in the three cool-season turfgrass species grown under low and high soil moisture environments. In the experiment with Kentucky bluegrass, application of HA at 5 l/ha plus SE at 326 g/ha also increased beta-carotene content and SOD activity under low and high soil moisture environments. There were close positive correlations between the antioxidant status and shoot or root growth in the three turfgrass species regardless of soil moisture levels. The antioxidant SOD activity, photosynthetic capacity in terms of Fvm690, and chlorophyll content in terms of Fm730/Fm690 exhibited a seasonal fluctuation in endophyte [Neotiphodium coenophialum (Morgan Jones and Gams) Glenn, Bacon, Price and Hanlin] -free and endophyte-infected tall fescue. Application of SE enhanced SOD activity, photosynthetic capacity, and chlorophyll content in tall fescue, especially at 4 weeks after SE treatment. The SOD activity, photosynthetic capacity and chlorophyll content were not significantly influenced by the endophyte infection. A close positive correlation between SOD and photosynthetic capacity during the summer was found in endophyte-free and endophyte-infected tall fescue. / Ph. D.

京都大学 / 新制・課程博士 / 博士(工学) / 甲第25311号 / 工博第5270号 / 京都大学大学院工学研究科合成・生物化学専攻 / (主査)教授 杉野目 道紀, 教授 中尾 佳亮, 教授 石田 直樹 / 学位規則第4条第1項該当 / Doctor of Philosophy (Engineering) / Kyoto University / DFAM

Thesis (Ph. D.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains x, 210 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 154-185).

Thesis (Ph. D.)--University of Texas at Austin, 2008. / Vita. Includes bibliographical references.

Thesis (doctoral)--Lund University, 1994.

The extent to which endogenous free radical-scavenging defense mechanisms are involved in experimental and human diabetes was investigated in various tissues of animals with chemically-induced or spontaneous diabetes (BB Wistar rats) and in erythrocytes of patients with either Type I or Type II diabetes. Diabetes was induced in female Wistar rats using alloxan (ALX) or streptozotocin (STZ), each administered in a dose of 50 mg/kg body wt., intravenously. The present study also included a group -of animals in which body wt. loss was induced by food-deprivation for 72 h. The effects of pharmacological interventions (insulin or allopurinol (ALP)), on these processes were also investigated in chemically-induced diabetes., The activities of catalase (CAT), CuZn-superoxide dismutase (CuZn-SOD), glutathione peroxidase (GSH-PX) and glutathione reductase (GSSG-RD) as well as levels of reduced glutathione (GSH) were examined in heart, pancreas, liver and kidney as well as in erythrocytes. Erythrocytes were also examined for their susceptibility to in vitro oxidative stress induced by hydrogen peroxide (H₂0₂). Criteria studied in this regard were GSH-depletion and malondi-aldehyde (MDA) production (an index of lipid peroxidation). The results obtained showed that tissue antioxidant systems are altered in experimental diabetes and that the magnitude of the alterations increased with the degree of body weight loss. Furthermore, the duration of hypoinsulinemia might contribute to the nature of alterations in antioxidant mechanisms. The complex patterns of the alterations observed varied from one tissue to another and may be the result of compensatory increases, usually involving enzymes whose activity in the particular tissue may be limiting, and direct inhibitory effects of endogenous oxidants on the enzymatic components of tissue antioxidant systems. The ability of insulin (9-12 U/kg body wt., subcutaneously) to reverse the many similar alterations of tissue antioxidant enzymes in diabetes induced by either STZ or ALX suggests that these changes are more likely attributable to hypoinsulinemia rather than to direct effects of either diabetogenic drug. The above-mentioned effects indicate that insulin can markedly influence tissue antioxidant status. However, the reason for the persistence of decreased CuZn-SOD activity in both liver and kidney of ALX-diabetic rats after 12 wk of treatment with insulin is not clear at present, and requires further investigation to determine whether this reflects the presence of a residual deficit in tissue antioxidant processes in liver and kidney despite insulin treatment, or whether it is the result of a direct effect exerted by ALX. Acute ALP administration (50 mg/kg body wt., intraperitoneally) was associated with reductions in ketonuria and early mortality among ALX-diabetic rats, and long-term ALP treatment (1.9 mg/day in drinking water) resulted in a normalization of renal CuZn-SOD activity in these animals. Comparable (although not identical) changes in tissue antioxidant status are present in insulin-dependent spontaneously diabetic BB (ISDBB) rats and in animals made diabetic by STZ or ALX administration. Our data also demonstate that the alterations in tissue GSH levels characterizing ALX-diabetes more closely paralleled changes seen in the ISDBB rat than did those in the diabetic state induced by STZ. If the alterations in antioxidant status in uncontrolled chemically-induced diabetes are attributable to a lack of insulin, the observed changes in ISDBB rats are suggestive of sub-optimal insulin therapy in these animals. The results obtained from BB rats demonstrate two types of alterations in antioxidant status: strain-related differences (increased CAT activity in pancreas and decreased GSH levels in pancreas and liver of both ISDBB and their non-diabetic littermates (NDLM)) and diabetes-related changes (mani- fested by an increase in cardiac GSH content and increases in activities of cardiac CAT and GSSG-RD, pancreatic CuZn-SOD and GSSG-RD, and renal GSH-PX). Whether or not these "strain-related" alterations in antioxidant status increase the susceptibility of these animals to developing diabetes remains unknown. Certain alterations were observed in red cells from diabetic patients and from animals with experimental diabetes suggesting that these alterations are more likely to be diabetes-related than species-dependent. Red cells in chemically-induced and clinical diabetes showed an increased resistance to peroxide-induced depletion of GSH, an effect attributed to hyperglycemia, which results in an increased supply of NADPH through the hexose monophosphate shunt for regeneration of GSH from GSSG via the GSSG-RD system. However, the susceptibility of red cells from diabetic patients and animals to lipid peroxidative damage was increased as reflected in augmented MDA production. In addition, insulin treatment did not normalize MDA production in red cells subjected to oxidative challenge and vigorous insulin treatment in both ALX- and STZ-diabetic rats resulted in a markedly decreased MDA production in response to H₂0₂. Moreover, GSSG-RD activity of red cells was increased in both uncontrolled and insulin-treated diabetic animals as well as in diabetic patients. However, some differences in erythrocyte antioxidant enzymes were also observed in erythrocytes from diabetic subjects and animals. For example, diabetic patients showed an increased activity of CuZn-SOD, while erythrocytes from diabetic animals showed no alterations in the activity of this enzyme. Erythrocyte membrane NADH-dehydrogenase activity was increased only in diabetic patients with Type I diabetes, but not in Type II diabetes or in diabetic animals. Erythrocytes from ALX- and STZ-diabetic animals showed an increase in the activity of GSH-PX and those from NDLM BB rats showed a decrease in CAT activity, alterations that were not observed in human diabetes. Finally, as far as antioxidant defense mechanisms are concerned, our results suggest that diabetes is associated with some common alterations in these mechanisms regardless of the model (chemically-induced versus the spontaneous type of diabetes) or the species used (animal versus human diabetes). Some of these alterations seem to be influenced by the degree of diabetic control, while others are apparently independent of it. Future studies will focus on the extent to which alterations in red cells of human diabetics can be used to predict the development of long-term sequelae of the disease. / Medicine, Faculty of / Anesthesiology, Pharmacology and Therapeutics, Department of / Graduate

Within the PhD. thesis the problems of H-transfer from selected types of phenols, aromatic secondary amines and compounds with acidic CH bond were investigated. This process was initiated by the action of redox agents, mostly PbO2, in nonpolar solvents. The abstraction of hydrogen atom results in the formation of radical intermediates, which were detected by EPR spectroscopy. Because in most cases, highly unstable radicals were produced, it was neccessary to apply the technique of indirect detection, so called spin trapping. This method enables to interpret the character of generated radicals on the basis of EPR parameters of radical adducts, which are formed by their reaction with suitably chosen compounds, spin traps, which are added to the reaction system. As spin traps, the aromatic nitrosocompounds were preferentially used. Due to the fact that EPR spectra of radical adducts were in most cases very complex, their interpretation was possible only using the computer simulation. Based on this approach, new information about the character of addition of phenoxyl tradicals to aromatic nitrosocompounds, stability of alkyl substituents in methyl substituted phenols and character of C-radicals, generated from substituted coumarines and beta-diketones, was obtained. Simultaneously, the small ability of nitrogen radicals, primary products of the splitting of NH bond, to enter the reaction with spin traps was proved by aromatic secondary amines.

NiSi and Ni(Pt)Si, and of the effects of dissociated ammonia on oxide reduction was carried out under controlled ultrahigh vacuum (UHV) conditions. X-ray photoelectron spectroscopy (XPS) has been used to characterize the evolution of surface composition. Vicinal surfaces on NiSi and Ni(Pt)Si were formed in UHV by a combination of Ar+ sputtering and thermal annealing. Oxidation of these surfaces in the presence of either O+O2 or pure O2 at room temperature results in the initial formation of a SiO2 layer ~ 7 Å thick. Subsequent exposure to O2 yields no further oxidation. Continued exposure to O+O2, however, results in rapid silicon consumption and, at higher exposures, the kinetically-driven oxidation of the transition metal(s), with oxides >35Ǻ thick formed on all samples, without passivation. The addition of Pt retards but does not eliminate oxide growth or Ni oxidation. At higher exposures, in Ni(Pt)Si surface the kinetically-limited oxidation of Pt results in Pt silicate formation. Substrate dopant type has almost no effect on oxidation rate. Reduction of the silicon oxide/metal silicate is carried out by reacting with dissociated NH3 at room temperature. The reduction from dissociated ammonia (NHx+H) on silicon oxide/ metal silicate layer shows selective reduction of the metal oxide/silicate layer, but does not react with SiO2 at ambient temperature.