Biomedical subjects

N Gedik

Publications and source records attributed to N Gedik.

7 recordsLinked to original sources

PubMed2006

L-Carnitine ameliorates methotrexate-induced oxidative organ injury and inhibits leukocyte death.

Methotrexate (MTX), a folic acid antagonist widely used for the treatment of a variety of tumors and inflammatory diseases, affects normal tissues that have a high rate of proliferation, including the hematopoietic cells of the bone marrow and the gastrointestinal mucosal cells. To elucidate the role of free radicals and leukocytes in MTX-induced oxidative organ damage and the putative protective effect of L-carnitine (L-Car), Wistar albino rats were administered a single dose of MTX (20 mg/kg) followed by either saline or L-Car (500 mg/kg) for 5 days. After decapitation of the rats, trunk blood was obtained, and the ileum, liver, and kidney were removed for histological examination and for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and collagen content. Our results showed that MTX administration increased the MDA and MPO activities and collagen content and decreased GSH levels in all tissues, while these alterations were reversed in L-Car-treated group. The elevated serum TNF-alpha level observed following MTX treatment was depressed with L-Car. The oxidative burst of neutrophils stimulated by Annexin V was reduced in the saline-treated MTX group, while L-Car abolished this inhibition. Similarly, flow cytometric measurements revealed that leukocyte apoptosis was increased in MTX-treated animals, while L-Car reversed these effects. Severe degeneration of the intestinal mucosa, liver parenchyma, and glomerular and tubular epithelium observed in the saline-treated MTX group was improved by L-Car treatment. These results suggest that L-Car, possibly via its free radical scavenging and antioxidant properties, ameliorates MTX-induced oxidative organ injury and inhibits leukocyte apoptosis. Thus, supplementation with L-Carnitine as an adjuvant therapy may be promising in alleviating the systemic side-effects of chemotherapeutics.

Animals↗

PubMed2006

Propylthiouracil-induced hypothyroidism protects ionizing radiation-induced multiple organ damage in rats.

The objective of this study was to examine the potential radioprotective properties of propylthiouracil (PTU)-induced hypothyroidism against oxidative organ damage induced by irradiation. Sprague-Dawley rats were pre-treated with saline or PTU (10 mg/kg i.p.) for 15 days, and were then exposed to whole-body irradiation (800 cGy). A group of rats were decapitated at 6 h after exposure to irradiation, while another group was followed for 72 h after irradiation, during which saline or PTU injections were repeated once daily. Lung, liver, kidney and ileum samples were obtained for the determination of malondialdehyde (MDA; an index of lipid peroxidation) and glutathione (GSH, an antioxidant) levels, myeloperoxidase activity (MPO; an index of tissue neutrophil accumulation) and collagen contents, while oxidant-induced DNA fragmentation was evaluated in the ileal tissues. All tissues were also examined microscopically and assayed for the production of reactive oxidants using chemiluminescence (CL). Lactate dehydrogenase (LDH), an indicator of tissue damage, and tumour necrosis factor-alpha (TNFalpha) were assayed in serum samples. Irradiation caused a significant decrease in GSH level, which was accompanied by significant increases in MDA levels, MPO activity, CL levels and collagen content of the tissues studied (P<0.05-0.001). Similarly, serum TNFalpha and LDH were elevated in the irradiated rats as compared with the control group. On the other hand, PTU treatment reversed all these biochemical indices, as well as histopathological alterations induced by irradiation. Our results suggested that PTU-induced hypothyroidism reduces oxidative damage in the lung, hepatic, renal and ileal tissues probably due to hypometabolism, which is associated with decreased production of reactive oxygen metabolites and enhancement of antioxidant mechanisms.

Animals↗

PubMed2005

Observation of spin Coulomb drag in a two-dimensional electron gas.

An electron propagating through a solid carries spin angular momentum in addition to its mass and charge. Of late there has been considerable interest in developing electronic devices based on the transport of spin that offer potential advantages in dissipation, size and speed over charge-based devices. However, these advantages bring with them additional complexity. Because each electron carries a single, fixed value (- e) of charge, the electrical current carried by a gas of electrons is simply proportional to its total momentum. A fundamental consequence is that the charge current is not affected by interactions that conserve total momentum, notably collisions among the electrons themselves. In contrast, the electron's spin along a given spatial direction can take on two values, +/- [planck]/2 (conventionally upward arrow, downward arrow), so that the spin current and momentum need not be proportional. Although the transport of spin polarization is not protected by momentum conservation, it has been widely assumed that, like the charge current, spin current is unaffected by electron-electron (e-e) interactions. Here we demonstrate experimentally not only that this assumption is invalid, but also that over a broad range of temperature and electron density, the flow of spin polarization in a two-dimensional gas of electrons is controlled by the rate of e-e collisions.

Journal Article↗

PubMed2005

Abrupt transition in quasiparticle dynamics at optimal doping in a cuprate superconductor system.

We report time-resolved measurements of the photoinduced change in reflectivity, DeltaR, in the Bi2Sr2Ca(1-y)Dy(y)Cu2O8+delta (BSCCO) system of cuprate superconductors as a function of hole concentration. We find that the kinetics of quasiparticle decay and the sign of DeltaR both change abruptly where the superconducting transition temperature T(c) is maximal. These coincident changes suggest that a sharp transition in quasiparticle dynamics takes place precisely at optimal doping in the BSCCO system.

Journal Article↗

PubMed2005

Ghrelin against alendronate-induced gastric damage in rats.

Alendronate sodium, a primary amino bisphosphonate, is widely used in the treatment of various diseases that are associated with bone resorption, such as postmenopausal osteoporosis and Paget's disease of bone. Although the adverse effects of biphosphonates on the gastrointestinal system have been demonstrated in experimental and clinical studies, the exact mechanisms underlying this damage are not clear yet. Ghrelin, a 28 amino acid peptide produced predominantly by the stomach, was shown to exert a potent protective action on the stomach of rats exposed to ethanol or stress. Our objective was to evaluate the possible anti-oxidant and anti-inflammatory effects of ghrelin against alendronate-induced gastric damage. Wistar albino rats were administered alendronate (20 mg/kg) by gavage for 4 days, along with either ghrelin (10 ng/kg per day) or saline given i.p. After decapitation, stomach tissues were removed for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and tissue collagen content, while the extent of tissue damage was analyzed microscopically. Formation of reactive oxygen species was determined by chemiluminesence using a luminol probe in fresh gastric tissues. Serum tumor necrosis factor (TNF-alpha) and lactate dehydrogenase levels were assessed in trunk blood. Oral administration of alendronate-induced significant gastric damage, accompanied by increased MPO activity, collagen content, MDA and luminol levels (P < 0.01-P < 0.001), while tissue GSH was decreased (P < 0.01). On the other hand, ghrelin treatment reversed these alterations (P < 0.05-P < 0.001) as well as elevating serum TNF-alpha levels significantly (P < 0.001). The findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect, and ghrelin ameliorates this damage by its possible antioxidant and anti-inflammatory properties.

Administration, Oral↗

PubMed2003

Diffusion of nonequilibrium quasi-particles in a cuprate superconductor.

We report a transport study of nonequilibrium quasi-particles in a high-transition-temperature cuprate superconductor using the transient grating technique. Low-intensity laser excitation (at a photon energy of 1.5 electron volts) was used to introduce a spatially periodic density of quasi-particles into a high-quality untwinned single crystal of YBa2Cu3O6.5. Probing the evolution of the initial density through space and time yielded the quasi-particle diffusion coefficient and the inelastic and elastic scattering rates. The technique reported here is potentially applicable to precision measurements of quasi-particle dynamics not only in cuprate superconductors but in other electronic systems as well.

Journal Article↗

PubMed2002

Photoinduced changes of reflectivity in single crystals of YBa2Cu3O6.5 (ortho II).

We report measurements of the photoinduced change in reflectivity of an untwinned single crystal of YBa2Cu3O6.5 in the ortho II structure. The decay rate of the transient change in reflectivity is found to decrease rapidly with decreasing temperature and, below T(c), with decreasing laser intensity. We interpret the decay as a process of thermalization of antinodal quasiparticles, with a rate determined by inelastic scattering of quasiparticle pairs.

Journal Article↗