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BÜYÜKUYSAL, RİFAT LEVENT

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BÜYÜKUYSAL

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RİFAT LEVENT

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    Biochemical changes in hemolymph of spinning and non-spinning silkworm larvae, bombyx mori (l., 1758) (Lepidoptera: Bombycidae), reared on fresh mulberry leaves: Possible reasons for non-spinning syndrome
    (Ege Üniversitesi, 2020-01-01) Şahan, Ümran; Gül, Zülfiye; Büyükuysal, Levent Rıfat; ŞAHAN, ÜMRAN; BÜYÜKUYSAL, RİFAT LEVENT; Bursa Uludağ Üniversitesi/Ziraat Fakültesi/Zootekni Bölümü; Bursa Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Farmakoloji Anabilim Dalı; AAH-2966-2021; IKI-0689-2023
    Non-spinning syndrome in Bombyx mori (L., 1758) (Lepidoptera: Bombycidae) is a serious issue for the sericulture industry. Determination of urea metabolism as an important parameter at the onset of spinning has shown the need for examining the role of urea metabolism in the non-spinning syndrome. The aim of this study was to investigate role of urea metabolism in the non-spinning syndrome by evaluating urease activity and L-arginine concentrations in the silkworm hemolymph and mulberry leaves. Additionally, urea concentrations were determined in hemolymph samples. Urease activities in hemolymph samples were almost twice as high in spinning larvae (SL) than in non-spinning larvae, 25 +/- 5.8 vs 10.9 +/- 2.4 units/l (P < 0.05). Urea concentrations in the SL hemolymph decreased significantly from day 5 (137 +/- 13 mg/l) to day 7 (97 +/- 17 mg/l) of the fifth instar (P < 0.01), it remained almost constant in NSL hemolymph (149 +/- 19 to 167 +/- 4 mg/l). Additionally, L-arginine concentrations in hemolymph samples obtained from NSL of 4.55 +/- 0.48 mM were significantly higher than in SL at 2.72 +/- 0.45 mM (P < 0.01). Changes in urease activity and L-arginine concentrations in hemolymph were similarly observed in mulberry leaves. These results suggested that changes in urea metabolism may cause or contribute to non-spinning syndrome in silkworms.
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    Glutamate-induced modulation in energy metabolism contributes to protection of rat cortical slices against ischemia-induced damage
    (Lippincott Williams & Wilkins, 2021-01-13) Gül, Zülfiye; Büyükuysal, R. Levent; BÜYÜKUYSAL, RİFAT LEVENT; 0000-0002-8872-0074; AAH-1657-2021
    Objectives: Glutamate excitotoxicity contributes to neurodegeneration during cerebral ischemia. Recent studies in the protective effect of glutamate against ischemia and hypoxia have shown the need for questioning the role of glutamate in energy metabolism during ischemia. Current study investigates the effect of glutamate on energy substrate metabolites such as alpha-ketoglutarate, lactate, and pyruvate release during control, oxygen-glucose deprivation (OGD), and reoxygenation (REO) conditions. Methods: The effects of 0.5 and 2 mM glutamate on spontaneous alpha-ketoglutarate, lactate, and pyruvate release were tested in vitro, on acute rat cortical slices. Alpha-ketoglutarate, lactate, and pyruvate levels were determined by HPLC with UV detector. Results: We observed that glutamate added into medium significantly increased alpha-ketogluarate release under control conditions. Although OGD and REO also had a glutamate-like effect, only REO-induced rise further enhanced by glutamate. In contrast to alpha-ketoglutarate, both OGD and REO conditions caused significant declines in pyruvate and lactate outputs. While OGD and REO-induced declines in pyruvate outputs were further potentiated, lactate output was not altered by glutamate added into the medium. Glutamate and alpha-ketoglutarate, moreover, also ameliorated OGD- and REO-induced losses in 2,3,5-triphenyltetrazolium chloride staining with a similar degree. Conclusion: These results indicate that glutamate probably increases alpha-ketoglutarate production as an alternative energy source for use in the TCA cycle under energy-depleted conditions. Thus, increasing the alpha-ketoglutarate production may represent a new therapeutic intervention for neurodegenerative disorders, including cerebral ischemia.
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    Temel farmakoloji: farmakokinetik prensipler ve hesaplamalar, advers ilaç reaksiyonları ve fitoterapi
    (Uludağ Üniversitesi Tıp Fakültesi , 2024) BÜYÜKUYSAL, RİFAT LEVENT; 0000-0003-0749-2426; AAH-1657-2021