Dovydas Levinas
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Dovydas Levinas has a total of 11 co-authors. Here are the top co-authors by number of shared publications:
- Arunas Liekis
Neuroscience Institute, Lithuanian University of Health Sciences, Eiveniu St. 4, LT-50161 Kaunas, Lithuania
1 shared publication - Dale Baranauskiene
Neuroscience Institute, Lithuanian University of Health Sciences, Eiveniu St. 4, LT-50009 Kaunas, Lithuania
1 shared publication - Dale Viezeliene
Department of Biochemistry, Medical Academy, Lithuanian University of Health Sciences, A. Mickeviciaus St. 9, LT-44307 Kaunas, Lithuania
1 shared publication - Giedre Miniotaite
Neuroscience Institute, Lithuanian University of Health Sciences, Eiveniu St. 4, LT-50009 Kaunas, Lithuania
1 shared publication - Ilona Sadauskiene
Neuroscience Institute, Lithuanian University of Health Sciences, Eiveniu St. 4, LT-50161 Kaunas, Lithuania
1 shared publication - Inga Staneviciene
Department of Biochemistry, Medical Academy, Lithuanian University of Health Sciences, A. Mickeviciaus St. 9, LT-44307 Kaunas, Lithuania
1 shared publication
Latest Publications
- Open Access
- 2 June 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (11) , 9704
Effect of Organic Selenium on the Homeostasis of Trace Elements, Lipid Peroxidation, and mRNA Expression of Antioxidant Proteins in Mouse Organs
(1) In this study we determined the effect of long-term selenomethionine administration on the oxidative stress level and changes in antioxidant protein/enzyme activity; mRNA expression; and the levels of iron, zinc, and copper. (2) Experiments were performed on 4–6-week-old BALB/c mice, which were given selenomethionine (0.4 mg Se/kg b.w.) solution for 8 weeks. The element concentration was determined via inductively coupled plasma mass spectrometry. mRNA expression of SelenoP, Cat, and Sod1 was quantified using real-time quantitative reverse transcription. Malondialdehyde content and catalase activity were determined spectrophotometrically. (3) After long-term SeMet administration, the amount of Se increased by 12-fold in mouse blood, 15-fold in the liver, and 42-fold in the brain, as compared to that in the control. Exposure to SeMet decreased amounts of Fe and Cu in blood, but increased Fe and Zn levels in the liver and increased the levels of all examined elements in the brain. Se increased malondialdehyde content in the blood and brain but decreased it in liver. SeMet administration increased the mRNA expression of selenoprotein P, dismutase, and catalase, but decreased catalase activity in brain and liver. (4) Eight-week-long selenomethionine consumption elevated Se levels in the blood, liver, and especially in the brain and disturbed the homeostasis of Fe, Zn, and Cu. Moreover, Se induced lipid peroxidation in the blood and brain, but not in the liver. In response to SeMet exposure, significant up-regulation of the mRNA expression of catalase, superoxide dismutase 1, and selenoprotein P in the brain, and especially in the liver, was determined.
- 2 June 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (11) , 9704
Open AccessEffect of Organic Selenium on the Homeostasis of Trace Elements, Lipid Peroxidation, and mRNA Expression of Antioxidant Proteins in Mouse Organs
(1) In this study we determined the effect of long-term selenomethionine administration on the oxidative stress level and changes in antioxidant protein/enzyme activity; mRNA expression; and the levels of iron, zinc, and copper. (2) Experiments were performed on 4–6-week-old BALB/c mice, which were given selenomethionine (0.4 mg Se/kg b.w.) solution for 8 weeks. The element concentration was determined via inductively coupled plasma mass spectrometry. mRNA expression of SelenoP, Cat, and Sod1 was quantified using real-time quantitative reverse transcription. Malondialdehyde content and catalase activity were determined spectrophotometrically. (3) After long-term SeMet administration, the amount of Se increased by 12-fold in mouse blood, 15-fold in the liver, and 42-fold in the brain, as compared to that in the control. Exposure to SeMet decreased amounts of Fe and Cu in blood, but increased Fe and Zn levels in the liver and increased the levels of all examined elements in the brain. Se increased malondialdehyde content in the blood and brain but decreased it in liver. SeMet administration increased the mRNA expression of selenoprotein P, dismutase, and catalase, but decreased catalase activity in brain and liver. (4) Eight-week-long selenomethionine consumption elevated Se levels in the blood, liver, and especially in the brain and disturbed the homeostasis of Fe, Zn, and Cu. Moreover, Se induced lipid peroxidation in the blood and brain, but not in the liver. In response to SeMet exposure, significant up-regulation of the mRNA expression of catalase, superoxide dismutase 1, and selenoprotein P in the brain, and especially in the liver, was determined.