J
Ján Lehotský
Researcher at Comenius University in Bratislava
Publications - 75
Citations - 1821
Ján Lehotský is an academic researcher from Comenius University in Bratislava. The author has contributed to research in topics: Ischemia & Endoplasmic reticulum. The author has an hindex of 24, co-authored 68 publications receiving 1627 citations. Previous affiliations of Ján Lehotský include Jessenius Faculty of Medicine & Academy of Sciences of the Czech Republic.
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The Molecular and Cellular Effect of Homocysteine Metabolism Imbalance on Human Health
Henrieta Škovierová,Eva Vidomanová,Silvia Mahmood,Janka Sopková,A Drgova,Tatiana Červeňová,Erika Halasova,Ján Lehotský +7 more
TL;DR: This review represents the current understanding of molecular mechanism of Hcy metabolism and its link to hyperhomocysteinemia-related pathologies in humans and examines the role of H Cy in thiolation of proteins, which results in their molecular and functional modifications.
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Effects of aging on activities of mitochondrial electron transport chain complexes and oxidative damage in rat heart.
Zuzana Tatarkova,Stanislav Kuka,Peter Racay,Ján Lehotský,Dusan Dobrota,Dušan Mištuna,Peter Kaplan +6 more
TL;DR: The present study suggests that non-uniform decline in activities of ETC complexes is due, at least in part, to mitochondrial oxidative damage; however, lipid peroxidation products appear to have a limited impact on enzyme functions.
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Role of Homocysteine in the Ischemic Stroke and Development of Ischemic Tolerance
Ján Lehotský,Barbara Tothova,Maria Kovalska,Dusan Dobrota,Anna Beňová,Dagmar Kalenska,Peter Kaplan +6 more
TL;DR: This review documents an increased oxidative stress and functional modification of enzymes involved in redox balance in experimentally induced hyperhomocysteinemia and describes the changes in the mitogen-activated protein kinase (MAPK) protein pathways following ischemic injury and IPC.
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Membrane ion transport systems during oxidative stress in rodent brain : protective effect of stobadine and other antioxidants
TL;DR: Stobadine (ST) seems to be at least as affective as BHT and 21-aminosteroids, and more potent than tocopherol acetate, and in combination with glutathione enhanced ST antioxidant efficacy, so drug combination might be beneficial therapeutically.
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Ischemic tolerance: the mechanisms of neuroprotective strategy.
TL;DR: It seems that the mechanisms of ischemic tolerance‐delayed postconditioning could be used not only after ischemia but also in some other processes leading to apoptosis, since pre‐ or post‐conditioners can be used plenty of harmful stimuli and some physiological compounds, such as norepinephrine, bradykinin.