Rotenone complex i mutants-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli
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PROVIDER: PRJNA481580 | ENA |
REPOSITORIES: ENA
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Project description:ra16-03_rotenone - rotenone - How does inhibition of CI enhance organogenesis? - NA
2019-01-01 | GSE107673 | GEO
Project description:rotenone-Effect of the inhibition of the mitochondrial respiratory chain complex I (CI) on shoot initiation on protoplast-derived calli
| PRJNA421272 | ENA
Project description:ra16-03_rotenone - rotenone_complex i mutants - How does inhibition of CI enhance organogenesis
2019-01-01 | GSE117269 | GEO
Project description:Rotenone is a naturally occurring toxic substance from the Leguminosa plant and belongs to the group of compounds known as rotenoids (Bové et al., 2005). It is commercially used as a pesticide and is epidemiologically linked to PD. Being lipophilic, rotenone can diffuse across biological membranes in the body and gain entry to all the organs and cells (Bové et al., 2005). Rotenone can bind to complex I of the electron transport chain (ETC) and inhibit the enzymatic activity of the NADH-ubiquinone reductase (Schuler and Casida, 2001). This interferes with the oxidation phosphorylation process, and eventually causes cell damage via oxidative stress. Rotenone may also cause the depolymerisation of microtubules into tubulin monomers (Marshall and Himes, 1978). Accumulation of tubulin monomers is potentially cytotoxic, and it is believed that parkin reverses cytotoxicity by ubiquitinating these monomers and targeting them for proteasome degradation (Ren et al., 2003.). Unfortunately, in PD patients with parkin mutations, this is not possible and tubulin accumulates to harmful levels in the cells. A total of 13 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 10nM rotenone over a time-course of 8h, 15h and 24h (n=3) in addition to the vehicle control (n=4).
2013-12-31 | E-GEOD-22997 | biostudies-arrayexpress
Project description:We investigated an subacute study in male Wistar rats, treated daily with 400 ppm rotenone for 1, 3, or 14 consecutive days, followed by necropsy 24h after the last application. Rotenone is a strong mitochondrial respiratory chain complex I inhibitor. Inhibitors of complex I are suggested to exert anti-tumor activity of those tumors relying on oxidative metabolism and are therefore of interest in oncology research. Nevertheless, the safety profile of these inhibitors needs to be rigorously assessed. Rotenone has shown anti-carcinogenic activity in several studies. In this context we used rotenone in our study as tool compound with the aim to identify suitable biomarker candidates and enhance mechanistic insights into the biologic and cellular effects of complex I inhibitors at the organ level after in vivo treatment. Various parameters, including hematology, clinical chemistry and histopathology, major blood cell population phenotyping using FACS and enzymatic activity assays were measured and/or evaluated. Moreover gene expression profiles were determined to investigate pathways and functions affected by rotenone at the molecular level. As organs, liver, heart and brain stem were chosen due to the high metabolic activity, the high energy demand and due to the known neurotoxic effect of rotenone, respectively. The strongest rotenone-induced effects on gene expression were observed in the liver (1444 deregulated genes) compared to heart (650 deregulated genes) and brain stem (52 deregulated genes). These findings, together with the histopathological results, show that liver is a target organ of rotenone.
2017-01-02 | GSE86352 | GEO
Project description:We investigated an subacute study in male Wistar rats, treated daily with 400 ppm rotenone for 1, 3, or 14 consecutive days, followed by necropsy 24h after the last application. Rotenone is a strong mitochondrial respiratory chain complex I inhibitor. Inhibitors of complex I are suggested to exert anti-tumor activity of those tumors relying on oxidative metabolism and are therefore of interest in oncology research. Nevertheless, the safety profile of these inhibitors needs to be rigorously assessed. Rotenone has shown anti-carcinogenic activity in several studies. In this context we used rotenone in our study as tool compound with the aim to identify suitable biomarker candidates and enhance mechanistic insights into the biologic and cellular effects of complex I inhibitors at the organ level after in vivo treatment. Various parameters, including hematology, clinical chemistry and histopathology, major blood cell population phenotyping using FACS and enzymatic activity assays were measured and/or evaluated. Moreover gene expression profiles were determined to investigate pathways and functions affected by rotenone at the molecular level. As organs, liver, heart and brain stem were chosen due to the high metabolic activity, the high energy demand and due to the known neurotoxic effect of rotenone, respectively. The strongest rotenone-induced effects on gene expression were observed in the liver (1444 deregulated genes) compared to heart (650 deregulated genes) and brain stem (52 deregulated genes). These findings, together with the histopathological results, show that liver is a target organ of rotenone.
2017-01-02 | GSE86350 | GEO
Project description:We investigated an subacute study in male Wistar rats, treated daily with 400 ppm rotenone for 1, 3, or 14 consecutive days, followed by necropsy 24h after the last application. Rotenone is a strong mitochondrial respiratory chain complex I inhibitor. Inhibitors of complex I are suggested to exert anti-tumor activity of those tumors relying on oxidative metabolism and are therefore of interest in oncology research. Nevertheless, the safety profile of these inhibitors needs to be rigorously assessed. Rotenone has shown anti-carcinogenic activity in several studies. In this context we used rotenone in our study as tool compound with the aim to identify suitable biomarker candidates and enhance mechanistic insights into the biologic and cellular effects of complex I inhibitors at the organ level after in vivo treatment. Various parameters, including hematology, clinical chemistry and histopathology, major blood cell population phenotyping using FACS and enzymatic activity assays were measured and/or evaluated. Moreover gene expression profiles were determined to investigate pathways and functions affected by rotenone at the molecular level. As organs, liver, heart and brain stem were chosen due to the high metabolic activity, the high energy demand and due to the known neurotoxic effect of rotenone, respectively. The strongest rotenone-induced effects on gene expression were observed in the liver (1444 deregulated genes) compared to heart (650 deregulated genes) and brain stem (52 deregulated genes). These findings, together with the histopathological results, show that liver is a target organ of rotenone.
2017-01-02 | GSE86351 | GEO
Project description:Rotenone is a naturally occurring toxic substance from the Leguminosa plant and belongs to the group of compounds known as rotenoids (Bové et al., 2005). It is commercially used as a pesticide and is epidemiologically linked to PD. Being lipophilic, rotenone can diffuse across biological membranes in the body and gain entry to all the organs and cells (Bové et al., 2005). Rotenone can bind to complex I of the electron transport chain (ETC) and inhibit the enzymatic activity of the NADH-ubiquinone reductase (Schuler and Casida, 2001). This interferes with the oxidation phosphorylation process, and eventually causes cell damage via oxidative stress. Rotenone may also cause the depolymerisation of microtubules into tubulin monomers (Marshall and Himes, 1978). Accumulation of tubulin monomers is potentially cytotoxic, and it is believed that parkin reverses cytotoxicity by ubiquitinating these monomers and targeting them for proteasome degradation (Ren et al., 2003.). Unfortunately, in PD patients with parkin mutations, this is not possible and tubulin accumulates to harmful levels in the cells.
2013-12-31 | GSE22997 | GEO
Project description:This experiment aimed to identify protoplast-induced genes in tomato seedling, for future use in single cell datasets.
2023-10-01 | GSE212404 | GEO