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{{Abstract | {{Abstract | ||
|title=[[File:Chakrabarti S.JPG|left|100px|Chakrabarti Sasanka]] Ganguly U, Bir A, <u>Chakrabarti Sasanka</u> (2022) Cytotoxicity of mitochondrial Complex I inhibitor rotenone: a complex interplay of cell death pathways. Bioblast 2022: BEC Inaugural Conference.<br>[[ | |title=[[File:Chakrabarti S.JPG|left|100px|Chakrabarti Sasanka]] Ganguly U, Bir A, <u>Chakrabarti Sasanka</u> (2022) Cytotoxicity of mitochondrial Complex I inhibitor rotenone: a complex interplay of cell death pathways. Bioblast 2022: BEC Inaugural Conference.<br>[[Ganguly 2022 MitoFit|»''MitoFit Preprint''«]] | ||
|info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference] | |info=[https://wiki.oroboros.at/index.php/Bioblast_2022#Submitted_abstracts Bioblast 2022: BEC Inaugural Conference] | ||
Revision as of 12:47, 20 May 2022
Ganguly U, Bir A, Chakrabarti Sasanka (2022) Cytotoxicity of mitochondrial Complex I inhibitor rotenone: a complex interplay of cell death pathways. Bioblast 2022: BEC Inaugural Conference. »MitoFit Preprint« |
Link: Bioblast 2022: BEC Inaugural Conference
Ganguly Upasana, Bir Aritri, Chakrabarti Sasanka (2022)
Event: Bioblast 2022
Ferroptosis has been identified as a type of regulated cell death triggered by a diverse set of agents with implications in various diseases like cancer and neurodegenerative diseases. Ferroptosis is iron-dependent and accompanied by an accumulation of reactive oxygen species (ROS) and lipid oxidation products, a depletion of reduced glutathione, mitochondrial morphological alterations and the rupture of cell membrane; the process is inhibited by specific antioxidants like ferrostatin-1 and liproxstatin-1 and by other general antioxidants like the iron-chelator deferoxamine, vitamin E and N-acetylcysteine. However, the mechanism of cell death in ferroptosis subsequent to the accumulation of ROS and lipid oxidation products is not clearly established. We show here that the classical mitochondrial Complex I inhibitor rotenone (0.5 µM) causes death of SH-SY5Y cells (a human neuroblastoma cell line) over a period of 48 h accompanied by mitochondrial membrane depolarization and intracellular ATP depletion. This is associated with an intracellular accumulation of ROS and the lipid oxidation product malondialdehyde or MDA and a decrease in reduced glutathione content. All these processes are inhibited very conspicuously by specific inhibitors of ferroptosis such as ferrostatin-1 and liproxstatin-1. However, the decrease in Complex I activity upon rotenone-treatment of SH-SY5Y cells is not significantly recovered by ferrostatin-1 and liproxstatin-1. When the rotenone-treated cells are analyzed morphologically by Hoechst 33258 and propidium iodide (PI) staining, a mixed picture is noticed with densely fluorescent and condensed nuclei indicating apoptotic death of cells (Hoechst 33258) and also significant numbers of necrotic cells with bright red nuclei (PI staining).
• Keywords: rotenone, mitochondria, ferroptosis, reactive oxygen species, neurodegeneration
• O2k-Network Lab: IN Haldia Chakrabarti S
Affiliations and support
- Ganguly U(1), Bir A(2), Chakrabarti S(1)
- Department of Biochemistry and Central Research Laboratory, Maharishi Markandeshwar Institute of Medical Sciences and Research, Maharishi Markandeshwar University (Deemed to be), Mullana, Ambala, India - [email protected]
- Department of Biochemistry, Dr. B.C. Roy Multispeciality Medical Research Centre, IIT Kharagpur, India
- Ganguly U(1), Bir A(2), Chakrabarti S(1)
Help
Labels: Pathology: Parkinson's Stress:Cell death, Oxidative stress;RONS
Tissue;cell: Nervous system, Neuroblastoma
Enzyme: Complex I, Complex III Regulation: ATP production, Inhibitor, mt-Membrane potential
Bioblast 2022
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