Chakrabarti 2022 Abstract Bioblast: Difference between revisions
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{{Abstract | {{Abstract | ||
|title='' | |title=''Not presented'' [[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. In: https://doi.org/10.26124/bec:2022-0001 <br>[[Ganguly 2022 MitoFit|ยป''MitoFit Preprint''ยซ]] | ||
|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] | ||
|authors=Ganguly Upasana, Bir Aritri, Chakrabarti Sasanka | |authors=Ganguly Upasana, Bir Aritri, Chakrabarti Sasanka |
Revision as of 15:59, 20 June 2022
Not presented 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. In: https://doi.org/10.26124/bec:2022-0001 ยปMitoFit Preprintยซ |
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 ยตM) 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).
โข Keywords: rotenone, mitochondria, ferroptosis, reactive oxygen species, neurodegeneration
โข O2k-Network Lab: IN Haldia Chakrabarti S
Affiliations and support
- Ganguly U1, Bir A2, Chakrabarti S1
- 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 U1, Bir A2, Chakrabarti S1
List of abbreviations, terms and definitions - MitoPedia
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