School Of Basic And Applied Sciences

Permanent URI for this communityhttps://kr.cup.edu.in/handle/32116/17

Browse

Has files: NoSubject: search.filters.subject.Mitochondria

Search Results

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    Role of platelet in Parkinson's disease: Insights into pathophysiology & theranostic solutions
    (Elsevier Ireland Ltd, 2022-07-04T00:00:00) Beura, Samir Kumar; Panigrahi, Abhishek Ramachandra; Yadav, Pooja; Singh, Sunil Kumar
    Parkinson's disease (PD) is the second-most-common neurodegenerative disease characterized by motor and non-motor dysfunctions, which currently affects about 10 million people worldwide. Gradual death and progressive loss of dopaminergic neurons in the pars compacta region of substantia nigra result in striatal dopamine deficiency in PD. Specific mutation with further aggregation of ??synuclein in the intraneuronal inclusion bodies is considered the neuropathological hallmark of this disease. PD is often associated with various organelle dysfunctions inside a dopaminergic neuron, including mitochondrial damage, proteasomal impairment, and production of reactive oxygen species, thus causing subsequent neuronal death. Apart from several genetic and non-genetic risk factors, emerging research establishes an association between cardiovascular diseases, including coronary heart disease, myocardial infarction, congestive heart failure, and ischemic stroke with PD. The majority of these cardiovascular diseases have an origin from atherosclerosis, where endothelial dysfunction following thrombus formation is significantly regulated by blood platelet. This non-nucleated cell fragment expresses not only neuron-specific molecules and receptors but also several PD-specific biomarkers such as ?-synuclein, parkin, PTEN-induced kinase-1, tyrosine hydroxylase, dopamine transporter, thus making platelet a suitable peripheral model for PD. Besides its similarity with a dopaminergic neuron, platelet structural alterations, as well as functional abnormalities, are also evident in PD. However, the molecular mechanism behind platelet dysfunction is still elusive and quite controversial. This state-of-the-art review describes the detailed mechanism of platelet impairment in PD, addressing the novel platelet-associated therapeutic drug candidates for plausible PD management. � 2022 Elsevier B.V.
  • No Thumbnail Available
    Item
    A Protein and Membrane Integrity Study of TiO2 Nanoparticles-Induced Mitochondrial Dysfunction and Prevention by Iron Incorporation
    (Springer, 2021-03-31T00:00:00) Barkhade, Tejal; Mahapatra, Santosh Kumar; Banerjee, Indrani
    The paper assessed the toxic effect of titanium dioxide (TiO2) nanoparticles (NPs) on isolated mitochondria and its dysfunction prevention after Iron (Fe) incorporation. TiO2 and Fe content TiO2 NPs were synthesized and characterized using XPS, PL spectroscopy, and TEM. The nanostructure interaction with isolated mitochondria was investigated using circular dichroism (CD) confocal microscopy, flow cytometry, atomic force microscopy (AFM), surface-enhanced Raman spectroscopy (SERS), and FT-IR spectroscopy via nonspecific pathway. Fe content TiO2 NPs helps to control the dissolution rate of parent nanomaterial of TiO2 on the mitochondrial membrane. Confocal micrographs and flow cytometry results confirmed that Rhodamine 123 dye intensity get increased after interaction with Fe content TiO2 NPs which states the integrity of the mitochondrial membrane. AFM results revealed that TiO2 induces the swelling of mitochondrial tubules and also impaired the mitochondrial structure, whereas Fe content TiO2 NPs interaction prevents the impairment of mitochondrial tubules. The denaturation of a membrane protein by TiO2 interactions was observed through CD Spectroscopy. Further, nano-bio-interface study was performed using SERS, through shifting and extinct of peaks affiliated to membrane proteins and lipids. However, Fe content TiO2-treated samples showed a significant increase in the membrane potential of mitochondria via flow cytometry results. Graphic Abstract: [Figure not available: see fulltext.] � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
  • No Thumbnail Available
    Item
    Evaluation of amyloid beta (aβ)-induced Mitochondrial dysfunction: Neuroprotective role of Apurinic/apyrimidinic endonuclease (ape1) Via its interaction with cysteamine Dioxygenase (ado)
    (Central University of Punjab, 2020) Kaur,Navrattan; Mantha, Anil K.
    Oxidative stress and damage to mitochondrial DNA during the aging process can impair mitochondrial energy metabolism and ion homeostasis in neurons, ultimately leading to neurodegeneration. Themain pathway for repairing oxidative base lesions is base excision repair (BER), and such repair is crucial for neurons owing to high rate of oxygen metabolism. Apurinic/apyrimidinic endonuclease (APE1) is a protein of this pathway involved in DNA repair and also in the redox co-activating function of different transcription factors. Thus, manipulation of DNA repair mechanisms can be thought of as a putative approach to prevent neuronal loss in neurodegenerative disorders like Alzheimer’s disease (AD). Ginkgo biloba has been studied as a possible treatment for dementia and AD. The ginkgolides present in G. biloba possess antioxidant, neuroprotective and cholinergic activities. The aim of the study was to explore the repair and redox functions of APE1 and a detailed mechanism of association of APE1 with ADO (a thiol dioxygenase) and functional cross-talk between them has been studied. In the present study, we have standardized the differentiation of SH-SY5Y neuroblastoma cells into the cells possessing a mature neuron-like phenotype. The results of cell viability assay showed that differentiated cells are more sensitive/vulnerable to oxidative stress, which is elicited by Aβ. H2DCFDA and DAF- FM-based detection of ROS and RNS strongly advocates that under oxidative stress conditions elicited by Aβ, GB exerts ameliorating effect to render neuroprotection to the SH-SY5Y cells due to its antioxidant nature. Significant decrease in nNOS expression was seen, when cells were pre-treated with GB and then given Aβ treatment in whole cell, cytosol and nucleus. This shows that GB pre-treatment decreases the RNS (NO) levels due to its anti-oxidant property. Determination of DNA damage in terms of measurement of 8-oxo-dG was seen to be more pronounced in mitochondria. In response to DNA damage, pre-treatment with GB decreased the expression of DNA repair enzyme APE1 expression in mitochondria, showing that GB aids in lowering the oxidative stress generated by Aβ in the mitochondria. In the nuclear extracts, upon treatment with GB, there was a significant increase in ADO expression and Aβ treatment also increased the expression of ADO. Whereas, combination treatment of Aβ and GB led to lower expression of ADO. This points towards the possibility that ADO might be translocating to nucleus under oxidative stress and GB might be affecting APE1 – ADO interaction in lowering oxidative stress by the anti-oxidant action of GB, which was clearly observed by immunostaining using confocal microscopy. JC-1 assay points toward GB’s role in restoring the mitochondrial membrane potential against Aβ- challenge. Determination of apoptotic markers (Caspase 9 and AIF) showed that Aβ(25-35) induced oxidative stress caused initiation of apoptosis and GB treatment was able to rescue apoptosis. Our study elucidates activation of synaptic CaMKII and CREB exerting neuroprotective effects; and GB acting to restore the expression and active, phosphorylated state of CaMKII and CREB in presence of Aβ-induced oxidative stress in the SH-SY5Y neuroblastoma cells. This study points towards the use of phytochemicals like GB which will may prove to be beneficial for the enhancement of synaptic functionality and promote neuroprotection.