School Of Basic And Applied Sciences
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Item Impact of mitochondrial transplantation on cancer cells(Central University of Punjab, 2014) Aggarwal, Alza; Bhardwaj, PankajMitochondria, the powerhouse of the cell, are small granular or filamentous bodies associated significantly with cellular respiration and are the main sources of energy, due to which they are present in maximum number in the organs that require large amounts of energy for doing their function like muscle cells, neural cells, etc. In case of any dysfunction of mitochondria, these organs are most affected culminating in a number of serious multi organs diseases, irrespective of age such as neurogenic weakness with ataxia and retinitis pigmentosa (NARP), or Leigh syndrome (LS), Cancer, etc. Although mutations in mitochondrial genes are common in cancer cells, they do not inactivate mitochondrial energy metabolism, but rather alter the mitochondrial bioenergetics and biosynthetic state. Literature survey also revealed that owing to mitochondrial dysfunction the clinical trial of many anticancer drugs has failed in patients. This study is focused on the impact of mitochondrial transplantation on cancer cells and their drug sensitivity against four human cancer cell lines HCT116 (WT & P53mutated), HepG2 and MCF7. The normal cell's Mitochondria was transplanted into cancer cells and then evaluated the Impact of transplantation of mitochondria from healthy cells into cancer cell upon their growth, ROS production and their drug sensitivity. The results of this study revealed that the healthy mitochondria transplanted to cancer cells decrease carcinogenesis and have drug sensitivity. So, it may be used as futuristic cancer remedy.Item Effect of amyloid beta (25-35) peptide on mitochondrial respiratiory function in neuroral cells over expressing ape1(Central University of Punjab, 2014) Kaur, Navrattam; Mantha, Anil K.Alzheimer's disease (AD) is an important public health problem which affects millions of people worldwide. The major pathological hallmarks associated with AD are the accumulation of amyloid beta (A?) in senile plaques and neurofibrillary tangles (NFTs) made up of hyperphosphorylated tau proteins. Accumulating evidences point towards the role of oxidative stress and mitochondrial dysfunction in the pathogenesis of AD. Aging is considered as one of the greatest risk factor for AD. In order to maintain genome integrity, base excision repair (BER) pathway is the predominant pathway for repairing oxidized base lesions in neuronal cells. APE1 is the central enzyme of the BER-pathway, having both repair and redox activities and shown to enhance neuronal survival after oxidative stress. In my study, effect of A?(25-35) on mitochondrial ROS/RNS levels and activities of respiratory complexes (I, III, & IV) in neuronal cells was studied with and without ectopic APE1 expression and the neuro- modulatory role of Ginkgolide B (from leaves of G. biloba) was evaluated. It was seen that A?(25-35) increases the ROS/RNS levels in these cells which was decreased when pre-treated with Ginkgolide B (G.B) before treating with A?(25-35). APE1 levels were found to be decreased on treating with A?(25-35) and were increased on pre- treatment with G.B and subsequent treatment with A?(25-35). These results indicate that ectopic APE1 expression in the mitochondria of the neuronal cells might overcome the oxidative damage caused by A?(25-35). Also, phytochemical G.B has shown to modulate the mitochondrial complex activity upon A?(25-35)-induced oxidative stress and modulate the ROS/RNS levels in the presence of APE1. Further studies are needed to understand the mechanism of action of APE1 in relation to the above results, which will be carried out during my Ph.D. work.