{"id":{"repo_id":"westminster","oai_identifier":"oai:westminsterresearch.westminster.ac.uk:v9v45"},"canonical_url":"https://search.dev.ndltd.org/etd/westminster/oai:westminsterresearch.westminster.ac.uk:v9v45","repository":{"repo_id":"westminster","name":"University of Westminster","base_url":"https://westminsterresearch.westminster.ac.uk/oai2"},"display":{"title":"Nanotechnology based therapeutic approaches to iron‐induced oxidative stress in an in vitro model of Parkinson’s disease","abstract":"In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model.","abstract_html":"In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model.","abstract_has_math":false,"creators":["Mursaleen, L."],"institution":"University of Westminster","degree_name":null,"degree_level":"PhD thesis","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2021,"date_issued":"2021","date_published":"2021","updated_at":"2026-07-24T06:01:26Z","subjects":[],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["oai:westminsterresearch.westminster.ac.uk:v9v45"],"render_values":[{"text":"oai:westminsterresearch.westminster.ac.uk:v9v45","href":null,"code":true}]}]},"links":{"outbound_url":"https://doi.org/10.34737/v9v45","outbound_label":"DOI","outbound_source":"dc:identifier.doi"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Mursaleen, L."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2021"]},{"key":"dc:date.issued","label":"Date","values":["2021"]},{"key":"dc:publisher","label":"Institution","values":["University of Westminster"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["School of Life Sciences"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["University of Westminster"]},{"key":"dc:relation","label":"Dc Relation","values":["https://westminsterresearch.westminster.ac.uk/item/v9v45/nanotechnology-based-therapeutic-approaches-to-iron-induced-oxidative-stress-in-an-in-vitro-model-of-parkinson-s-disease"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://westminsterresearch.westminster.ac.uk/item/v9v45/nanotechnology-based-therapeutic-approaches-to-iron-induced-oxidative-stress-in-an-in-vitro-model-of-parkinson-s-disease"]},{"key":"dc:type","label":"Dc Type","values":["Thesis or dissertation"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["PhD thesis"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["oai:westminsterresearch.westminster.ac.uk:v9v45"]},{"key":"dc:identifier.doi","label":"DOI","values":["https://doi.org/10.34737/v9v45"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://westminsterresearch.westminster.ac.uk/download/9ec8673be9962c3d78161e10524900c44b9ae6a255a8b85d927f4947909ba28b/19096794/20211111_%20Leah%20Mursaleen_Final%20thesis_Awarded.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model."]},{"key":"dc:description.abstract","label":"Abstract","values":["In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model."]},{"key":"dc:title","label":"Title","values":["Nanotechnology based therapeutic approaches to iron‐induced oxidative stress in an in vitro model of Parkinson’s disease"]}]}],"canonical_facts":{"dc:creator":["Mursaleen, L."],"dc:date":["2021"],"dc:date.issued":["2021"],"dc:description":["In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model."],"dc:description.abstract":["In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model. In Parkinson’s disease (PD), excess free iron drives the accumulation of toxic hydroxyl radicals within mitochondria of dopaminergic neurons, resulting in sustained oxidative stress and cellular damage. The blood‐brain barrier (BBB) prevents most pharmaceuticals from entering the brain, therefore, to enable the advancement of potential antioxidant and iron chelator therapies for PD, limiting factors such as brain penetrance and bioavailability need to be overcome. This study aimed to develop novel nanocarrier delivery systems of the antioxidants curcumin, n‐acetylcysteine (NAC) and hydroxytyrosol (HT), alone or combined with the iron chelator deferoxamine (DFO), to protect against rotenone‐induced parkinsonism in SH‐SY5Y cells, and in a co‐cultured hCMEC/D3 ‐ SH‐SY5Y cellular BBB model."],"dc:identifier":["oai:westminsterresearch.westminster.ac.uk:v9v45"],"dc:identifier.doi":["https://doi.org/10.34737/v9v45"],"dc:identifier.uri":["https://westminsterresearch.westminster.ac.uk/download/9ec8673be9962c3d78161e10524900c44b9ae6a255a8b85d927f4947909ba28b/19096794/20211111_%20Leah%20Mursaleen_Final%20thesis_Awarded.pdf"],"dc:publisher":["University of Westminster"],"dc:publisher.department":["School of Life Sciences"],"dc:publisher.institution":["University of Westminster"],"dc:relation":["https://westminsterresearch.westminster.ac.uk/item/v9v45/nanotechnology-based-therapeutic-approaches-to-iron-induced-oxidative-stress-in-an-in-vitro-model-of-parkinson-s-disease"],"dc:relation.isreferencedby":["https://westminsterresearch.westminster.ac.uk/item/v9v45/nanotechnology-based-therapeutic-approaches-to-iron-induced-oxidative-stress-in-an-in-vitro-model-of-parkinson-s-disease"],"dc:title":["Nanotechnology based therapeutic approaches to iron‐induced oxidative stress in an in vitro model of Parkinson’s disease"],"dc:type":["Thesis or dissertation"],"dc:type.qualificationlevel":["PhD thesis"]},"updated_at":"2026-07-24T06:01:26Z"}