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Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway

Thesis (MSc)--Stellenbosch University, 2025.

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Main Author: Slabber, Johann
Other Authors: Abdul, Naeem Sheik
Format: Thesis
Published: Stellenbosch : Stellenbosch University 2026
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access_status_str Open Access
author Slabber, Johann
author2 Abdul, Naeem Sheik
author_browse Abdul, Naeem Sheik
Slabber, Johann
author_facet Abdul, Naeem Sheik
Slabber, Johann
author_sort Slabber, Johann
collection Thesis
dc_rights_str_mv Stellenbosch University
description Thesis (MSc)--Stellenbosch University, 2025.
format Thesis
id oai:scholar.sun.ac.za:10019.1/134823
institution Stellenbosch University (South Africa)
last_indexed 2026-06-10T12:41:56.100Z
license_str Other — see source repository
provenance_str_mv Harvested via OAI-PMH from SUNScholar — Stellenbosch University Repository
publishDate 2026
publishDateRange 2026
publishDateSort 2026
publisher Stellenbosch : Stellenbosch University
publisherStr Stellenbosch : Stellenbosch University
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source_str SUNScholar — Stellenbosch University Repository
spelling oai:scholar.sun.ac.za:10019.1/134823 Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway Slabber, Johann Abdul, Naeem Sheik Stellenbosch University. Faculty of Science. Dept. of Biochemistry. Microplastics -- Toxicology Polystyrene -- Oxidation Kidneys -- Cytopathology Oxidative stress Nephrotoxicology UCTD Thesis (MSc)--Stellenbosch University, 2025. Slabber, J. 2025. Oxidative Stress Induced by Polystyrene Microplastics in HEK 293 Cells: Exploring the Impact on the NRF2 Pathway. Unpublished masters thesis. Stellenbosch: Stellenbosch University [online]. Available: https://scholar.sun.ac.za/items/2e693383-09f3-4ca4-8247-ab5e73413708 ENGLISH ABSTRACT: Polystyrene microplastics (PSMPs), arising from widespread single-use plastics, have become common environmental contaminants. Recent studies report their accumulation in human organs, notably the kidney, a primary site for toxin filtration and elimination. This makes the kidney especially vulnerable to PSMP toxicity and bioaccumulation. Exposure to PSMPs promote excessive reactive oxygen species (ROS) formation by disrupting mitochondrial membrane potential and impairing the electron transport chain (ETC), culminates in cellular oxidative stress (OS) . This results in damage to cell macromolecules, induces mutations, and drives cell death. While the precise mechanisms of toxicity in kidney cells remain unclear, PSMP-induced oxidative damage is a key concern for renal health. This study aims to verify the kidney toxicity of PSMPs on OS and the molecular mechanism involved by using spectrophotometric, luminometric and protein expression techniques. This study investigated the toxicity of three selected PSMP concentrations (25, 100 and 239 μg/mL) to elucidate the effect at physiologically relevant levels and to determine the mechanism of toxicity after 48 hours of exposure. Results indicated that kidney cell metabolic function remained stable until a critical threshold, after which it declined. The cell viability assay indicated that the halfmaximal inhibition concentration (IC50) was 239 μg/mL. Even minimal PSMP exposure elevated hydrogen peroxide (H2O2) in a dose-dependent manner, yet antioxidant (AO) enzymes did not respond proportionally. Total superoxide dismutase (SOD) activity decreased, catalase (CAT) rose only at the highest dose, and total glutathione declined, highlighting a complex OS response. Further protein expression analysis showed downregulation of SOD I while SOD II was marginally upregulated, and CAT increased only at the highest PSMP concentration. The AO master transcription factor, nuclear factor erythroid 2-related factor 2 (NRF2) was also found to be significantly decreased. Protein expression analysis further, revealed an increase in pro-apoptotic BCL2-associated X protein (BAX) and a decrease in anti-apoptotic B-cell lymphoma 2 (BCL2). Initiation of apoptosis was confirmed by upregulation of caspases-8 and -9, but executioner caspases-3 and -7 were downregulated. This study elucidated the molecular mechanism by which PSMPs induce nephrotoxicity, demonstrating how they induce OS via excessive ROS production and inhibition of AO enzymes linked with the NRF2 pathway. Furthermore, this investigation highlights the urgent need for broader investigation into MP-induced organ and pathway toxicity. Masters 2026-01-09T11:56:34Z 2026-01-09T11:56:34Z 2025-12 Thesis https://scholar.sun.ac.za/handle/10019.1/134823 Stellenbosch University xv, 80 pages : illustrations application/pdf Stellenbosch : Stellenbosch University
spellingShingle Microplastics -- Toxicology
Polystyrene -- Oxidation
Kidneys -- Cytopathology
Oxidative stress
Nephrotoxicology
UCTD
Slabber, Johann
Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title_full Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title_fullStr Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title_full_unstemmed Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title_short Oxidative stress Induced by polystyrene microplastics in HEK 293 cells: exploring the impact on the NRF2 pathway
title_sort oxidative stress induced by polystyrene microplastics in hek 293 cells exploring the impact on the nrf2 pathway
topic Microplastics -- Toxicology
Polystyrene -- Oxidation
Kidneys -- Cytopathology
Oxidative stress
Nephrotoxicology
UCTD
url https://scholar.sun.ac.za/handle/10019.1/134823
work_keys_str_mv AT slabberjohann oxidativestressinducedbypolystyrenemicroplasticsinhek293cellsexploringtheimpactonthenrf2pathway