protective effects of vitamin c on polyethylene terephthalate nanoplastic–induced oxidative stress and membrane damage: an in vitro study

Background: nanoplastics originating from polyethylene terephthalate (pet) are increasingly found in environmental and biological samples, where they have been linked to oxidative stress-driven cell injury. because of their tiny size and high surface reactivity, pet nanoplastics (pet-nps) can cross cellular barriers and disturb redox balance. although antioxidants like vitamin c might counteract such effects, human cell-based evidence remains scarce.objectives: this work examined whether pet-nps induce oxidative toxicity in human embryonic kidney (hek293) cells and whether vitamin c can protect against the resulting cellular damage.methods: in this experimental study, hek293 cells were exposed to pet nanoparticles (pet-nps), vitamin c, or their combination at concentrations based on half-maximal inhibitory values. cell viability was assessed using the mtt assay, while membrane integrity was evaluated by measuring lactate dehydrogenase (ldh) release. oxidative stress was assessed by quantifying lipid peroxidation (lpo), total antioxidant capacity (tac), and the activities of superoxide dismutase (sod) and catalase (cat). results: pet-np exposure significantly lowered sod and cat activities and reduced tac compared to untreated controls (p<0.05). a pronounced rise in ldh release was also observed, signaling compromised membrane integrity. co-treatment with vitamin c significantly blunted ldh elevation and brought antioxidant enzyme activities and tac back toward control levels (p<0.05). lipid peroxidation increased after pet-np exposure and was partially corrected by vitamin c supplementation.conclusion: pet nanoplastics trigger oxidative stress and cytotoxicity in hek293 cells by weakening antioxidant defenses and promoting lipid peroxidation. vitamin c lessens these harmful effects by boosting cellular antioxidant capacity and limiting membrane damage. these findings suggest that vitamin c could serve as a protective agent against nanoplastic-induced oxidative injury and reinforce oxidative stress as a core mechanism of pet-np toxicity.