Induction Of Oxidative Stress Research Articles

DNA repair efficiency in young hypertensive: Is lifestyle a prooxidant factor?

Background: High prevalence of hypertension (HTN) is of major concern among the middle-aged population of Kerala. Understudied in the context of HTN is oxidative damage to DNA, which is caused by free radical assaults. The modern lifestyle associated with an unhealthy diet and lack of exercise plays a key role in oxidative stress induction. Aims and Objectives: The objective of this study was to assess the significance of oxidative stress and the effectiveness of DNA repair mechanisms in young hypertensives along with how it correlates with aspects of lifestyle. Materials and Methods: This prospective case–control study enrolled clinically proven hypertensive patients referred from the outpatient department of Hridayalaya, Institute of Preventive Cardiology, Thiruvananthapuram, to Genetika, a research center for Cytogenetic Studies in South Kerala. Hypertensive patients (n=180) within the age group of 18–39 were compared with matched healthy controls (n=140). Associated lifestyle factors were determined. Results: In comparison to controls, cases had noticeably higher mean levels of malondialdehyde (MDA) and mean break per cell (P<0.05). There was a difference that was statistically significant (P<0.05) between the patients and controls in terms of diet, exercise, physical activity, obesity, mental stress, alcohol, and tobacco use. On comparing MDA and mean break per cell values with lifestyle factors, a statistically significant difference was detected (P<0.05). Observed a significant positive correlation of break per cell value with MDA (P<0.05). Conclusion: The current study demonstrated increased DNA damage and decreased DNA repair efficiency in young hypertensive and was strongly associated with lifestyle factors. Appropriate measures such as regular BP checkups, regular exercises, and abstinence from alcohol and smoking are to be taken for the prevention and control of HTN.

Acute and chronic effects of the antifouling booster biocide Irgarol 1051 on the water flea Moina macrocopa revealed by multi-biomarker determination

Irgarol 1051 is an herbicide extensively utilized in antifouling paint due to its ability to inhibit photosynthesis. Irgarol and its photodegradation products are highly persistent in waters and sediments, although they are present in low concentrations. However, our understanding of the harmful effects of Irgarol on non-target organisms remains limited. In this study, we assessed the effects of acute (24 h) and chronic (14 days across three generations) exposure to different concentrations (including the 1/10 NOEC, NOEC, and 1/10 LC50 calculated from the 24-h acute toxicity test) of Irgarol using the water flea Moina macrocopa. Acute exposure to 1/10 LC50 significantly decreased survival, feeding rate, thoracic limb activity, heart rate, and acetylcholinesterase activity. Elevated levels of intracellular reactive oxygen species and malondialdehyde, along with a significant increase in catalase and superoxide dismutase activity, suggested the induction of oxidative stress in response to 1/10 LC50. An initial boost in glutathione level and the enzymatic activities of glutathione peroxidase and glutathione reductase, followed by a plunge, implies some compromise in the antioxidant defense system. Upon chronic exposure to the NOEC value, both generations F1 and F2 displayed a significant decrease in survival rate, body length, number of neonates per brood, and delayed sexual maturation, suggesting maternal transfer of potential damage through generations. Taken together, Irgarol induced acute toxicity through physiological and cholinergic damage, accompanied by the induction of oxidative stress, in the water flea. Even its sub-lethal concentrations can induce detrimental effects across generations when consistently exposed.

Protective Effect of Tertiary Butylhydroquinone against Obesity-induced Skeletal Muscle Pathology in Post-weaning High Fat Diet Fed Rats.

Obesity deleteriously affects skeletal muscle functionality starting from infancy to adulthood, leading to dysfunctional skeletal muscle. This study, therefore, evaluated the protective action of tert-butylhydroquinone (tBHQ) against obesity-induced skeletal muscle pathology in high-fat diet (HFD) fed rats. Twenty post-weaning male albino rats were randomized into four groups of five rats each as: Group 1 (control), Group 2 (HFD), Group 3 (orlistat) and Group 4 (tBHQ). Group one received rat pellets for 12 weeks, while groups 2 to 4 received HFD for 12 weeks. At the end of week 8, obesity was confirmed with Lee Obesity Index and body mass index values of ≥ 303 and ≥ 0.68 gcm2, respectively. Group 3 was given oral administration of orlistat (10 mg/kg, once daily), while group 4 was given oral administration of tBHQ (25 mg/kg, once daily). Administration of orlistat and tBHQ commenced from week 9 to the end of the experiment. Chronic exposure of post-weaning rats to HFD led to their development of the metabolic syndrome phenotypes in adulthood, characterized by obesity, hyperglycemia, dyslipidaemia, hyperinsulinaemia, insulin resistance as well as induction of oxidative stress and alteration of skeletal muscle markers, which were mitigated following supplementation with orlistat and tBHQ. The study showed the anti-obesity potentials of tBHQ and its protective action against HFD obesity-induced skeletal muscular pathology.

Copper mediated follicular atresia: Implications for granulosa cell death

3-nitropropanoic acid is a potent oxidative stress inducer that is conventionally regarded as a regulator of follicular atresia by regulating granulosa cells (GCs) death through the apoptosis pathway. There has been no research investigating the impact of copper metal overload induced Cuproptosis in ovarian GCs as a factor contributing to hindered follicular development.To elucidate whether 3-NP-induced oxidative stress plays a contributory role in promoting Cuproptosis, and discuss the role of Cuproptosis in the development of ovarian follicles.We conducted an analysis of cuproptosis occurrence in murine GCs and C57BL/6 J mice under the influence of 3-NP and 3-NP with added exogenous copper.The results revealed that 3-NP serving as a robust facilitator of exogenous copper uptake by upregulating the expression of copper transporter 1 (CTR1). In turn, culminated in the accumulation of intracellular copper within mouse granulosa cells (mGCs). Furthermore, 3-NP promoted mitochondrial permeability transition pore opening and concurrently reduced the stability of lipoic acid proteins. These actions collectively induced the oligomerization of Dihydrolipoamide S-Acetyltransferase (DLAT), ultimately leading to cuproptosis in GCs and consequent follicular atresia. Heavy metal copper and fungal decomposition product 3-NP, induce ovarian atresia via cuproptosis, modulating the reproductive performance of female animals.

CS and ZnO Nanoparticles as Fungicides against Potato Fungal Pathogens Alternaria solani and Fusarium solani. Mechanism Underlining Their Antifungal Activity

Fusarium solani (F. solani) and Alternaria solani (A. solani) are among the most destructive pathogenic fungi affecting potatoes, causing significant crop losses in both field and post-harvest conditions. Current control relies heavily on synthetic fungicides which pose serious environmental and health risks. Therefore, there is a growing need to find efficient and environmentally friendly alternatives to combat fungal infections in potatoes. This study offers chitosan (CS) and zinc oxide (ZnO) nanoparticles (NPs) as potential fungicides against A. solani and F. solani. We evaluated their antifungal properties and elucidated the mechanism underlining their activity. Our results revealed that both CS and ZnO NPs exhibited pronounced antifungal activity against the two pathogenic strains by effectively inhibiting the mycelium growth. Furthermore, we discovered that the activity of the NPs involved the induction of oxidative stress in fungal cells and changes in the molecular organization of their membranes.

Pharmacologic inhibition of eIF4A blocks NRF2 synthesis to prevent osteosarcoma metastasis.

Effective therapies for metastatic osteosarcoma (OS) remain a critical unmet need. Targeting mRNA translation in metastatic OS offers a promising option, as selective translation drives synthesis of cytoprotective proteins under harsh microenvironmental conditions to facilitate metastatic competence. We assessed expression levels of eukaryotic translation factors in OS, revealing high expression of the eIF4A1 initiation factor. Using a panel of metastatic OS cell lines and PDX models, eIF4A1 inhibitors were evaluated for their ability to block proliferation and reduce survival under oxidative stress, mimicking harsh conditions of the lung microenvironment. Inhibitors were also evaluated for their anti-metastatic activity using the ex vivo pulmonary metastasis assay (PuMA) and in vivo metastasis models. Proteomics were performed to catalog which cytoprotective proteins or pathways were affected by eIF4A1 inhibition. CR-1-31B, a rocaglate-based eIF4A1 inhibitor, exhibited nanomolar cytotoxicity against all metastatic OS models tested. CR-1-31B exacerbated oxidative stress and apoptosis when OS cells were co-treated with a tert-butylhydroquinone (tBHQ), a chemical oxidative stress inducer. CR-1-31B potently inhibited OS growth in the PuMA model and in experimental and spontaneous models of OS lung metastasis. Proteomic analysis revealed that tBHQ-mediated upregulation of the NRF2 antioxidant factor was blocked by co-treatment with CR-1-31B. Genetic inactivation of NRF2 phenocopied the anti-metastatic activity of CR-1-31B. Finally, the clinical grade eIF4A1 phase 1-2 inhibitor, Zotatifin, similarly blocked NRF2 synthesis and the OS metastatic phenotype. Collectively, our data reveal that pharmacologic targeting of eIF4A1 is highly effective in blocking OS metastasis by blunting the NRF2 antioxidant response.

Design and synthesis of visible light-activatable photocaged peroxides for optical control of ROS-mediated cellular signaling

We designed and synthesized two novel photocaged peroxide compounds, N5TBHP and N6TBHP, featuring nitrogen-containing fused ring coumarin skeletons. Notably, a tetrahydroquinoline fused coumarin derivative, N6TBHP demonstrated significantly higher photocleavage efficiency under visible light at 455 nm compared to N5TBHP, which contains an indoline fused coumarin. This process effectively releases the oxidative stress inducer tert-butylhydroperoxide (TBHP). Additionally, N6TBHP exhibits high resistance to glutathione (GSH), and its UV spectral analysis suggests enhanced intracellular stability due to reduced reactivity with GSH through self-assembly. Furthermore, N6TBHP can release an optimal amount of TBHP into cells under visible light irradiation with minimal cell damage. These properties position N6TBHP as a promising tool for advancing research in intracellular redox signaling.

Oxidative damage and cell cycle delay induced by vanadium(III) in human peripheral blood cells

Vanadium (V) is a metal that can enter the environment through natural routes or anthropogenic activity. In the atmosphere, V is present as V oxides, among which vanadium(III) oxide (V2O3) stands out. Cytogenetic studies have shown that V2O3 is genotoxic and cytostatic and induces DNA damage; however, the molecular mechanisms leading to these effects have not been fully explored. Therefore, we treated human peripheral blood lymphocytes in vitro, evaluated the effects of V2O3 on the phases of the cell cycle and the expression of molecules that control the cell cycle and examined DNA damage and the induction of oxidative stress. The results revealed that V2O3 did not affect cell viability at the different concentrations (2, 4, 8 or 16 μg/mL) or exposure times (24 h) used. However, V2O3 affected the percentage of G1- and S-phase cells in the cell cycle, decreased the expression of mRNAs encoding related proteins (cyclin D, cyclin E, CDK2 and CDK4) and increased the expression of γH2AX and the levels of reactive oxygen species. The ability of V2O3 to cause a cell cycle delay in G1-S phase may be associated with a decrease in the mRNA and protein expression of the cyclins/CDKs and with intracellular oxidative stress, which may cause DNA double-strand damage and H2AX phosphorylation.

Stimuli-Responsive Hydrogels Potentiating Photothermal Therapy against Cancer Stem Cell-Induced Breast Cancer Metastasis.

The self-renewal and differentiation properties of cancer stem cells (CSCs) result in chemoresistance in breast cancer. Even though numerous drugs have been developed to target CSCs, they have suffered from inefficient delivery and accumulation at the focal site. Here, a thermoresponsive hydrogel is developed by coencapsulating aggregation-induced emission (AIE)-active photothermal agent and thioridazine (THZ), demonstrating a controllable delivery system triggered by the AIE agent to augment THZ-mediated CSC ablation. Upon near-infrared laser stimuli, the photothermal effect from the AIE agent induces hydrogel deformation for burst drug release. The precise in situ tumor administration of the hydrogel accelerates drug diffusion and accumulation in deep breast cancer lesions. Thus, THZ can invade tumors and provoke massive CSC apoptosis via dopamine receptor blockage and oxidative stress induction. Consequently, effective CSC inhibition and significant suppression of tumor recurrence and metastasis are demonstrated in mice with breast cancer. We believe that this intelligent hydrogel-based delivery system represents a promising treatment strategy for metastatic breast cancer with clinical potential.

Reproductive Toxicity Caused by Zearalenone on Animals and Its Possible Interventions

Zearalenone (ZEN) is a mycotoxin that is usually found in moldy grains. ZEN causes reproductive toxicity to domestic animals by interfering with follicular and embryonic development, reducing sperm vitalityand destroying the homeostasis of endogenous hormones, leading to reproductive system diseases such as abortion, ovarian dysfunctionand stillbirth. The reproductive damage caused by zearalenone is mainly attributed to the factors as follows: (1) interaction with estrogen receptor; (2) induction of oxidative stress; (3) induction of apoptosis, necrosis, autophagyand iron prolapse and (4) interference with cell replication cycle. Natural compounds and micro-nutrients have the potential to alleviate the oxidative stress caused by ZEN. In addition, some microorganisms and enzymes have also shown good detoxification effects. Therefore, in this review, we focus on the damage caused by ZEN on animal gamete development and embryonic development, its molecular mechanismsand suggested some potential mitigation measures for the prevention of ZEN-induced toxicity to provide information for preventing toxicity associated with ZEN as well as serve as a foundation for further development of drug candidates for the treatment of ZEN induced damage.

Dynamics of Inflammatory and Pathological Changes Induced by Single Exposure of Particulate Matter (PM2.5) in Mice: Potential Implications in COPD.

Chronic Obstructive Pulmonary Disease (COPD) is a progressive disorder of lungs marked by chronic bronchitis and emphysema. Particulate matter (PM2.5), a major component of air pollution has been correlated with COPD incidence. The present work aimed to understand dynamics of cellular/molecular players behind PM2.5-mediated COPD pathogenesis in mice by conducting dose and time-course studies. Single intratracheal exposure of PM2.5 at a dose of either 100 or 200 μg induced inflammatory response in lungs at 4 days. Time course studies showed that inflammation once triggered by PM2.5 is progressive in nature as reflected by data on BALF inflammatory cells at 7/14 days. Similarly, various cytokines/chemokines (KC/IL-6/TNF-α/IL-1β/G-CSF/MCP-1) peak at either 7 or 14 days. However, inflammation declined sharply at 21 days. Data on LPO/GSH and activities of SOD/Catalase show induction of continuous oxidative stress in lung tissue. Next, enhanced mtROS in the CD11b+ inflammatory cells confirms the redox imbalance in neutrophils/macrophages. A continuous decline in lung function was observed till 28 days. Further, histological analysis of lung tissues at 28 days confirmed the presence of emphysematous lesions, validating the potency of PM2.5 to cause irreversible damage to lungs through complex interplay of various cellular/molecular players which may be exploited as potential preventive/therapeutic targets.

Assessing the impact of Ag-ZnO nanoparticle on the induction of oxidative stress, hematological, and molecular changes in zebrafish (Danio rerio) and McCoy fibroblast cell lines

Assessing the impact of Ag-ZnO nanoparticle on the induction of oxidative stress, hematological, and molecular changes in zebrafish (Danio rerio) and McCoy fibroblast cell lines

Effects of Brookite TiO2/CeO2 Nanocomposite on Artemia salina: Induction of Oxidative Stress and Apoptosis Assessment

TiO2 and CeO2 NPs are widely used in the medical field, for drug administration, oncological therapies, disinfection or diagnostic imaging. To date, their effects on aquatic ecosystems and their impacts on human health are little known but several scientific evidences show how CeO2 NPs are able to store and release oxygen, giving them antioxidant activity against oxidative stress while TiO2 NPs seem to be responsible for cytotoxicity and genotoxicity. In this study, the effects of combined nanoparticles, brookite TiO2/CeO2 nanocomposites, on A. salina nauplii following acute exposure were evaluated. Although the cytotoxicity of nanoparticles is generally dose-dependent and time-dependent, in the following investigation, exposure to combined nanoparticles, brookite TiO2/CeO2 nanocomposites, in A. salina nauplii would appear not to have had a statistically significant negative impact on the viability of the specimens. One of the mechanisms by which NPs exert toxic effects is the induction of oxidative stress. In this study, an assessment of potential oxidative stress and apoptotic damage on exposed organisms was conducted through the use of the DCFH2DA probe and acridine orange. The results obtained suggest that although acute exposure to different concentrations of brookite TiO2/CeO2 nanocomposites did not have lethal effects, the positivity to DCFH2DA and acridine orange observed does not exclude potential sublethal effects.

Dermatan Sulfate Affects the Activation of the Necroptotic Effector MLKL in Breast Cancer Cell Lines via the NFκB Pathway and Rac-Mediated Oxidative Stress.

Dermatan sulfate (DS) is a glycosaminoglycan characterized by having a variable structure and wide distribution in animal tissues. We previously demonstrated that some structural variants of DS were able to rapidly induce moderate necroptosis in luminal breast cancer cells when used at a high concentration. We have now investigated the mechanisms underlying the DS-mediated activation of the necroptotic executor MLKL using immunofluorescence, Western blotting and pharmacological inhibition. The two main processes, by which DS influences the phosphorylation of MLKL, are the activation of NFκB, which demonstrates a suppressive impact, and the induction of oxidative stress, which has a stimulatory effect. Moreover, the triggering of the redox imbalance by DS occurs via the modulatory influence of this glycosaminoglycan on the rearrangement of the actin cytoskeleton, requiring alterations in the activity of small Rho GTP-ase Rac1. All of these processes that were elicited by DS in luminal breast cancer cells showed a dependence on the structure of this glycan and the type of cancer cells. Furthermore, our results suggest that a major mechanism that is involved in the stimulation of necroptosis in luminal breast cancer cells by high doses of DS is mediated via the effect of this glycan on the activity of adhesion molecules.

The Antioxidative Role of Moringa Oil extract in Modulating Histological and Biochemical Changes in the Salivary Glands of Rats Under Oxidative Stress Induction

The Antioxidative Role of Moringa Oil extract in Modulating Histological and Biochemical Changes in the Salivary Glands of Rats Under Oxidative Stress Induction

Tau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation.

Neurodegenerative diseases are often characterized by mitochondrial dysfunction. In Alzheimer's disease, abnormal tau phosphorylation disrupts mitophagy, a quality control process through which damaged organelles are selectively removed from the mitochondrial network. The precise mechanism through which this occurs remains unclear. Previously, we showed that tau which has been mutated at Thr-231 to glutamic acid to mimic an Alzheimer's-relevant phospho-epitope expressed early in disease selectively inhibits oxidative stress-induced mitophagy in C. elegans. Here, we use immortalized mouse hippocampal neuronal cell lines to extend that result into mammalian cells. Specifically, we show that phosphomimetic tau at Ser-396/404 (EC) or Thr-231/Ser-235 (EM) partly inhibits mitophagy induction by paraquat, a potent inducer of mitochondrial oxidative stress. Moreover, a combination of immunologic and biochemical approaches demonstrates that the levels of the mitophagy receptor FKBP8, significantly decrease in response to paraquat in cells expressing EC or EM tau mutants, but not in cells expressing wildtype tau. In contrast, paraquat treatment results in a decrease in the levels of the mitophagy receptors FUNDC1 and BNIP3 in the presence of both wildtype tau and the tau mutants. Interestingly, FKBP8 is normally trafficked to the endoplasmic reticulum during oxidative stress induced mitophagy, and our results support a model where this trafficking is impacted by disease-relevant tau, perhaps through a direct interaction. We provide new insights into the molecular mechanisms underlying tau pathology in Alzheimer's disease and highlight FKBP8 receptor as a potential target for mitigating mitochondrial dysfunction in neurodegenerative diseases.

Antitumor Effects of Resveratrol Opposing Mechanisms of Helicobacter pylori in Gastric Cancer.

Gastric cancer is an aggressive and multifactorial disease. Helicobacter pylori (H. pylori) is identified as a significant etiological factor in gastric cancer. Although only a fraction of patients infected with H. pylori progresses to gastric cancer, bacterial infection is critical in the pathology and development of this malignancy. The pathogenic mechanisms of this bacterium involve the disruption of the gastric epithelial barrier and the induction of chronic inflammation, oxidative stress, angiogenesis and metastasis. Adherence molecules, virulence (CagA and VacA) and colonization (urease) factors are important in its pathogenicity. On the other hand, resveratrol is a natural polyphenol with anti-inflammatory and antioxidant properties. Resveratrol also inhibits cancer cell proliferation and angiogenesis, suggesting a role as a potential therapeutic agent against cancer. This review explores resveratrol as an alternative cancer treatment, particularly against H. pylori-induced gastric cancer, due to its ability to mitigate the pathogenic effects induced by bacterial infection. Resveratrol has shown efficacy in reducing the proliferation of gastric cancer cells in vitro and in vivo. Moreover, the synergistic effects of resveratrol with chemotherapy and radiotherapy underline its therapeutic potential. However, further research is needed to fully describe its efficacy and safety in treating gastric cancer.

Protective Role of Ellagic Acid Against Ethanol-Induced Neurodevelopmental Disorders in Newborn Male Rats: Insights into Maintenance of Mitochondrial Function and Inhibition of Oxidative Stress.

Ellagic acid (EA) exerts, neuroprotective, mitoprotective, anti-oxidative and anti-inflammatory effects. We evaluated protective effect of EA on ethanol-induced fetal alcohol spectrum disorders (FASD). A total of 35 newborn male rats were used, divided into five groups, including; control (normal saline), ethanol (5.25 g/kg per day), ethanol (5.25 g/kg per day) + EA (10 mg/kg), ethanol (5.25 g/kg per day) + EA (20 mg/kg) and ethanol (5.25 g/kg per day) + EA (40 mg/kg). Thirty-six days after birth behavioral tests (Morris water maze and Elevated Plus Maze), tumor necrosis factor-α (TNF-α) levels, oxidative markers (malondialdehyde, glutathione and superoxide dismutase), mitochondrial examination such as succinate dehydrogenases (SDH) activity, mitochondrial swelling, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) formation were analyzed. The results revealed that ethanol exposure adversely affected cognitive and mitochondrial functions and as well as induced oxidative stress and inflammation in brain tissue. However, EA (20 and 40 mg/kg) administration effectively prevented the toxic effects of ethanol in FASD model. These findings demonstrate that ethanol application significantly impairs the brain development via mitochondrial dysfunction and induction of oxidative stress. These data indicate that EA might be a useful compound for prevention of alcohol-induced FASD.

Combined toxicity of abamectin and carbendazim on enzymatic and transcriptional levels in the soil-earthworm microcosm.

To reveal the toxicological mechanisms of pesticide mixtures on soil organisms, this study concentrated on evaluating enzymatic activity and gene expression changes in the earthworm Eisenia fetida (Savigny 1826). Despite being frequently exposed to multiple pesticides, including the common combination of abamectin (ABA) and carbendazim (CAR), environmental organisms have primarily been studied for the effects of individual pesticides. Acute toxicity results exhibited that the combination of ABA and CAR caused a synergistic impact on E. fetida. The levels of MDA, ROS, T-SOD, and caspase3 demonstrated a significant increase across most individual and combined groups, indicating the induction of oxidative stress and cell death. Additionally, the expression of three genes (hsp70, gst, and crt) exhibited a significant decrease following exposure to individual pesticides and their combinations, pointing toward cellular damage and impaired detoxification function. In contrast, a noteworthy increase in ann expression was observed after exposure to both individual pesticides and their mixtures, suggesting the stimulation of reproductive capacity in E. fetida. The present findings contributed to a more comprehensive understanding of the potential toxicity mechanisms of the ABA and CAR mixture, specifically on oxidative stress, cell death, detoxification dysfunction, and reproductive capacity in earthworms. Collectively, these data offered valuable toxicological insights into the combined effects of pesticides on soil organisms, enhancing our understanding of the underlying risks associated with the coexistence of different pesticides in natural soil environments.

One-step green synthesis of platinum mesoporous nanoparticles by riboflavin for light activated antitumoral therapy

Photodynamic therapy (PDT) has been established as one of the most promising novel cancer therapies with fewer side-effects and enhanced efficacy compared to the currently available conventional treatments. However, its application has been hindered by the limitations that photosensitizers (PS) have. The combination of PS with metallic nanoparticles like platinum nanoparticles (PtNPs), can help to overcome these intrinsic drawbacks. In this work, the combination of PtNPs and the natural photosensitizer riboflavin (RF) is proposed. PtNPs are synthesized using RF (Pt@RF) as reducing and stabilizing agent in a one-step method, obtaining nanoparticles with mesoporous structure for UV triggered PDT. In view of possible future UV irradiation treatments, the degradation products of RF, ribitol (RB) and lumichrome (LC), this last being a photosensitizing byproduct, are also employed for the synthesis of porous PtNPs, obtaining Pt@LC and Pt@RB. When administered in vitro to lung cancer cells, all the samples elicit a strong decrease of cell viability and a decrease of intracellular ATP levels. The antitumoral effect of both Pt@RF and Pt@LC is triggered by UV-A irradiation. This antitumoral activity is caused by the induction of oxidative stress, shown in our study by the decrease in intracellular glutathione and increased expression of antioxidant enzymes.