Jul 2026· International Journal of Applied and Experimental Biology· Vol 6· 0 citations· 22 references
TL;DR
It is suggested that citronellol confers protective effects against ethanol-induced cytotoxicity in human embryonic kidney cells, potentially by enhancing cell viability, attenuating oxidative stress, and modulating apoptosis-related pathways.
Abstract
Alcohol-induced toxicity is a significant health concern that can lead to organ damage, including renal impairment. Citronellol has demonstrated several bioactive properties, including antioxidant, anti-inflammatory, antimicrobial, and anticancer activities. The study aimed to investigate the ameliorative properties of citronellol against alcohol-induced toxicity in human embryonic kidney (HEK) cells. The HEK cells were exposed to ethanol to induce cellular toxicity, followed by treatment with different concentrations of citronellol to assess its cytoprotective potential. Cell viability was examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and crystal violet (CV) assay. Oxidative stress parameters, including glutathione levels and superoxide dismutase (SOD) activity, were measured. Apoptotic potential was evaluated by assessing the expression levels of CYR61 and p53 proteins. Experiments were conducted in triplicate. Citronellol treatment improved cell viability in the ethanol-exposed HEK cells without causing cytotoxicity. A significant reduction in CYR61 protein expression was observed, while the p53 protein levels showed only a mild elevation. In addition, citronellol treatment did not significantly alter glutathione reductase or SOD activities compared with the control group. Overall, these findings suggest that citronellol confers protective effects against ethanol-induced cytotoxicity in human embryonic kidney cells, potentially by enhancing cell viability, attenuating oxidative stress, and modulating apoptosis-related pathways.
Prolonged administration of cisplatin, a widely used chemotherapeutic agent, induces nephrotoxicity. Identifying natural compounds that attenuate cisplatin's adverse effects on renal tissues would be of clinical value. Thus, the present study aimed to evaluate the cytoprotective effects of Cudrania tricuspidata leaf-derived polysaccharides (CTP) in human embryonic kidney (HEK) 293T cells to explore their potential as a chemotherapeutic adjuvant. In the cell viability assay, CTP alone showed no inherent cytotoxic effects, whereas co-treatment with cisplatin led to a significant improvement in cell viability. These observations were corroborated by Annexin V/propidium iodide staining, which demonstrated that CTP effectively attenuated cisplatin-induced cell damage in HEK 293T cells. CTP also increased the total antioxidant capacity in the 2,2-diphenyl-1-picrylhydrazyl, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid), and ferric reducing antioxidant power assays in a dose-dependent manner while elevating the activities of intracellular antioxidant enzymes, including catalase and superoxide dismutase, which correlated with the expression of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1. Moreover, CTP reduced malondialdehyde levels, indicating that it protected against oxidative-stress-induced membrane damage. Mechanistically, CTP mitigated cisplatin-induced apoptosis by upregulating B cell lymphoma 2 (Bcl-2) expression while suppressing the expression of Bcl-2-associated X protein, cleaved caspase-3, and caspase-9. Collectively, the findings demonstrate that pretreatment with CTP protected HEK 293T cells from cisplatin-induced damage, highlighting its potential as a functional food ingredient.
Hea-Ju Cho, Eui-Hong Byun· Journal of Medicinal Food· 0 citations
Antimony (Sb), a heavy metal employed in PET manufacturing, is an emerging contaminant due to its ability to leach into food and beverages. Chronic exposure can impair intestinal health by disrupting epithelial barrier functionality and promoting oxidative stress, inflammation, and apoptosis. This study investigated the protective effects of cyanidin-3-O-glucoside (C3G), a dietary anthocyanin, against continuous exposure to low concentrations of Sb(III) during intestinal epithelial Caco-2 cell differentiation. C3G (20-40μM) attenuated barrier dysfunction, increasing TEER values and reducing fluorescein permeability, and reduced reactive oxygen species, mitigating inflammatory responses by inhibiting NF-κB activation and downregulating IL-6 and COX-2 expression. C3G alleviated endoplasmic reticulum (ER) stress, decreasing eIF2α phosphorylation and ATF4 and CHOP expression. Furthermore, it reduced apoptosis, as shown by lower caspase-3 activation, and displayed antioxidant activity, partly mediated by the Nrf2‑related pathway. Overall, C3G protects intestinal epithelial function from Sb-induced stress by modulating oxidative, inflammatory, ER stress, and apoptotic pathways.
F. L. Salamone, M. S. Molonia, Santi Trischitta et al.· Environmental Toxicology and...· 0 citations
BACKGROUND/OBJECTIVES Cisplatin is a widely used drug clinically for the treatment of numerous solid malignant tumors. However, the use of cisplatin has resulted in serious side effects, of which renal toxicity and renal dysfunction are the most common. In this study, we explored the effect of isothiocyanates in cisplatin-treated human embryonic kidney (HEK)-293 cells. Allyl isothiocyanate (AITC) and benzyl isothiocyanate (BITC) are substances found in cruciferous vegetables such as watercress and broccoli. They possess various physiological activities including anti-inflammatory, anticancer and antioxidant. However, the protective effect of AITC and BITC against cisplatin-induced nephrotoxicity has not yet been elucidated. MATERIALS/METHODS HEK-293 cells were treated with cisplatin (50 µM) in AITC and BITC (0.3–1.25 µM) in the absence or presence for 24 h. MTT assays detected cell viability, and Hoechst 33342 staining allowed us to observe nuclear morphology changes such as chromatin condensation and apoptotic nuclei. Reactive oxygen species (ROS) detection assays measured intracellular ROS production and the griess reaction assays assessed nitric oxide (NO) production. Western blotting and quantitative polymerase chain reactions quantified corresponding proteins and mRNA. RESULTS Cisplatin treatment for 24 h increased the generation of intracellular ROS and NO production compared to untreated cells. In contrast, pretreatment with AITC and BITC significantly reduced intracellular ROS generation and NO production. AITC and BITC also significantly inhibited cisplatin-induced inflammation-related genes expression. AITC and BITC decreased cisplatin-induced mitogen-activated protein kinase (MAPK) protein expression. Pretreatment of cells with AITC and BITC in cisplatin-treated cells downregulated the Bax/Bcl-2 expression ratio, resulting in a dose-dependent inhibition of apoptosis. CONCLUSION Our results suggest that the inhibition of inflammation and cell death via MAPK signaling in HEK-293 cells plays a protective role in kidney damage. Therefore, AITC and BITC may be potential candidates to attenuate and prevent the onset and progression of nephrotoxicity.
Ha-Rin Moon, Jung-Mi Yun· Nutrition Research and Pract...· 0 citations
Acrylamide (Acr) is a widely encountered environmental and dietary toxicant known to induce oxidative stress and disrupt male reproductive function. Leydig cells, due to their high metabolic activity and mitochondrial dependence, are particularly vulnerable to redox imbalance. N-acetylcysteine (Nac), a thiol-containing antioxidant and glutathione precursor, has been extensively studied for its cytoprotective properties. However, its modulatory effects on Acr-induced toxicity in Leydig cells and its pharmacodynamic interaction profile remain incompletely characterized. In this study, TM3 Leydig cells were exposed to Acr in the presence or absence of Nac. Cell viability was assessed by MTT assay, and chemical interaction profiles were evaluated using ZIP, Bliss, and Chou-Talalay combination index analyses. Oxidative stress parameters, including intracellular reactive oxygen species (ROS), lipid peroxidation, antioxidant enzyme activities (SOD, CAT, GPx), and glutathione levels, were measured. Apoptotic responses were analyzed through double fluorescence staining, RT-qPCR of apoptosis-related genes (Bax, Bcl2, Casp3, Trp53), and Western blot analysis of CASP3 protein expression. Acr exposure significantly reduced cell viability, increased ROS and lipid peroxidation levels, suppressed antioxidant defenses, and activated the mitochondrial apoptotic pathway. Nac treatment markedly improved cell viability, restored antioxidant capacity, reduced oxidative stress markers, and suppressed p53/Bax/Casp3-mediated apoptotic signaling. Combination analyses revealed an antagonistic interaction profile, indicating that Nac biologically limits Acr-induced cytotoxicity. Collectively, these findings demonstrate that Nac exerts protective effects in Leydig cells by modulating redox homeostasis and mitochondrial apoptosis, suggesting its potential as a protective regulator against Acr-induced reproductive toxicity.
Banu Orta Yilmaz, Iremnur Sarialioglu, Gokce Elmaci et al.· Drug and chemical toxicology...· 0 citations
Findings indicate that black mulberry fruit extract partially mitigates VPA-induced hepatocellular injury, primarily by enhancing glutathione-dependent antioxidant defenses.
Iza Oblak, Nebojša Pavlović, S. Vukmirović et al.· Biomolecules & biomedicine· 0 citations
Protein aggregation and increased reactive oxygen species (ROS) driving oxidative stress are hallmarks of neurodegenerative diseases. This study investigated the protective potential of the natural antioxidants ferulic acid (FA) and quercetin (Qc) against cytotoxicity induced by the Alzheimer's-associated β-amyloid peptide (Aβ42), using Saccharomyces cerevisiae as a eukaryotic model. Assays were performed using a wild-type strain (BY4741), an isogenic mutant deficient in the antioxidant transcription factor Yap1p (Δyap1), and a transformed strain expressing Aβ42. Experiments evaluated cell proliferation, mitochondrial membrane potential (ΔΨ), and intracellular oxidation levels. Results showed that both FA and Qc significantly reduced intracellular oxidation in WT and Δyap1 strains under H₂O₂-induced stress, as well as in the Aβ42-expressing strain. However, this antioxidant activity failed to rescue yeast metabolism from Aβ42 toxicity, which severely compromised cell proliferation rates and ΔΨ. These findings demonstrate that while FA and Qc effectively modulate the redox imbalance caused by Aβ42, their antioxidant effect does not directly translate into cellular protection against β-amyloid cytotoxicity. Consequently, although oxidative stress contributes to Aβ42-induced damage, mitigating this condition alone is insufficient to neutralize the fundamental pathological mechanisms that compromise eukaryotic cell survival.
Rodrigo P. Osorio, D. C. N. Grillo, T. A. Cruz et al.· ARACÊ· 0 citations
