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    Boric acid and quercetin supplementations alleviated paraquat-induced neurotoxic and irritation effects in human SH-SY5Y cells and in ovo models
    (Bmc, 2025) Guner, Adem; Tekin, Askin
    BackgroundParaquat (PQ) is a herbicide that causes neurotoxicity through oxidative stress, mitochondrial dysfunction and apoptosis. Boric acid (BA) and quercetin (Qe) are bioactive compounds with antioxidant and anti-inflammatory properties, but their combined effect against PQ-induced neuronal damage is still unexplored. This study aimed to investigate the individual and synergistic protective effects of BA and Qe in SH-SY5Y neuroblastoma cells and in ovo models.MethodsHuman SH-SY5Y neuroblastoma cells were exposed to PQ (400 mu M) with or without BA (50 mu M), Qe (50 mu M) or their combination for 48 h. ROS production, mitochondrial membrane potential (MMP, Delta Psi m) and intracellular calcium levels (Ca-2(+)) were measured. Apoptotic (BAX, BCL2, Casp-3) and inflammatory (NFKB, VEGF, TNF, TRAF1) gene expression and DNA fragmentation were determined by qRT-PCR and DPA assay. NRF2 activation was determined by gene expression. In parallel, irritation and vascularization were evaluated using the hen's egg chorioallantoic membrane (HET-CAM) assay after exposure to PQ, BA, Qe and their combinations.ResultsPQ significantly increased ROS, interfered with MMP, increased Ca-2(+) levels, regulated pro-apoptotic and inflammatory genes, and induced DNA fragmentation. BA or Qe alone reduced oxidative stress, partially restored Delta Psi m and Ca-2(+) homeostasis, downregulated BAX and Casp-3, and increased BCL2 expression. The combined treatment with BA + Qe showed the strongest protection by significantly reducing ROS, restoring Delta Psi m and Ca-2(+) homeostasis, suppressing inflammatory genes, enhancing NRF2 activation and minimizing DNA fragmentation, indicating synergistic antioxidant and anti-apoptotic effects. In the HET-CAM assay, PQ induced hemorrhage, lysis, and severe irritation with an IS of 9.1 +/- 0.2, whereas BA, Qe, and BA + Qe alone showed no irritation. Co-treatments (BA + PQ and Qe + PQ) caused moderate irritation (IS 6.2 +/- 0.1 and 6.0 +/- 0.2, respectively), while the combined treatment with BA + Qe + PQ markedly alleviated irritation, showing only mild effects (IS 4.1 +/- 0.2).ConclusionsBA and Qe, particularly in combination, protect neuronal cells from PQ-induced oxidative and mitochondrial damage by restoring redox balance, stabilizing mitochondria, regulating Ca-2(+) homeostasis and modulating apoptosis and attenuating irritation in the in ovo model. These results suggest that BA and Qe may be promising complementary therapeutics to attenuate neurotoxicity caused by environmental toxins.
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    Öğe
    Protective Effect of Boric Acid Against Ochratoxin A-Induced Toxic Effects in Human Embryonal Kidney Cells (HEK293): A Study on Cytotoxic, Genotoxic, Oxidative, and Apoptotic Effects
    (Springernature, 2025) Tekin, Askin; Guner, Adem; Akkan, Tamer
    The present study evaluates the protective properties of boric acid (BA) against the toxic effects induced by ochratoxin A (OTA) in human embryonic kidney cells (HEK293). The focus is on various parameters such as cytotoxicity, genotoxicity, oxidative stress, and apoptosis. OTA is a known mycotoxin that has harmful effects on the liver, kidneys, brain, and nervous system. BA, on the other hand, a boron-based compound, is known for its potential as a vital micronutrient with important cellular functions. The results show that BA administration not only increases cell viability but also mitigates the cytotoxic effects of OTA. This is evidenced by a reduction in the release of lactate dehydrogenase (LDH), indicating less damage to cell membranes. In addition, BA shows efficacy in reducing genotoxic effects, as the frequency of micronucleus (MN) and chromosomal aberrations (CA) decreases significantly, suggesting a protective role against DNA damage. In addition, the study shows that treatment with BA leads to a decrease in oxidative stress markers, highlighting its potential as a therapeutic intervention against the deleterious effects of OTA. These results emphasize the need for further research into the protective mechanisms of boron, particularly BA, in combating cell damage caused by OTA.