Background and objectives: Previous studies have shown anti-tumor activity of quercetin (QT). However, the low bioavailability of QT has restricted its use. This study aimed to assess the toxic effect of QT encapsulated in solid lipid nanoparticles (QT-SLNs) on the growth of MCF-7 human breast cancer cells. Materials and Methods: MCF-7 and MCF-10A (non-tumorigenic cell line) cell lines treated with 25 µmol/mL of QT or QT-SLNs for 48 h. Cell viability, colony formation, oxidative stress, and apoptosis were evaluated to determine the toxic effects of the QT-SLNs. Results: The QT-SLNs with appropriate characteristics (particle size of 85.5 nm, a zeta potential of −22.5 and encapsulation efficiency of 97.6%) were prepared. The QT-SLNs showed sustained QT release until 48 h. Cytotoxicity assessments indicated that QT-SLNs inhibited MCF-7 cells growth with a low IC₅₀ (50% inhibitory concentration) value, compared to the free QT. QT-SLNs induced a significant decrease in the viability and proliferation of MCF-7 cells, compared to the free QT. QT-SLN significantly increased reactive oxygen species (ROS) level and MDA contents and significantly decreased antioxidant enzyme activity in the MCF-7 cells. Following QT-SLNs treatment, the expression of the Bcl-2 protein significantly decreased, whereas Bx expression showed a significant increase in comparison with free QT-treated cells. Furthermore, The QT-SLNs significantly increased apoptotic and necrotic indexes in MCF-7 cells. Viability, proliferation, oxidative stress and apoptosis of MCF-10A cells were not affected by QT or QT-SLNs. Conclusions: According to the results of this study, SLN significantly enhanced the toxic effect of QT against human breast cancer cells.

Quercetin induces apoptosis and necroptosis in MCF-7 breast cancer cells

Exposure to glucocorticoids (GCs) leads to numerous changes in various biological systems including the reproductive system. This work evaluated effects of dexamethasone (Dex), a widely used GC, on mouse testicular germ cells. Experimental groups (E1-E3) received one of the following treatments daily for 7 days: 4, 7 and 10 mg kg(-1) Dex respectively. Control groups were treated with equivalent volumes of saline. Testicular histopathology, morphometric analysis and deoxy-UTP-digoxigenin nick end labeling (TUNEL) assessment were performed for evaluation of the toxic effects of Dex and detection of the apoptotic cells. The results showed that Dex induces histopathological alterations such as epithelial vacuolisation, atrophy and reduction in testicular spermatozoid. Morphometrical data showed that Dex significantly reduced tubular diameter and epithelial height (P < 0.05). Johnsen's scoring also showed poor spermatogenesis in E2 and E3 groups (P < 0.05). Apoptotic index of germ cells was significantly increased in E2 (18.9% versus 1.76%, P < 0.01) and E3 (24.6 versus 1.76%, P < 0.001) groups. It is concluded that Dex acts as testicular toxicant and that further studies are needed to establish its mechanism of action upon spermatogenesis.