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Objective: To investigate the effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (Ⅱ) and Fe (Ⅱ) ions. Methods: The antiproliferative effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu (Ⅱ) and Fe (Ⅱ) ions were examined by MTT assay. Additionally, colony-forming, reactive oxidative species (ROS) generation, apoptosis induction, autophagy, mitochondrial membrane potential, and mitochondrial mass were investigated. Results: At 24 and 72 h, no significant differences were observed in the viability of HepG2 cells between the control and syringic acid + Fe (Ⅱ) groups. However, exposure of HepG2 cells to syringic acid + Cu (Ⅱ) for 72 h reduced the cell viability significantly. Furthermore, ROS formation, induction of apoptosis, and autophagic vacuoles were significantly increased in HepG2 cells without marked changes in mitochondrial membrane potential and mitochondrial mass. Moreover, syringic acid + Cu (Ⅱ) reduced the plating efficiency and surviving fraction significantly. Conclusions: The combination of syringic acid with Cu (Ⅱ) was toxic to cancer cells and showed pro-oxidant activity. In addition, this combination induced autophagy in cancer cells with less cytotoxic effects on normal cells, which is a potential candidate for the development of novel therapeutics towards cancer. [ABSTRACT FROM AUTHOR]

Background: Sodium benzoate, a food preservative, prevents the growth of fungi and bacteria. Numerous studies have reported the protective effects of sodium benzoate on the nervous system. This study investigated the effect of sodium benzoate on cell apoptosis and mitochondrial function in an aluminum cell toxicity model. Methods: After 48 hr of treating PC-12 cells with varying concentrations of sodium benzoate (0.125, 0.25 or 0.5 mg/ml) in the presence of aluminum maltolate (500 µM), the cell viability was assessed by MTT assay. The type of cell death (necrosis or apoptosis) was analyzed by flow cytometry (7-ADD/An V-PE staining). Also, rhodamine 123 was used to measure the Mitochondrial Membrane Potential (MMP). The acetylcholinesterase activity (AChE) was assessed by Ellman's method. Results: It was observed that sodium benzoate inhibited aluminum induced cell death within 48hr. Sodium benzoate at a concentration of 0.5 mg/ml significantly reduced the apoptotic cells that had been exposed to aluminum. Exposure of PC-12 cells with sodium benzoate and aluminum, increased the AChE activity, although, no significant changes in mitochondrial membrane potential were observed. Conclusion: Sodium benzoate may provide its protective effects through increased AChE activity and inhibiting apoptosis induced by aluminum toxicity. It is likely that the disruption of MMP is neither involved in the induction of apoptosis by aluminum nor in the protective effect of sodium benzoate. [ABSTRACT FROM AUTHOR]

The aim of the present investigation was to determine the effects of sodium fluoride (NaF) on aluminum-induced toxicity in PC12 cells, a rat pheochromocytoma cell line, including cell death and changes in apoptosis, mitochondrial membrane potential (MMP), and oxidative stress. Aluminum (Al) and the fluoride ion (F) are known as plausible pathological factors in the pathogenesis of neurodegenerative disease. Conflicting results have been reported on the interaction of fluoride and aluminum on cell toxicity. PC12 cells were treated with various concentrations of aluminum maltolate (Almal) in the presence and absence of NaF (50-2400 µM) in vitro. A MTT (3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay was used to determine cell viability. 7AAD/annexin-V and 2',7'-dichlorofluorescin diacetate (DCFDA) flow cytometric methods were used to quantify the effects of NaF on Al-induced apoptosis and reactive oxygen species (ROS) generation, respectively. The mitochondrial membrane potential (MMP) was monitored using the retention of rhodamine 123. Catalase activity was determined by measuring the rate of H2O2 decomposition. Almal exposure increased cell death dose dependently and significantly (IC50=1090 µM). ROS generation and apoptosis were increased while MMP and catalase activity were reduced following treatment with Almal. NaF ameliorated the Almal-induced cell toxicity in low concentrations while augmenting the Almal effects at high concentrations. The present data suggest F has antagonistic impacts on Al-induced cell toxicity in low concentrations while acting synergistically with Al to induce cell toxicity at high concentrations. [ABSTRACT FROM AUTHOR]

Small supernumerary marker chromosomes (sSMCs), or markers, are abnormal chromosomal fragments that can be hereditary or de novo. Despite the importance of sSMCs diagnosis, de novo sSMCs are rarely detected during the prenatal diagnosis process. Usually, prenatally diagnosed de novo sSMCs cannot be correlated with a particular phenotype without knowing their chromosomal origin and content; therefore, molecular cytogenetic techniques are applied to achieve this goal. The present study aimed to characterize an sSMC in a case of Klinefelter syndrome using an in-house microsatellite analysis method and fluorescent in situ hybridization (FISH) technique. Amniotic fluid was collected from a pregnant woman who was considered to have risk factors for trisomy higher than the screening cut-off. Karyotype analysis was followed by the amplification of different microsatellite loci and FISH technique. Karyotype analysis identified a fetus with an extra X chromosome and also an sSMC with unknown identity. Further investigation of the parents showed that the sSMC is de novo. Microsatellite amplification by quantitative fluorescent PCR (QF-PCR) and FISH analysis showed that the sSMC is a derivative of chromosome 18. Eventually, the patient decided to terminate the pregnancy. Here, the first case of the coincidence of sSMC 18 in a Klinefelter fetus is reported. [ABSTRACT FROM AUTHOR]

Metastasis to lymph nodes and distant organs is the main challenge in the treatment of papillary thyroid cancer. In the current investigation, we aimed to evaluate the synergistic effects of celecoxib (CX) and sodium valproate (VPA) against cell survival, invasiveness properties, and expression of metalloproteinase-2 and -9 (MMP-2 and MMP-9) in papillary thyroid cancer cell line, B-CPAP cells. The effect of CX and VPA on B-CPAP cells viability and apoptosis were investigated using MTT assay and annexin V/7-AAD flowcytometry, respectively. The effects of the drugs on invasiveness properties of B-CPAP cells and expression of MMP-2 and MMP-9 were evaluated using transwell assay and real time PCR, respectively. MTT assay showed that CX and VPA decreased viability of B-CPAP cells dose dependently (IC50 32.4μM and 6.8 mM, respectively). Combination of CX (5 μM) and VPA (2.5 and 5 mM) increased apoptosis, and reduced cell migration and invasion of B-CPAP cell, synergistically. Real time PCR results showed that both CX (5 μM) and VPA (2.5 and 5 mM) reduced MMP-2 expression (P < 0.05) but had no significant effects on the expression of MMP-9. Our findings suggest that CX and VPA synergistically increase apoptosis and suppress migration and invasion of B-CPAP cells through inhibition of MMP-2 expression. [ABSTRACT FROM AUTHOR]

Sodium benzoate (SB) is one of the food additives and preservatives that prevent the growth of fungi and bacteria. SB has been shown to improve the symptoms of neurodegenerative disease such as Alzheimer's disease. The aim of this study was to evaluate the effect of SB on the cell survival and cellular antioxidant indices after exposure to aluminum maltolate (Almal) in PC12 cell line as a model of neurotoxicity. The cells exposed to different concentrations of SB (0.125 to 3 mg/mL) in the presence of Almal (500 µM) and cell viability, the level of reactive oxygen species (ROS), glutathione content and catalase activity were measured. The results showed that low concentrations of SB caused an increase in the cell survival, but cell viability was reduced in high concentrations. SB could neither prevent the level of ROS production nor change glutathione content. SB (0.5 mg/mL) significantly increased the catalase enzyme activity as compared to the Almal. This study suggested that SB did not completely protect the cell to aluminuminduced free radicals toxicity. Possibly SB improves the symptoms of neurodegenerative disease by other mechanisms. [ABSTRACT FROM AUTHOR]

Objective(s): The role of aluminum (Al) in the pathogenesis of neurodegenerative diseases has been implicated in several studies. However, the exact mechanisms of cytotoxic effects of Al have not been elucidated yet. The aim of this study was to investigate the effect of L-type calcium channel antagonist, nimodipine (NM), and lithium chloride (LiCl) on Al-induced toxicity in PC12 cells. Materials and Methods: PC12 cells were treated with Al-maltolate (Almal) in the presence and absence of different concentrations of NM (50-150 μm) and/or LiCl (0.5-1.0 mM) for 48 hr. Cell viability, apoptosis, and catalase (CAT) activity, a marker of oxidative stress, were then measured using MTT, flow cytometry and enzyme assay, respectively. Results: The results showed that Almal, dose dependently induced cell death, apoptosis and CAT activity in the PC12 cells. NM significantly increased cell viability and decreased apoptosis and CAT activity of Almal-treated cells in a dose dependent mode. LiCl reduced CAT activity and increased cell viability in Almal-treated cells, without significant effect on apoptosis (P=0.74). Conclusion: These findings suggest that NM and Li may have benefits in the prevention of Al-induced cytotoxicity through decreasing oxidative stress. [ABSTRACT FROM AUTHOR]