The vicious circle between mitochondrial oxidative stress and dynamic abnormality mediates triethylene glycol dimethacrylate-induced preodontoblast apoptosis.

Oxidative stress (OS) plays crucial roles in triethylene glycol dimethacrylate (TEGDMA, a major component in dental resin)-induced apoptosis of dental pulp cells. Mitochondria are important target organelles for regulating the balance of OS, meanwhile, imbalance of the mitochondrial dynamic associated with mitochondrial dysfunction is one major molecular mechanism for oxidative damages. However, whether these mitochondrial dependent pathways were involved in the apoptosis of dental pulp cells induced by TDGDMA remains unclarified. We demonstrated that TEGDMA decreased viability and induced apoptosis of mouse preodontoblasts (mDPC6T cell line) in a time- and dose-dependent manner. Furthermore, TEGDMA elevated the mitochondrial OS status and induced mitochondrial dysfunction, as reflected by the significant decrease of mitochondrial membrane potential, ATP production, the activity of Complex III and citrate synthase. In this process, we detected a dramatically impaired mitochondrial dynamic that was reflected by significantly enhanced mitochondrial fragmentation. Consistently, we also found a significant enhancement of the key upstream regulators for mitochondrial fission, such as short form of optic atrophy 1, dynamic related protein 1 oligomer and Fission 1. The respective inhibition of mitochondrial OS or mitochondrial fission could mutually attenuate each other, thereby significantly preventing both mitochondrial dysfunction and cell apoptosis. In conclusion, TEGDMA-induced preodontoblasts apoptosis was mediated by the vicious circle between mitochondrial OS and dynamic abnormality, which represented a new target to prevent TEGDMA-induced dental pulp cells apoptosis.

Effect of ammonium on liquid- and gas-phase protonation and deprotonation in electrospray ionization mass spectrometry.

The electrospray ionization (ESI) is a complex process and there has been a long debate regarding the gas-phase effect on ion generation in the process. In this paper we investigated the effect of liquid chromatographic mobile phase additives (formic acid, aqueous ammonia and their combination) on the ESI signal intensities for a wide variety of compounds. The addition of a trace amount of aqueous ammonia to the common formic acid-methanol mobile phase significantly enhances the ESI signals of protonated molecules and suppresses the formation of sodium adduct ions. This effect is well observed for the compounds containing the -N-C=O group but not for those without N or O atoms. The ESI signal intensity of deprotonated molecules increases with increase in pH of the mobile phase for neutral compounds, such as substituted urea, whereas this trend is not observed for acidic compounds such as phenoxy acids. The mechanistic analysis regarding liquid- and gas-phase protonation and deprotonation is discussed.

Apoptotic-induced cleavage shifts HuR from being a promoter of survival to an activator of caspase-mediated apoptosis.

Little is known about the cellular mechanisms modulating the shift in balance from a state of survival to cell death by caspase-mediated apoptosis in response to a lethal stress. Here we show that the RNA-binding protein HuR has an important function in mediating this switch. During caspase-mediated apoptosis, HuR is cleaved to generate two cleavage products (CPs). Our data demonstrate that the cleavage of HuR switches its function from being a prosurvival factor under normal conditions to becoming a promoter of apoptosis in response to a lethal stress. In the absence of an apoptotic stimuli, HuR associates with and promotes the expression of caspase-9 and prothymosin α (ProT) mRNAs, and pro- and antiapoptotic factors, respectively, both of which have been characterized as important players in determining cell fate. During the early steps of caspase-mediated apoptosis, however, the level of caspase-9 protein increases, while ProT remains unchanged. Under these conditions, the two HuR-CPs selectively bind to and stabilize caspase-9 mRNA, but do not bind to ProT. Hence, taken together, our data show that by maintaining a threshold of expression of proapoptotic factors such as caspase-9 in response to a lethal stress, the HuR-CPs help a cell to switch from resisting death to undergoing apoptosis.

Chemical degradation of drinking water disinfection byproducts by millimeter-sized particles of iron-silicon and magnesium-aluminum alloys.

The candidature of Fe-Si and Mg-Al alloys at millimeter-scale particle sizes for chemical degradation of disinfection byproducts (DBPs) in drinking water systems was substantiated by their enhanced corrosion resistance and catalytic effect on the degradation. The Mg-Al particles supplied electrons for reductive degradation, and the Fe-Si particles acted as a catalyst and provided the sites for the reaction. The alloy particles are obtained by mechanical milling and stable under ambient conditions. The proposed method for chemical degradation of DBPs possesses the advantages of relatively constant degradation performance, long-term durability, no secondary contamination, and ease of handling, storage and maintenance in comparison with nanoparticle systems.

A novel approach for the determination of detection limits for metal analysis of environmental water samples.

Despite the widespread use of the USEPA method (U.S. Environmental Protection Agency, 40 CFR 136 Appendix B) for the determination of method detection limit (MDL), criticisms have been raised that the method does not account for measurement bias and outliers that subsequently lead to a common misunderstanding of the requirement for the determination of MDL. This paper demonstrates that it is difficult to follow the USEPA method for verifying the MDL for analysis involving multiple metals and proposes a precision and bias criterion for determining the MDL. A multiple-point fitted profile, based on the correlation between relative standard deviation (RSD) and concentration, is used to derive a robust MDL value. Representative examples of As, Ca, Cr, and Cu are used to illustrate this procedure. A procedure for identifying outliers is also discussed.