Selenocysteine insertion sequence binding protein 2 (Sbp2) in the sex-specific regulation of selenoprotein gene expression in mouse pancreatic islets.

Selenoproteins are a group of selenocysteine-containing proteins with major roles in cellular antioxidant defense and thyroid hormone metabolism. Selenoprotein expression is determined by hierarchical mechanisms that result in tissue-specific levels. Current data inadequately explain the abundance of various selenoproteins under normal and pathological conditions, including in pancreatic ß-cells. Selenocysteine insertion sequence binding protein 2 (SBP2) is a critical protein in selenoprotein translation that also plays an essential role in stabilizing selenoprotein transcripts by antagonizing nonsense-mediated decay (NMD). Importantly, dysfunctional SBP2 is associated with endocrine disorders in humans. Here we describe the impact of induced Sbp2 deficiency in pancreatic ß-cells on selenoprotein transcript profiles in the pancreatic islets of C57BL/6J mice. Sex differences were noted in control mice, in which female islets showed 5 selenoproteins decreased and one increased versus male islets. Induced Sbp2 deficiency in pancreatic ß-cells altered expression of only 3 selenoprotein transcripts in male islets, whereas 14 transcripts were reduced in female islets. In all cases, decreased transcription was observed in genes known to be regulated by NMD. The differential impact of Sbp2 deletion on selenoprotein transcription between sexes suggests sex-specific hierarchical mechanisms of selenoprotein expression that may influence islet biology and consequentially metabolic disease risk.

Sphingomyelin: a natural modulator of membrane homeostasis and inflammation.

Although membrane sphingomyelin (SPH) serves as the precursor for many signaling molecules, its presence in large amounts, and its specific localization in the outer monolayer of the plasma membrane suggest that it may have a cytoprotective function. We propose that SPH helps maintain the integrity of the plasma membrane by protecting phosphatidylcholine (PC) against oxidative damage and phospholipase degradation. Since it contains mostly saturated longchain hydrocarbon groups, we postulate that SPH impedes the lateral propagation of the lipid peroxides by decreasing membrane fluidity, while also acting as an 'insulating' molecule. By virtue of its structural similarity to PC, it acts as a competitive inhibitor of the phospholipases, which may otherwise hydrolyze PC excessively. Because phospholipase reaction is the rate-limiting step in eicosanoid synthesis, SPH may serve as an endogenous anti-inflammatory molecule.

Spectral changes in metal halide and high-pressure sodium lamps equipped with electronic dimming.

Electronic dimming of high-intensity discharge lamps offers control of photosynthetic photon flux (PPF) but is often characterized as causing significant spectral changes. Growth chambers with 400-W metal halide (MH) and high-pressure sodium (HPS) lamps were equipped with a dimmer system using silicon-controlled rectifiers (SCR) as high-speed switches. Phase control operation turned the line power off for some period of the alternating current cycle. At full power, the electrical input to HPS and MH lamps was 480 W (root mean squared) and could be decreased to 267 W and 428 W, respectively, before the arc was extinguished. Concomitant with this decrease in input power, PPF decreased by 60% in HPS and 50% in MH. The HPS lamp has characteristic spectral peaks at 589 and 595 nm. As power to the HPS lamps was decreased, the 589-nm peak remained constant while the 595-nm peak decreased, equaling the 589-nm peak at 345-W input, and the 589-nm peak was almost absent at 270-W input. The MH lamp has a broader spectral output but also has a peak at 589 nm and another smaller peak at 545 nm. As input power to the MH lamps decreased, the peak at 589 diminished to equal the 545-nm peak. As input power approached 428 W, the 589-nm peak shifted to 570 nm. While the spectrum changed as input power was decreased in the MH and HPS lamps, the phytochrome equilibrium ratio (Pfr : Ptot) remains unchanged for both lamp types.