Search

As nanoparticles (NPs) are readily absorbed across gastrointestinal tract, it is hypothesized that Zinc oxide nanoparticles (ZnO-NPs) will not interfere with intestinal glucose transport. The current study aims to investigate the in vitro effects of ZnO-NPs on Na linked glucose transport across jejunal mucosa in laying hens. A total of 12 White Leghorn laying hens (1.73 ± 0.176 kg), 40 wk of age, housed in individual cages were killed and mid-jejunum was divided into 4 segments to be mounted on the Ussing chambers. The mucosal side of jejunum was bathed with either no ZnO, ZnO (70 μM), ZnO-NPs (70 μM), or ZnO-NPs (35 μM) followed by addition of D-glucose (10 mM) mucosally in all the 4 experimental groups. Peak electrical response was measured 2 min after the addition of D-glucose. Results demonstrate that there was a decrease (P< 0.05) in short-circuit current (Isc) of tissues treated with ZnO compared to either control or ZnO-NPs suggesting that ZnO and not ZnO-NPs appears to interfere with electrogenic current across jejunal tissues of the laying hens. The increases in Isc following the addition of D-glucose was higher (P< 0.05) in the tissues pretreated with ZnO-NPs compared with the tissues mucosally bathed with only ZnO while the tissue conductance (Gt) remained unchanged. In conclusion, ZnO-NPs did not interfere with glucose transport and can be used as a feed supplement.

The transport of nitrogen across the rumen epithelium is characterized by absorption of ammonia from the rumen and by an influx of urea into the rumen. The transport rates of both compounds are large and exhibit wide variation. The transport of ammonia occurs in two forms: in the lipophilic form as NH3, the magnitude of which is linearly related to the pH in the ruminal fluid at pH values above 7, while at a physiological pH of 6.5 or lower, ammonia is predominantly absorbed as NH4+ via putative potassium channels in the apical membrane. The uptake of NH4+ depends on the potential difference of the apical membrane, Pda, and shows competition with K uptake. The pathway for basolateral exit of NH4+ is unknown. Hence, the relative transport rates of NH3 or NH4+ are determined by the ruminal pH according to the Henderson–Hasselbalch equation. Transport of ammonia interacts with the transport of Na and Mg mainly via changes of the intracellular pH. Urea recycling into the rumen has been known for many years and the transport across the rumen epithelium is mediated via urea transporters in the luminal and basolateral membrane of the epithelium. Transport of urea occurs by simple diffusion, but is highly variable. A significant increase of urea influx is caused by the fermentation products CO2 and short-chain fatty acids. Conversely, there is some evidence of inhibition of urea influx by ruminal ammonia. The underlying mechanisms of this modulation of urea transport are unknown, but of considerable nutritional importance, and future research should be directed to this aspect of ruminal transport.

The aim of this study is to characterize the subtype of tyrosine kinase-regulated L-type Ca2+ channels in retinal pigment epithelial (RPE) cells. Ca2+ channel α1D-subunits were enriched by immunoprecipitation from membrane proteins isolated from rat RPE cells. Western blot analysis of the precipitates revealed coprecipitation of pp60c-src. In addition, in precipitates obtained with antibodies against pp60c-src, α1D-subunits were identified. The same was observed in immunoprecipitations from rat brain neurons. Tyrosine phosphorylation of α1D-subunits was confirmed using anti-phosphotyrosine antibodies. Ba2+ currents through L-type channels in cultured rat RPE cells were increased by intracellular application of active pp60c-src (30 U/ml) (heat-inactivated pp60c-src had no effect). Thus, L-type channels of the neuroendocrine subtype can be expressed in epithelial cells and are activated by tyrosine kinase of the src subtype. This kind of regulation is also suggested for brain-derived neurons.

Trabecularf2f2Parts of this work were published in abstract form: Steinhausen, K., Stumpff, F., Strauß, O., Wiederholt, M. 1998. Trabecular meshwork cells express L-type Ca2+channels. Pflügers Arch. 437 (Suppl.): R79.meshwork (TM), a smooth muscle-like tissue with contractile properties, is involved in the regulation of aqueous humor outflow. However, little is known about the regulation of Ca2+influx in trabecular meshwork cells. We investigated the influence of acetylcholine and tyrosine kinases on Ca2+conductances of bovine TM (BTM) and human TM (HTM) cells using the perforated-patch configuration of the patch-clamp technique and measurements of intracellular free Ca2+([Ca2+]i). Depolarization of the cells in the presence of 10 m mBa2+or Ca2+led to an activation of inward currents at potentials positive to -30 mV with characteristics typical of L-type Ca2+currents: when using 10 m mBa2+, maximal inward current and inactivation time constant (τ) increased; the L-type Ca2+channel blocker nifedipine (1 μm) reduced and the L-type Ca2+channel agonist BayK8644 (5 μm) enhanced maximal inward current.

AbstractAmple evidence supports the theory that trabecular meshwork possesses smooth-muscle-like properties. Trabecular meshwork cells express a large number of transporters, channels and receptors, many of which are known to regulate smooth-muscle contractility. It has been shown that trabecular meshwork can be induced to contract and relax in response to pharmacological agents. In the model of the bovine eye, confirmed in some cases by experiments on primates, agents that contract trabecular meshwork reduce outflow. On the cellular level, this is coupled with depolarization and a rise in intracellular calcium. Relaxation of trabecular meshwork, on the other hand, appears to be coupled to a stimulation of the maxi-K channel, inducing hyperpolarization and a closure of L-type calcium channels. No significant differences between cells from a human and a bovine source emerged, either in classical measurements of membrane voltage, in measurements of intracellular calcium or patch-clamp experiments. Thus, pharmacological agents that relax trabecular meshwork seem promising candidates for further research – the ultimate goal being an improvement of glaucoma therapy in humans.Copyright © 2000 S. Karger AG, Basel