Zooplankton as a compound mineralising and synthesizing system: phosphorus excretion

Data on phosphate excretion rates of zooplankton are based on measurements using the pelagic crustacean zooplankton of Lake Vechten and laboratory-cultured Daphnia galeata. In case of Daphnia sp we measured the effects of feeding on P-rich algae and P-poor algae (Scenedesmus) as food on the P-excretion rates at 20°C. The excretion rates of the natural zooplankton community, irrespective of the influence of the factors mentioned, varied by an order of magnitude: 0.025–0.275µg PO₄-Pmg^–1C in zooplankton (C _zp ) h^–1. The temperature accounted for about half the observed variation in excretion rates. The mean excretion rates in the lake, computed for 20°C, varied between 0.141 and 0.260 µg Pmg^–1C _zp h^–1. Based on data of zooplankton biomass in the lake the P-regeneration rates by zooplankton covered between 22 and 239% of the P-demand of phytoplankton during the different months of the study period.In D. galeata, whereas the C/P ratios of the Scenedesmus used as food differed by a factor 5 in the experiments, the excretion rates differed by factor 3 only. Despite the higher P-excretion rates (0.258± 0.022 µg PO₄-P mg^–1 C h^–1) of the daphnids fed with P-rich food than those fed with P-poor food (0.105 ± 0.047 µg PO₄-P mg^–1 C h^p–1), both the categories of the animals were apparently conserving P. A survey of the literature on zooplankton excretion shows that in Daphnia the excretion rates vary by a factor 30, irrespective of the species and size of animals and method of estimation and temperature used.About two-thirds of this variation can be explained by size and temperature. A major problem of comparability of studies on P-regeneration by zooplankton relates to the existing techniques of P determination, which necessitates concentrating the animals several times above the in situ concentration (crowding) and prolonged experimental duration (starving), both of which manifest in marked changes that probably lead to underestimation of the real rates.     

Anti-Hepatitis A Virus Antibody Response Elicited in Mice by Different Forms of a Synthetic VP1 Peptide

Peptide VP1 (11-25) of the capsid of hepatitis A virus was synthesized by the Fmoc-polyamide solid phase method, and administered to mice in different forms: (1) free, (2) encapsulated in multilamellar liposomes, (3) coupled to keyhole limpet hemocyanin (KHL), and (4) incorporated into a tetrameric branched lysine core. The highest anti-VP1 peptide responses were generated by synthetic peptides entrapped into liposomes and coupled to KLH. No anti-HAV response was generated with the free peptide, while all the other forms induced both anti-HAV and HAV-neutralizing antibodies. Maximum neutralization indices were observed in ascites from mice treated with liposome-entrapped and KLH peptides.     

Autoradiography of nucleoside uptake into the retina

A selective uptake mechanism for some nucleosides and related substances was found in retinae of light adapted rabbits and fish. After the intravitreal injection in vivo of [³H]adenosine, [³H]inosine, [³H]guanosine and certain related compounds, the distribution of radioactivity was studied by autoradiography. Retinae were also incubated in [³H]adenosine and [³H]inosine and then were similarly processed.In rabbits, the accumulation of radioactivity from [³H]adenosine and [³H]guanosine was predominantly into glial cells, but also into neurons. [³H]Inosine labelled glia almost exclusively. However, the adenosine analog, [³H]methylphenylethyl-adenosine, resulted in well-defined neuronal labelling in this species. In fish, a few photoreceptor cell bodies exhibited strong radioactivity with the nucleosides, presumably representing incorporation into nucleic acids of replicating cells. Labelling was also seen in horizontal cells, amacrine cells and ganglion cells after the injection of either [³H]adenosine, [³H]guanosine or [³H]inosine.To some extent, the selective accumulation of radioactivity is likely to be due to cell replication, but in most neurons, other factors must be responsible. Judging from what is known about the actions of adenosine in central nervous tissue, signal transmission in the retina could be such a factor.