Response of phytoplankton and bacteria to nutrients and zooplankton: a mesocosm experiment

Although both nutrient inputs and zooplankton grazing are importantto phytoplankton and bacteria in lakes, controversy surroundsthe relative importance of grazing pressure for these two groupsof organisms. For phytoplankton, the controversy revolves aroundwhether zooplankton grazers, especially large cladocerans likeDaphnia, can effectively reduce phytoplankton populations regardlessof nutrient conditions. For bacteria, little is known aboutthe balance between possible direct and indirect effects ofboth nutrients and zooplankton grazing. However, there is evidencethat bacteria may affect phytoplankton responses to nutrientsor zooplankton grazing through direct or apparent competition.We performed a mesocosm experiment to evaluate the relativeimportance of the effects of nutrients and zooplankton grazingfor phytoplankton and bacteria, and to determine whether bacteriamediate phytoplankton responses to these factors. The factorialdesign crossed two zooplankton treatments (unsieved and sieved)with four nutrient treatments (0, 0.5, 1.0 and 2.0 µgphosphorus (P) l^–1 day^–1 together with nitrogen(N) at a N:P ratio of 20:1 by weight). Weekly sieving with 300µm mesh reduced the average size of crustacean zooplanktonin the mesocosms, decreased the numbers and biomass of Daphnia,and increased the biomass of adult copepods. Nutrient enrichmentcaused significant increases in phytoplankton chlorophyll a(4–5x), bacterial abundance and production (1.3x and 1.6x,respectively), Daphnia (3x) and total zooplankton biomass (2x).Although both total phytoplankton chlorophyll a and chlorophylla in the <35 µm size fraction were significantly lowerin unsieved mesocosms than in sieved mesocosms, sieving hadno significant effect on bacterial abundance or production.There was no statistical interaction between nutrient and zooplanktontreatments for total phytoplankton biomass or bacterial abundance,although there were marginally significant interactions forphytoplankton biomass <35 µm and bacterial production.Our results do not support the hypothesis that large cladoceransbecome less effective grazers with enrichment; rather, the differencebetween phytoplankton biomass in sieved versus unsieved zooplanktontreatments increased across the gradient of nutrient additions.Furthermore, there was no evidence that bacteria buffered phytoplanktonresponses to enrichment by either sequestering P or affectingthe growth of zooplankton.     

Re-evaluation of the mutagenic potential of quinacrine dihydrochloride dihydrate.

Quinacrine has been used for voluntary female non-surgical sterilization for its ability to produce tubal occlusion. Safety issues regarding quinacrine have been raised because it has been shown to intercalate with DNA. Therefore, safety issues need to be resolved by appropriate toxicology studies to support a review for human transcervical use. Such toxicology studies include mutagenicity assays. Here we report an evaluation of the genotoxicity of quinacrine dihydrochloride dihydrate (QH) using a battery of assays. In the bacterial mutagenicity assay, QH was strongly positive in Salmonella typhimurium tester strain TA1537 with and without S9-activation and in S. typhimurium tester strain TA98 with S9-activation; QH was also strongly positive in Escherichia coli WP2 uvrA without S9-activation. QH was not mutagenic in S. typhimurium tester strains TA100 and TA1535 with and without S9-activation. QH was mutagenic in the mouse lymphoma assay in the absence of S9-activation. QH was clastogenic in Chinese hamster ovary (CHO) cells, with and without S9-activation. QH was negative for polyploidy in the same chromosome aberration test. Using a triple intraperitoneal injection treatment protocol in both male and female mice, QH was negative in the in vivo mouse micronucleated erythrocyte (micronucleus) assay. These results confirm that QH is mutagenic and clastogenic in vitro and suggest a potential risk to human health due to QH exposure after intrauterine exposure.     

Identification of New Regulatory Sequences Far Upstream of the Mouse Monocyte Chemoattractant Protein-1 Gene

We systematically searched for sequences influencing the expression of the mouse monocyte chemoattractant protein-1 (MCP-1) gene (Scya2) by mapping DNase I hypersensitive sites (HS) in the chromatin of mesangial cells in a 40-kb interval around the gene. We found nine HS located between -24 kb and +12.7 kb. Three HS coincided with previously known regulatory sequences (HS-2.4, HS-1.0, and HS-0.2). We tested two of the previously unknown HS located far upstream of Scya2 (HS-19.4 and HS-16.3) in transfection experiments using luciferase reporter constructs and mouse mesangial cells as recipients. In transient transfections, both HS had a moderate effect on basal promoter activity as well as promoter activity stimulated by tumor necrosis factor-alpha. In stable transfection experiments, we found much higher activity. A DNA fragment containing HS-19.4 and HS-16.3 caused a considerable increase in the number of stably integrated luciferase copies. We determined the nucleotide sequence of the 5' flanking region to -28.6 kb. Computer-assisted sequence analysis did not yield evidence of an additional gene. These HS are located within the 5' flanking region of a gene cluster consisting of Scya2 (MCP-1), Scya7 (MCP-3), Scya11 (eotaxin), Scya12 (MCP-5), and Scya8 (MCP-2). This report represents the first comprehensive chromatin analysis of the mouse MCP-1 locus leading to the identification of a complex regulatory region located far upstream of Scya2.     

Size-dependent predator–prey relationships between perch and their fish prey

Size-dependent interactions between piscivorous perch Perca fluviatilis (age ≥1 year) and their fish prey age 0 year perch, pikeperch Sander lucioperca and roach Rutilus rutilus in the biomanipulated Bautzen Reservoir indicated that the highest ratio of prey total length ( L _T) to predator L _T was 59%. Perch L _T and prey fish L _T were positively and linearly related. Perch L _T was strongly related with both gape width and gape height. Within the range 80–110 mm L _T, the gape height of perch exceeded gape width, while beginning at 120 mm L _T the gape width exceeded gape height. The minimum, maximum and mean prey L _T and prey body depths of all three prey species increased with increasing predator size, but the increases in mean sizes of perch and pikeperch as prey were less than that of roach. The low limit of the 'predation window' observed in this study coupled with results of previous studies on perch in the Bautzen Reservoir indicated that perch had a major impact on the population dynamics of both perch and pikeperch.     

Vitamin E up-regulates arachidonic acid release and phospholipase A2 in megakaryocytes

The alteration in calcium transport in the liver nuclei of rats orally administered carbon tetrachloride (CCl4) was investigated. Rats received a single oral administration of CCl₄(5, 10, and 25%, 1.0ml/100 g body weight), and 5, 24 and 48 h later the animals were sacrificed. The administration of CCl₄ (25%) caused a remarkable elevetion of calcium content in the liver tissues and the nuclei of rats. Liver nuclear Ca2+-ATPase activity was markedly decreased by CCl₄ (25%) administration. The presence of dibutyryl cyclic AMP(10^-4 and 10^-3 M) or inositol 1,4,5-trisphosphate (10^-6 and 10^-5 M) in the enzyme reaction mixture caused a significant decrease in Ca²⁺-ATPase activity in the liver nuclei obtained from normal rat, while the enzyme activity was significantly increased by calmodulin (1.0 and 2.0 g/ml). These signaling factor's effects were completely impaired in the liver nuclei obtained from CCl₄ (25%)-administered rats. DNA fragmentation in the liver nuclei obtained from CCl₄ -administered rats was significantly decreased by the presence of EGTA (2 mM) in the reaction mixture, suggesting that the endogenous calcium activates nuclear DNA fragmentation. The present study demonstrates that calcium transport system in the liver nuclei is impaired by liver injury with CCl₄ administration in rats.     

The effect of heat on photosynthesis,dark respiration and cellular ultrastructure of the arctic-alpine psychrophyte Ranunculus glacialis

Effects of high temperatures on the leaves of Ranunculus glacialis were studied in plants taken from sites located between 2400-2550 m in the Central Alps. Changes in CO2 exchange rates, in vivo chlorophyll fluorescence, and cellular ultrastructure were investigated during and after an experimental heat exposure. The earliest heat stress effect was inactivation of the net photosynthetic rate at 38-39 °C. Between 40-42 °C, disorders appeared in the photosynthetic apparatus and in the tonoplast. Heat shock granules were observed at 42 °C in chloroplasts, and at 44 °C also in mitochondria. In this temperature range, the dark respiration rate was reversibly enhanced, and an increased number of polyribosomes indicated repair after the primary injury. Above 44 °C, the degradation progress entered the phase of chronic impairment leading to irreversible damage at 45-46 °C. An unusually wide temperature range from the start of reversible photosynthetic inhibition to incipient necrosis indicated a pronounced heat sensitivity, particularly in cellular functions, of this arctic-alpine species.