Azaspiracids (AZA) are lipophilic marine biotoxins associated with shellfish poisoning which are produced by some species of Amphidomataceae. Diversity and global biogeography of this family are ...still poorly known. In summer 2017 plankton samples were collected from the central Labrador Sea and western Greenland coast from 64° N (Gothaab Fjord) to 75° N for the presence of Amphidomataceae and AZA. In the central Labrador Sea, light microscopy revealed small Azadinium-like cells (9200 cells l
−1
). Clonal strains established from plankton samples and scanning electron microscopy of fixed plankton samples revealed at least eight species of Amphidomataceae: Azadinium obesum, Az. trinitatum, Az. dexteroporum, Az. spinosum, Az. polongum, Amphidoma languida, Azadinium spec., and a new species described here as Azadinium perforatum sp. nov. The new species differed from other Azadinium species by the presence of thecal pores on the pore plate. All samples, including cultured strains, filtered seawater samples, and solid phase adsorption toxin tracking (SPATT) samplers deployed during the expedition in a continuous water-sampling system (FerryBox), were negative for AZA. DNA samples and PCR assays were positive for Amphidomataceae from most stations, whereas species-specific assays for three toxigenic species were rarely positive (two stations for Az. poporum, one station for Am. languida). The results highlight the presence of Amphidomataceae in the area but the lack of toxins and low abundance of toxigenic species currently indicate a low risk of toxic Amphidomataceae blooms in Arctic coastal waters.
Lake Baikal is inhabited by more than 300 endemic amphipod species, which are narrowly adapted to certain thermal niches due to the high interspecific competition. In contrast, the surrounding ...freshwater fauna is commonly represented by species with large-scale distribution and high phenotypic thermal plasticity. Here, we investigated the thermal plasticity of the energy metabolism in two closely-related endemic amphipod species from Lake Baikal (Eulimnogammarus verrucosus; stenothermal and Eulimnogammarus cyaneus; eurythermal) and the ubiquitous Holarctic amphipod Gammarus lacustris (eurythermal) by exposure to a summer warming scenario (6-23.6 °C; 0.8 °C d
). In concert with routine metabolic rates, activities of key metabolic enzymes increased strongly with temperature up to 15 °C in E. verrucosus, whereupon they leveled off (except for lactate dehydrogenase). In contrast, exponential increases were seen in E. cyaneus and G. lacustris throughout the thermal trial (Q
-values: 1.6-3.7). Cytochrome-c-oxidase, lactate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase activities were found to be higher in G. lacustris than in E. cyaneus, especially at the highest experimental temperature (23.6 °C). Decreasing gene expression levels revealed some thermal compensation in E. cyaneus but not in G. lacustris. In all species, shifts in enzyme activities favored glycolytic energy generation in the warmth. The congruent temperature-dependencies of enzyme activities and routine metabolism in E. verrucosus indicate a strong feedback-regulation of enzymatic activities by whole organism responses. The species-specific thermal reaction norms reflect the different ecological niches, including the spatial distribution, distinct thermal behavior such as temperature-dependent migration, movement activity, and mating season.
Despite cold adaptation, Antarctic fish show lower growth than expected from the van’t Hoff’s Q
10
rule. Protein synthesis is one of the main energy-consuming processes, which is downregulated under ...energy deficiency. Considering the effect of temperature on growth performance, we tested if temperature-dependent cellular energy allocation to protein synthesis correlates with temperature-dependent whole-animal growth and thus thermal tolerance. Cell respiration and energy expenditure for protein synthesis were determined in hepatocytes of the circumpolar-distributed Antarctic eelpout
Pachycara brachycephalum
after warm acclimation (0 °C vs 5 °C) and, of two notothenioids the sub-Antarctic
Lepidonotothen squamifrons
and the high-Antarctic icefish
Chionodraco hamatus
. We used intermittent-flow respirometry to analyse cellular response to acute warming from 5 to 10 °C (
P. brachycephalum
) and from 1 to 5 °C (
L. squamifrons, C. hamatus
). Warming-induced rise in respiration was similar between 0- and 5 °C-acclimated
P. brachycephalum
and between
L. squamifrons
and
C. hamatus
. Irrespective of acclimation, warming decreased energy expenditure for protein synthesis in
P. brachycephalum
, which corresponds to reduced whole-animal growth at temperatures > 5 °C. Warming doubled energy expenditure for protein synthesis in
L. squamifrons
but had no effect on
C. hamatus
indicating that
L. squamifrons
might benefit from warmer waters. The species-specific temperature effect on energy expenditure for protein synthesis is discussed to mirror thermal sensitivity of whole-animal growth performance, thereby paralleling the degree of cold adaptation. Clearly more data are necessary including measurements at narrower temperature steps particularly for
C. hamatus
and an increased species’ number per ecotype to reinforce presented link between cellular and whole-animal thermal sensitivity.
In August 1993 during a synoptic evaluation of the plankton of the Northfrisian Wadden Sea, the infection of two diatom species (
Guinardia delicatula,
Guinardia flaccida) with parasitic protists was ...observed and quantified. The morphological appearance of infected cells suggests that nanoflagellates of the genera
Pirsonia and
Cryothecomonas were responsible for the infection.
Guinardia delicatula dominated the phytoplankton community in the northern part of the Northfrisian Wadden Sea with densities of up to 520 cells cm
−3. A second population was found in the outer Elbe estuary. In the whole area infection of
G. delicatula could be observed. The percentage of infected cells was highest in the inner part of the northern Wadden Sea, reaching up to 35%.
Guinardia flaccida occurred in lower densities (up to 3.6 cells cm
−3) but with a higher fraction affected (up to 65%). The large-scale occurrence of heavy infection indicates that in the Wadden Sea phytoplankton parasites may at times be successful competitors to zooplankton in controlling energy flow and food web dynamics and that they may play a regulating role in phytoplankton succession due to their pronounced species selection.
T3 has been shown to exert cardiovascular effects. These effects have not yet been defined with regard to the mode of action (nongenomic vs. genomic) and with regard to an interaction with the ...adrenergic system in humans. To address these issues we conducted a randomized, double blind, 6-fold cross-over trial in 18 healthy male volunteers. After pretreatment with the β-agonist dobutamine, the β-blocking agent esmolol, or placebo (0.9% NaCl), 100 μg T3 or placebo were injected. Primary target variables were systemic vascular resistance (SVR) and cardiac output (CO) within 45 min after injection of T3 vs. placebo after placebo pretreatment. Sympatho-vagal balance was assessed by measurement of heart rate variability.
T3 caused a lower SVR and a higher CO than placebo (P < 0.001) after pretreatment with placebo. An increased low frequency (LF)/high frequency (HF) ratio (power in LF/power in HF band) after T3 compared with placebo (P = 0.004) suggests an increase in sympathetic tone. After pretreatment with dobutamine, the effects of T3 on SVR and CO were abolished, and the effect on LF/HF ratio was reversed. After pretreatment with esmolol, the effects on SVR and LF/HF ratio were reversed. Our data show, for the first time, nongenomic cardiovascular effects of T3 in humans.
Interactions between the renin-angiotensin-aldosterone system and the adrenergic system are complex and have mainly been attributed to angiotensin II, with knowledge about aldosterone action much ...less advanced. Only recently has evidence been forthcoming that aldosterone blunts the baroreceptor reflex and lowers heart rate variability in humans. Both effects point to an adrenergic-like action of aldosterone. It has been proposed that this blunting of baroreceptor sensitivity is mediated nongenomically and that nongenomic aldosterone action itself is modulated by the adrenergic system. The aim of the present study was to prove the hypothesis of an interaction between the autonomic nervous system and rapid, nongenomic aldosterone effects. We conducted a randomized, double blind, 8-fold cross-over trial on 18 healthy male volunteers. After pretreatment with the beta-blocking agent esmolol, the beta-agonist dobutamine, the alpha(1)-agonist phenylephrine, or placebo, placebo (0.9% NaCl) or aldosterone (0.5 mg) was injected. After aldosterone injection the peak plasma levels were supraphysiological, reaching nanomolar concentrations. Primary target variables were differences in changes in mean arterial blood pressure, systemic vascular resistance, and cardiac output depending on the pretreatment. Cardiovascular parameters were measured by impedance cardiography during the maintained infusion of the adrenergic modulators for 45 min. Comparing pretreatments, diverse acute, and thus nongenomic, effects of aldosterone on mean arterial blood pressure were observed. After esmolol pretreatment, aldosterone caused an increase in mean arterial blood pressure by 4.1%, whereas after dobutamine pretreatment mean arterial blood pressure decreased by 1.6%, and the difference was statistically significant (P < 0.01). These effects were significant (P < 0.005) for the first 12 min, underlining their nongenomic nature. Our data support the hypothesis that aldosterone, via nongenomic mechanisms, has diverse effects on the cardiovascular system that depend on the preexisting adrenergic state. Furthermore, aldosterone blunts the blood pressure-lowering effect of the beta-blocking agent esmolol by a nongenomic mechanism.
T(3) has been shown to exert cardiovascular effects. These effects have not yet been defined with regard to the mode of action (nongenomic vs. genomic) and with regard to an interaction with the ...adrenergic system in humans. To address these issues we conducted a randomized, double blind, 6-fold cross-over trial in 18 healthy male volunteers. After pretreatment with the beta-agonist dobutamine, the beta-blocking agent esmolol, or placebo (0.9% NaCl), 100 microg T(3) or placebo were injected. Primary target variables were systemic vascular resistance (SVR) and cardiac output (CO) within 45 min after injection of T(3) vs. placebo after placebo pretreatment. Sympatho-vagal balance was assessed by measurement of heart rate variability. T(3) caused a lower SVR and a higher CO than placebo (P < 0.001) after pretreatment with placebo. An increased low frequency (LF)/high frequency (HF) ratio (power in LF/power in HF band) after T(3) compared with placebo (P = 0.004) suggests an increase in sympathetic tone. After pretreatment with dobutamine, the effects of T(3) on SVR and CO were abolished, and the effect on LF/HF ratio was reversed. After pretreatment with esmolol, the effects on SVR and LF/HF ratio were reversed. Our data show, for the first time, nongenomic cardiovascular effects of T(3) in humans.
Interactions between the renin-angiotensin-aldosterone system and the
adrenergic system are complex and have mainly been attributed to
angiotensin II, with knowledge about aldosterone action much ...less
advanced. Only recently has evidence been forthcoming that aldosterone
blunts the baroreceptor reflex and lowers heart rate variability in
humans. Both effects point to an adrenergic-like action of aldosterone.
It has been proposed that this blunting of baroreceptor sensitivity is
mediated nongenomically and that nongenomic aldosterone action itself
is modulated by the adrenergic system. The aim of the present study was
to prove the hypothesis of an interaction between the autonomic nervous
system and rapid, nongenomic aldosterone effects.
We conducted a randomized, double blind, 8-fold cross-over trial on 18
healthy male volunteers. After pretreatment with the β-blocking agent
esmolol, the β-agonist dobutamine, the α1-agonist
phenylephrine, or placebo, placebo (0.9% NaCl) or aldosterone (0.5 mg)
was injected. After aldosterone injection the peak plasma levels were
supraphysiological, reaching nanomolar concentrations. Primary target
variables were differences in changes in mean arterial blood pressure,
systemic vascular resistance, and cardiac output depending on the
pretreatment. Cardiovascular parameters were measured by impedance
cardiography during the maintained infusion of the adrenergic
modulators for 45 min.
Comparing pretreatments, diverse acute, and thus nongenomic, effects of
aldosterone on mean arterial blood pressure were observed. After
esmolol pretreatment, aldosterone caused an increase in mean arterial
blood pressure by 4.1%, whereas after dobutamine pretreatment mean
arterial blood pressure decreased by 1.6%, and the difference was
statistically significant (P < 0.01). These
effects were significant (P < 0.005) for the first
12 min, underlining their nongenomic nature. Our data support the
hypothesis that aldosterone, via nongenomic mechanisms, has diverse
effects on the cardiovascular system that depend on the preexisting
adrenergic state. Furthermore, aldosterone blunts the blood
pressure-lowering effect of the β-blocking agent esmolol by a
nongenomic mechanism.
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