Anoxic Survival Research Articles

Anoxia tolerant brains.

While medical science has struggled to find ways to counteract anoxic brain damage with limited success, evolution has repeatedly solved this problem. The best-studied examples of anoxia-tolerant vertebrates are the crucian carp and some North American Freshwater turtles. These can survive anoxia for days to months, depending of temperature. Both animals successfully fight any major fall in brain ATP levels, but the strategies they use to accomplish this are quite divergent. The anoxic turtle suppresses brain activity to such a degree that it becomes virtually comatose. The underlying mechanisms involve closing down ion conductances and releasing GABA and adenosine. By contrast, the crucian carp remains active in anoxia, although it suppresses selected brain functions, and avoids lactate self-poisoning by producing an exotic anaerobic end-product. These animals provide unique models for studying anoxic survival mechanisms both on a molecular and physiological level.

Hemoglobin and Hypoxic Acclimation in Maize Root Tips

Class 1 hemoglobins (Hbs) have a wide distribution in the plant kingdom and have been demonstrated in root, seed, stem, and leaf tissues. They are present at low concentrations in aerobic tissue, but their synthesis is rapidly induced by hypoxic stress. The pattern of expression of the maize Hb gene in roots of young maize plants exposed to hypoxia has been examined. Root Hb gene expression increased rapidly to a maximum within first two hours of hypoxia, then declining to prehypoxia levels within 48-h hypoxic exposure. Limiting oxygen supply to the roots by total plant immersion and darkness did not alter the time course of hemoglobin expression. Hb gene expression was about 20-fold higher in the stele than in the cortex of control, aerobically grown roots. Stele Hb expression increased about fourfold under hypoxic conditions, whereas its expression in the cortex increased about 60-fold. In these samples, alcohol dehydrogenase (Adh) gene expression increased about four- and ten fold in the stele and cortex, respectively. The effect of the state of the Hb on anoxic survival of maize root tips was assessed by exposing root tips to a carbon monoxide atmosphere to maximize the proportion of hemoglobin in the carbonmonoxy form. Carbon monoxide had no significant effect on the survival or the ATP levels in anoxic maize roots, regardless of whether they had been acclimated by exposure to a hypoxic pretreatment. This would suggest that the presence of oxyhemoglobin is not essential for the survival of anoxic root tips.

The role of nitrate reduction in the anoxic metabolism of roots I. Characterization of root morphology and normoxic metabolism of wild type tobacco and a transformant lacking root nitrate reductase

Two tobacco lines with (Nicotiana tabacum cv. Gatersleben, WT) or without (transformant LNR-H) nitrate reductase in roots were chosen as model systems to re-evaluate the role of root nitrate reduction for survival of anoxia. In this first paper, the two hydroponically grown lines were compared with respect to their root morphology, root respiration and the root content of inorganic cations, anions, and metabolites. Leaf transpiration in relation to root morphology was also determined. In comparison to WT roots containing NR, the NR-free LNR-H transformants had slightly shorter and thicker roots with a lower root surface area per g leaf FW. Consistent with that, LNR-H leaves had lower transpiration rates than WT. LNR-H-roots also showed consistently higher respiration and higher contents of ATP, starch and hexose monophosphates than WT roots. Concentrations of free sugars were only slightly higher in LNR-H roots. Total soluble protein content was identical in both lines, whereas amino acids were higher in LNR-H. Contents of major inorganic cations and anions were also almost identical in both lines. We conclude that WT versus LNR-H plants are a suitable tool to re-evaluate the role of nitrate reduction in flooding tolerance.

Hypoxia induces anoxia tolerance in roots and shoots of lupine seedlings

Lupine seedlings were exposed to 4 kPa partial pressure oxygen (hypoxically pretreated) for 18 hours before treatment with strictly anaerobic conditions (anoxia). Seedlings previously exposed to hypoxia were more tolerant than the controls (not hypoxically pretreated) to anoxic stress in both roots and shoots. Hypoxic pretreatment induced roots and shoots survival in anoxia. Improved viability of roots, following hypoxic pretreatment, was associated with increased activity of ADH. In nonacclimated roots and shots significant increase in LDH activity occurd during the first hours under anoxia but the in vitro activity of LDH was two orders of magnitude lower than that of ADH. The results are discussed in relation to the ability of lupine seedlings to survive anoxia.

Effect of anoxia and pharmacological anoxia on whole-cell NMDA receptor currents in cortical neurons from the western painted turtle.

The mammalian brain undergoes rapid cell death during anoxia that is characterized by uncontrolled Ca(2+) entry via N-methyl-D-aspartate receptors (NMDARs). In contrast, the western painted turtle is extremely anoxia tolerant and maintains close-to-normal [Ca(2+)](i) during periods of anoxia lasting from days to months. A plausible mechanism of anoxic survival in turtle neurons is the regulation of NMDARs to prevent excitotoxic Ca(2+) injury. However, studies using metabolic inhibitors such as cyanide (NaCN) as a convenient method to induce anoxia may not represent a true anoxic stress. This study was undertaken to determine whether turtle cortical neuron whole-cell NMDAR currents respond similarly to true anoxia with N(2) and to NaCN-induced anoxia. Whole-cell NMDAR currents were measured during a control N(2)-induced anoxic transition and a control NaCN-induced transition. During anoxia with N(2) normalized, NMDAR currents decreased to 35.3%+/-10.8% of control values. Two different NMDAR current responses were observed during NaCN-induced anoxia: one resulted in a 172%+/-51% increase in NMDAR currents, and the other was a decrease to 48%+/-14% of control. When responses were correlated to the two major neuronal subtypes under study, we found that stellate neurons responded to NaCN treatment with a decrease in NMDAR current, while pyramidal neurons exhibited both increases and decreases. Our results show that whole-cell NMDAR currents respond differently to NaCN-induced anoxia than to the more physiologically relevant anoxia with N(2).

Gap junctions do not underlie changes in whole-cell conductance in anoxic turtle brain

An acute reduction in cell membrane permeability could provide an effective strategy to prolong anoxic survival. A previous study has shown that in the western painted turtle whole-cell neuronal conductance ( G w) decreases during anoxia, which may be mediated by the activation of adenosine A 1 receptors and calcium. Reduction in G w is thought to be the result of ion channel closure, but closure of gap junctions could also be responsible for this phenomenon. In our study, antibody staining of connexin 32 and 43 (Cx32 and Cx43) suggested the presence of gap junctional components in the turtle cortex. To examine if gap junctions were involved in the previously measured anoxic decrease in G w, neuronal connectivity was assessed through the measurement of whole-cell capacitance ( C w). Turtle cortical sheets were perfused with normoxic (95%O 2/5%CO 2), anoxic (95%N 2/5%CO 2), high calcium (4 mM) and adenosine (200 μm) artificial cerebral spinal fluid (aCSF). No significant change in C w was observed under any of the above conditions. However, during hypo-osmotic aCSF perfusion C w decreased significantly, with the lowest value of 50±10.4 pF ( P<0.05) occurring at 30 min. To visualize changes in gap junction permeability lucifer yellow was loaded into turtle neurons during normoxic, anoxic, 0 calcium, hypo-osmotic, cold shock, (+)-isoproterenol, nitric oxide donor S-nitoso-acetyl penicillamine, and 8-bromo-guanosine 3′,5′-cyclic monophosphate aCSF perfusion. Dye propagation was only observed in 3 of 20 cold shock experiments (4 °C). We conclude that gap junctions are not involved in the acute reduction in G w previously observed during anoxia and that our results support the hypothesis that ion channel arrest is involved.

Influence of abiotic factors on bacterial proliferation and anoxic survival of the sea mussel Mytilus edulis L.

The effect of several abiotic factors (salinity, temperature and pH) on bacterial proliferation and survival time of the sea mussel Mytilus edulis L. were studied under anoxic incubations. In addition, the presence in the incubation media of ammonium and the volatile fatty acids propionate and acetate, both excreted fermentation products of the bivalve, was tested. Anoxic incubations with seawater diluted with demineralised water showed at the lowest salinity (50% seawater, SW) a significant increase in the capacity of M. edulis to survive anoxia as compared to both 75% SW and control [100% SW, corresponding to 32 practical salinity units (psu)]. Formation of biotic sulphide and ammonium occurred in all incubations. However, bacterial proliferation was postponed by 2–3 days at lowest salinity and accordingly, concentrations of both compounds were lower. Anoxic survival profiles of mussels collected from different habitats in the Dutch Scheldt area, characterised by differences in salinity (range from 17 to 31 psu), corresponded with the above salinity effect. Walsoorden mussels (17 psu) showed the longest ( P<0.001) survival time under anoxia (LT 50=17.2 days) as compared with Paulina (27 psu) and Wemeldinge (31 psu) mussels (LT 50=12.8 and 9.8 days, respectively). Condition index (ratio of soft body weight to shell volume) was not correlated with anoxic survival time in untreated mussels, although this was clearly the case when the antibiotic chloramphenicol was added to the anoxic seawater. Acidification of the anoxic incubation medium had a positive effect on survival time. LT 50 values significantly ( P<0.001) increased from 10.2 days at pH 8.1 to 11.6 and 11.5 days at pH 7.3 and 6.5, respectively. Biotic sulphide and ammonium accumulation as well as bacterial numbers were significantly lower at pH 7.3 and 6.5 as compared with pH 8.1. Anoxic incubations at 10 °C (LT 50=12.0 days) strongly increased survival time as compared to 18 °C (LT 50=5.9 days). The benefit of antibiotic addition was also stronger at lower temperature (10 °C). Addition of both propionate and acetate (0.5 mM) displayed no effect on mortality of mussels under anoxia, but ammonium (0.5 mM) caused a negative effect ( P<0.001). Biotic sulphide and ammonium concentrations measured in both volatile fatty acid incubations were lower than the control situation, as well as total bacterial numbers. This study shows that environmental factors play a significant role in determining the course of bacterial infection and death of bivalves exposed to anoxia.

Mechanisms for maintaining extracellular glutamate levels in the anoxic turtle striatum.

The turtle Trachemys scripta is one of a limited group of vertebrates that can withstand hours to days without oxygen. One facet of anoxic survival is the turtle's ability to maintain basal extracellular glutamate levels, whereas in most vertebrates, anoxia triggers massive excitotoxic glutamate release. We investigated glutamate release and reuptake in the anoxic turtle and the effects of adenosine and ATP-sensitive potassium (K(ATP)) channels on glutamate homeostasis. Striatal extracellular glutamate was measured in anesthetized T. scripta by microdialysis in normoxia and over 2-h anoxia. Glutamate release is decreased by 44% in the early anoxic turtle; this anoxia-induced decrease in glutamate release was prevented when K(ATP) channels and adenosine receptors were blocked simultaneously but not when either mechanism was blocked individually. We hypothesize that the continued release and reuptake of glutamate during anoxia help maintain neuronal tone and aid in the recovery of a functional neuronal network after long periods of anoxia, whereas activation of adenosine and/or K(ATP) conserves energy by reducing glutamate release and lowering transport costs.

Dephosphorylation of cell cycle-regulated proteins correlates with anoxia-induced suspended animation in Caenorhabditis elegans.

Some metazoans have evolved the capacity to survive severe oxygen deprivation. The nematode, Caenorhabditis elegans, exposed to anoxia (0 kPa, 0% O(2)) enters into a recoverable state of suspended animation during all stages of the life cycle. That is, all microscopically observable movement ceases including cell division, developmental progression, feeding, and motility. To understand suspended animation, we compared oxygen-deprived embryos to nontreated embryos in both wild-type and hif-1 mutants. We found that hif-1 mutants survive anoxia, suggesting that the mechanisms for anoxia survival are different from those required for hypoxia. Examination of wild-type embryos exposed to anoxia show that blastomeres arrest in interphase, prophase, metaphase, and telophase but not anaphase. Analysis of the energetic state of anoxic embryos indicated a reversible depression in the ATP to ADP ratio. Given that a decrease in ATP concentrations likely affects a variety of cellular processes, including signal transduction, we compared the phosphorylation state of several proteins in anoxic embryos and normoxic embryos. We found that the phosphorylation state of histone H3 and cell cycle-regulated proteins recognized by the MPM-2 antibody were not detectable in anoxic embryos. Thus, dephosphorylation of specific proteins correlate with the establishment and/or maintenance of a state of anoxia-induced suspended animation.

Characterization of a novel gene up-regulated during anoxia exposure in the marine snail, Littorina littorea

Gene expression was investigated during anoxia exposure in the marine snail, Littorina littorea. Differential screening of a cDNA library made from hepatopancreas of anoxic L. littorea yielded a 525 bp clone coding for the novel gene kvn. The deduced amino acid sequence of the KVN protein contained 99 amino acid residues with a predicted molecular weight of 12 kDa and showed an N-terminal secretory signal. Analysis of hepatopancreas samples over a time course of anoxia exposure showed a maximum increase in transcript levels of 5.8-fold after 48 h relative to normoxic animals, with a subsequent decrease in transcript levels during normoxic recovery. Nuclear run-off assays confirmed the observed transcriptional up-regulation of kvn during anoxia. Organ culture experiments were performed to determine a possible pathway of up-regulation of kvn, with data indicating a putative role for cGMP in signal transduction. Profiles of ribosome distribution in polysomes versus monosomes revealed a reduction in the polysome peak during anoxia and a shift in the position of kvn transcripts to association with the lower density polysome/higher density monosome region. The data suggest that the kvn transcript is both transcribed and translated during anoxia, indicating a possible significant role for the KVN protein in the survival of anoxia by L. littorea.

Anoxic survival potential of bivalves: (arte)facts

The anoxic survival time of the bivalves Chamelea gallina, Cerastoderma edule and Scapharca inaequivalvis from two different ecosystems and differing anoxia tolerances was studied in static (closed) and flow-through systems. The antibiotics chloramphenicol, penicillin and polymyxin were added, and molybdate (specific inhibitor of the process of sulfate reduction). Survival in (near) anoxic seawater of Chamelea was studied in a static system by comparing untreated seawater with autoclaved seawater and untreated clams with clams incubated in well-aerated seawater, containing the broad-spectrum antibiotic chloramphenicol, prior to the anoxic survival test. With untreated clams and natural seawater (median mortality time 2.4 days) a decrease in pH and exponential accumulation of sulfide and ammonium was observed in the anoxic medium, indicating excessive growth of (sulfate reducing) bacteria. In sterilized seawater LT 50 (2.1 days) was not significantly different and again considerable amounts of ammonium and sulfide accumulated. However, pre-treatment of clams with chloramphenicol resulted in an increase of LT 50 (11.0 days) by approximately fivefold. Accumulation of ammonium and sulfide was retarded, but was finally even stronger than in the medium containing untreated clams. Median mortality times were 2.5 and 2.4 days for Chamelea and 2.7 and 2.9 days for Cerastoderma for static and flow-through incubations, respectively. Addition of chloramphenicol increased strongly survival time in both systems with corresponding values of 11.0 and 16.3 days for Chamelea, and 6.4 and 6.5 days for Cerastoderma. LT 50 of Scapharca in anoxic seawater was 14.4 days. Chloramphenicol and penicillin increased median survival time to 28.5 and 28.7 days, respectively, whereas polymyxin displayed no effect (LT 50=13.6 days). Molybdate added to artificial sulfate free seawater blocked biotic sulfide formation, but did not improve survival time (LT 50=13.7 days). Overall the results indicate that proliferation of anaerobic pathogenic bacteria, firmly associated with the bivalves, is a main cause of death besides lack of oxygen. Bacterial damage is probably caused by injury of the tissues of the clams and not by the release of noxious compounds to the medium.

Surviving anoxia with the brain turned on.

Crucian carp is one of few vertebrates that tolerate anoxia. It maintains brain ATP during anoxia partially by reducing ATP consumption. However, unlike turtles, which become comatose during anoxia, this fish remains physically active. This striking difference in anoxic survival strategy is reflected all the way down to the cellular level.

Studies on the causes of mortality of the estuarine bivalve Macoma balthica under conditions of (near) anoxia

Survival of the bivalve Macoma balthica in (near) anoxic seawater was studied in a static system and a flow-through system and compared with emersed exposure to air and N2. In the static system, a decrease in pH and exponential accumulation of sulphide in the incubation medium were observed, indicating excessive growth of (sulphate-reducing) bacteria. These changes in the chemical environment were prevented by the use of a flow-through system. However, this treatment hardly affected survival time. Median mortality times were 8.3 and 9.0 days for the static and flow-through incubation, respectively. Addition of the antibiotic chloramphenicol strongly increased survival time in both systems with corresponding values of 17.9 and 23.0 days. A similar value was obtained for survival in air (LT50= 21.7 days). In a second experiment (1 year later), we obtained much lower values for anoxic survival in a static system, although laboratory conditions, season and temperature were similar. The pH values were adjusted to 6.5, 7.2 and 8.2 by buffering the media (25 mM Tris-HCl), and the corresponding LT50 values were 5.5, 5.7 and 4.7 days, respectively. In the presence of chloramphenicol the values were 10.8, 10.9 and 9.5 days, respectively. These values show that a slightly acidic medium increased survival time. Exposure to an atmosphere of N2 resulted in a survival time close to that in anoxic seawater without chloramphenicol (LT50= 6.4 days). Overall the results indicate that proliferation of anaerobic bacteria associated with the bivalves was the main cause of death. Since chloramphenicol also displayed a strong positive effect in the flow-through system, which prevented the accumulation of released waste products and a decrease of pH, bacterial damage must have been by injury of the tissues of the clams and not by the release of noxious compounds to the medium. Bacterial outbreaks are a part of every anoxic event (eutrophication), and therefore, in their habitats, direct bacterial infection may also be the cause of clam mortality. It is concluded that laboratory studies on anoxic tolerance, or impact of sulphide, may produce artefacts when no precautions are taken to suppress bacterial proliferation.

Factors involved in the (near) anoxic survival time of Cerastoderma edule: associated bacteria vs. endogenous fuel

The effect of several antibiotics, molybdate and hydrogen sulfide was tested on anoxic tolerance of the cockle Cerastoderma edule, as well as utilisation of glycogen. The aim was to evaluate the role of fuel depletion and growth of bacteria as a cause of mortality. The exponential increase of sulfide and ammonium occurred in anoxic natural seawater incubations and to a lesser extend in artificial, sulfate free, seawater. This could be strongly decreased by antibacterial agents, which led to improved survival time by approximately two-fold. Molybdate suppressed sulfide formation also, but did not affect survival time. Exogenous sulfide showed a negative effect on survival time at pH 6.8 and induced stronger accumulation of free glucose, d-lactate and l-alanine. This was not the case at pH 8.2. Fifty percent (LT 50) of cockles in anoxic seawater died after 3.5 days still with half the initial glycogen concentration present. However, in the presence of chloramphenicol (LT 50 7.9 days), the cockles utilised their endogenous fuel almost completely. In both incubations there was initially a strong increase of d-lactate and l-alanine. The d-lactate levels subsequently decreased again, probably due to bacterial consumption. This study strongly indicates that in anoxic closed systems, infection by pathogenic bacteria is the first cause of death and not exhaustion of endogenous fuel depots.

Anoxic survival of Macoma balthica: the effect of antibiotics, molybdate and sulphide.

In anoxic semi-closed systems, the survival time of the clam Macoma balthica was compared to clams which were incubated in the presence of several antibiotics (chloramphenicol, 5-oxytetracycline hydrochloride, penicillin, streptomycin, a mix of penicillin and streptomycin and a mix of chloramphenicol, polymyxin, neomycin and penicillin), sulphide and chloramphenicol at pH 6.8 and 8.2 and molybdate (specific inhibitor of the process of sulphate reduction). The aim was to detect maximum survival times of this clam and indications for the cause of mortality under the conditions tested. Median survival time (LT(50)) of the clam was 4.8 days (at 19 degrees C) in incubations without any addition. Added sulphide (200 µM) decreased survival time. At pH 8.2, LT(50) decreased by 20.8% and at pH 6.8 by 35.2%. However, added molybdate, which suppressed biotic sulphide formation, did not improve survival time (LT(50)=4.4 days). Biotic sulphide probably did not speed up mortality rate, but indicated excessive growth of sulphate reducing bacteria once mortality started. The presence of different antibiotics increased significantly survival time (LT(50)) from 8.9 to 14.9 days. Qualitative estimations were made of the numbers of bacteria present in the systems. Compared to a seawater control, highest numbers were observed in the incubation of clams without additions and in the presence of molybdate. Nevertheless, due to the presence of molybdate, bacteria numbers were significantly lower. However, very low numbers of bacteria were observed in the incubations of clams in the presence of chloramphenicol. These data demonstrated that the presence and proliferation of bacteria was probably the cause of death of the clams.

Influence of incubation conditions on the anoxic survival of marine bivalves. Static and semi-static incubations

MEPS Marine Ecology Progress Series Contact the journal Facebook Twitter RSS Mailing List Subscribe to our mailing list via Mailchimp HomeLatest VolumeAbout the JournalEditorsTheme Sections MEPS 211:169-179 (2001) - doi:10.3354/meps211169 Influence of incubation conditions on the anoxic survival of marine bivalves. Static and semi-static incubations Albertus de Zwaan1,*, Otello Cattani2, Giovanni Vitali2, Paolo Cortesi2 1Netherlands Institute of Ecology, Centre for Estuarine and Coastal Ecology, PO Box 140, 4400 AC Yerseke, The Netherlands 2Department of Biochemistry, Veterinary Section, University of Bologna, Via Tolara di sopra 50, 40064 Ozzano Emilia (Bologna), Italy *E-mail: zwaan@cemo.nioo.knaw.nl ABSTRACT: In a comparative study of 4 bivalve species we show that the apparent widely different tolerances in survival time observed in a closed system filled with N2-gassed seawater is mainly due to the experimental conditions. Both a high dose of cadmium and the antibiotic chloramphenicol increase survival time 2- to 4-fold. Without precautions for bacterial growth, the survival time of the most tolerant species, Scapharca inaequivalvis, is about 4 times longer than that of the most sensitive species, Venus gallina. The other bivalves Tapes philippinarum and Mytilus galloprovincialis, have intermediate survival times. When proliferation of bacteria is prevented by chloramphenicol, the survival time of S. inaequivalvis remains the highest; however under these conditions the other 3 species show similar survival times. Bacteria cause a drop in pH of the incubation medium and the accumulation of sulphide. S. inaequivalvis exhibits a significant decrease in survival time in the presence of exogenous sulphide. The antibiotic postpones the accumulation of sulphide, but a significant population of sulphate-reducing bacteria is able to survive in its presence. In the case of V. gallina and M. galloprovincialis, exogenous sulphide (up to 400 µM) does not affect the improved survival time due to the antibiotic. This holds also for a decrease in pH. Bacterial toxins other than sulphide or direct action on the integrity of the organism must be responsible for the adverse effects on survival. The responsible micro-organisms are associated with the bivalves, and anoxia induces their proliferation. For this reason, accumulation of bacterial noxious products cannot be avoided by frequent renewal of the medium. KEY WORDS: Benthic macrofauna · Bivalves · Hydrogen sulphide · Anaerobiosis · Cadmium · Chloramphenicol · Anoxic resistance Full text in pdf format PreviousNextExport citation RSS - Facebook - Tweet - linkedIn Cited by Published in MEPS Vol. 211. Online publication date: February 14, 2001 Print ISSN: 0171-8630; Online ISSN: 1616-1599 Copyright © 2001 Inter-Research.

Anoxia survival and metabolic arrest in the turtle

Anoxia survival and metabolic arrest in the turtle

Role of metallothionein against oxidative stress in the mussel Mytilus galloprovincialis.

Metallothionein (MT) is a sulfhydryl-rich protein involved mainly in heavy metal homeostasis and detoxification. In this study, the use of the mussel as an experimental model allowed us to test MT antioxidant properties at the molecular, cellular, and organism level. MT induction was achieved by mussel exposure to Cd (200 microg/l) in aquaria for 7 days followed by detoxification in the sea for 28 days. Cd-preexposed and nonexposed mussels were then treated with Fe (300-600 microg/l) in aquaria for 3 days. Biochemical assays on digestive gland tissue showed that treatment with Fe led to a significant increase in oxyradical production and malondialdehyde level only in mussels not preexposed to Cd. The Cd-dependent resistance to oxidative stress was ascribed to MT induction, as Cd produced no significant variation of reduced glutathione and major antioxidant enzymes. Digital imaging of isolated digestive gland cells showed lower oxyradical rise and higher viability in cells from Cd-preexposed mussels after treatments with 0.5-5 mM H2O2. Analyses on whole organisms showed that anoxic survival was lowered in mussels that had been treated with Fe, but such an effect was less pronounced in Cd-preexposed mussels compared with nonpreexposed ones. In conclusion, data suggest an antioxidant role for MT, which seems to occur through oxyradical scavenging and is able to protect both isolated cells and the entire organism from oxidative stress.

Habitat-related differences in the responses to oxygen deficiencies in Idotea baltica and Idotea emarginata (Isopoda, Crustacea)

Abstract Two apparently ecologically similar sublittoral isopod species, Idotea baltica and Idotea emarginata , were studied with respect to their abilities to cope with deficiencies in environmental oxygen concentration. In a first series of experiments, respiration rates of both species were measured, at different temperatures (5, 10, 15°C), as a function of oxygen partial pressure. Whereas I. baltica showed the characteristics of an oxyconformer, I. emarginata regulates oxygen consumption from normoxia down to distinct hypoxic conditions. In a second series of experiments, anoxia survival times (LD 50 ) were determined for different types of individuals of both species (mancas, juveniles, adult females, adult males). In both species, survival times increased with developmental stage. Adult males were more resistant to anoxia than adult females. In all types of individuals, the LD 50 values of I. emarginata were significantly higher than those of I. baltica . The interspecific differences are clearly adaptive, correlating with respective habitat differences. Idotea baltica is associated with seaweed drifting at the water surface where oxygen is in the normoxic range. In contrast, I. emarginata lives among accumulations of macroalgal debris on the seabed where hypoxia is common. The different abilities of the species to sustain periods of hypoxia may contribute to the maintenance of habitat segregation.

Survival of Immersion and Anoxia by Larval Tiger Beetles, Cicindela togata

Abstract The sedentary terrestrial larvae of the tiger beetle, Cicindela togata, inhabit areas that are often flooded for days or weeks. We tested the ability of these larvae to survive immersion and anoxia. Maximum survival time of immersed, anoxic C. togata was 6 days at 25 C. Time to 50% mortality (LT50) in these conditions was 85.9 ± 23.5 h. Survival times were more than eight times longer than those of similarly treated larvae of Tenebrio molitor (LT50 10.1 ± 3.2 h). Similar or somewhat longer survival times were observed in larvae of C. togata exposed to an anoxic nitrogen atmosphere (LT50 102 ± 31 h) and of T. molitor (LT5014.4 ± 6.5 h). At 10 C, LT50 of C. togata in anoxic atmospheres exceeded 10 days. Tiger beetle larvae are physiologically capable of surviving several days of inundation during floods without mechanisms to prevent burrow flooding. By entering a quiescent state, C. togata larvae survive much longer periods of anoxia than has been previously reported for terrestrial insect larvae.