scholarly journals Effect of Cadmium and Nickel Exposure on Early Development in Zebrafish (Danio rerio) Embryos

Water ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3005
Author(s):  
Seyed Javid Aldavood ◽  
Louise C. Abbott ◽  
Zachary R. Evans ◽  
Daniel J. Griffin ◽  
MaKenzie D. Lee ◽  
...  

Exposure to even low concentrations of heavy metals can be toxic to aquatic organisms, especially during embryonic development. Thus, this study aimed to investigate the toxicity of nickel and cadmium in zebrafish (Danio rerio) embryos exposed to environmentally relevant concentrations of each metal alone or in combination from 4 h through to 72 h postfertilization. Neither metal altered survival, but individual and combined exposures decreased hatching rate. Whereas cadmium did not affect total body length, trunk area, eye diameter, or eye area, nickel alone and in combination with cadmium decreased each morphological parameter. Yolk sac area, an index of metabolic rate, was not affected by nickel, but was larger in embryos exposed to high cadmium concentrations or nickel and cadmium combined at high concentrations. Nickel decreased spontaneous movement, whereas cadmium alone or nickel and cadmium combined had no effect. Neither metal altered elicited movement, but nickel and cadmium combined decreased elicited movement. Myosin protein expression in skeletal muscle was not altered by cadmium exposure. However, exposure to nickel at low concentrations and combined exposure to nickel and cadmium decreased myosin expression. Overall, nickel was more toxic than cadmium. In conclusion, we observed that combined exposures had a greater effect on movement than gross morphology, and no significant additive or synergistic interactions were present. These results imply that nickel and cadmium are toxic to developing embryos, even at very low exposure concentrations, and that these metals act via different mechanisms.

2019 ◽  
Vol 68 (8) ◽  
pp. 718-730 ◽  
Author(s):  
Barzah Muazzam ◽  
Kashif Munawar ◽  
Imtiaz Ahmad Khan ◽  
Sarwat Jahan ◽  
Mazhar Iqbal ◽  
...  

Abstract Fish and other aquatic biota are hampered by mixtures of pesticides which pollute natural water through agricultural runoff and other sources. Toxicity of combined exposures of endosulfan and imidacloprid on zebrafish in terms of oxidative stress and deoxyribonucleic acid (DNA) damage in liver and histological alterations in gills and muscles was investigated. Zebrafish were exposed to three different sub-lethal concentrations of endosulfan and imidacloprid along with control selected for each treatment for 21 days: control treatment (CT), treatment 1 (T1), treatment 2 (T2) and treatment 3 (T3). T1, T2 and T3 groups were exposed to 0.1, 0.5 and 1 μg/L of endosulfan, respectively, while imidacloprid concentration was maintained at 1 ppm in all three treatments. Oxidative stress was evaluated by measuring levels of catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA). Comet assay was applied to measure degree of DNA damage. Dose- and time-dependent decrease in SOD and CAT activity was observed after 21 days of exposure while low concentrations of pesticides induced SOD and CAT activities after early exposure to reduce the oxidative stress. MDA content was found to be increased in T3 having high concentrations of pesticides. Substantial increase in DNA damage was noticed after 21 days' exposure to pesticides. Significant morphological changes were observed in gills relative to muscles.


Author(s):  
Huihui Chen ◽  
Huiting Yang ◽  
Yanyan Zhao ◽  
Xiaohong Gu ◽  
Christopher J. Martyniuk

Concerns regarding environmental exposures and the impacts of pharmaceuticals on non-target aquatic organisms continue to increase. The antiepileptic drug carbamazepine (CBZ) is often detected as an aquatic contaminant and can disrupt various behaviors of fishes. However, there are few reports which investigate the mechanism of CBZ action in fish. The aim of the current study was to evaluate the effects of CBZ on embryonic development (i.e., hatching rate, heart rate, and body length) and early spontaneous movement. Moreover, we sought to investigate potential mechanisms by focusing on the gamma-aminobutyric acid (GABA) neurotransmitter system in zebrafish 6 days after of exposure. The results show that CBZ exposure did not cause significant effects on embryo development (hatching rate, heart rate, nor body length) at the test concentrations. However, the early spontaneous movement of embryos was inhibited following 10 μg/L CBZ exposure at 28–29 h post-fertilization (hpf). In addition, acetylcholinesterase (AChE) activity and GABA concentrations were increased with exposure, whereas glutamate (Glu) concentrations were decreased in larval zebrafish. Gene expression analysis revealed that GABA and glutamate metabolic pathways in zebrafish larvae were altered following exposure to CBZ. GABA transaminase (abat) and glutamic acid decarboxylase (gad1b) decreased to 100 µg/L, and glutamate receptor, ionotropic, N-methyl D-aspartate 1b (grin1b) as well as the glutamate receptor, ionotropic, α-amino-3hydroxy-5methylisoxazole-4propionic 2b (gria2b) were down-regulated with exposure to 1 µg/L CBZ. Our study suggests that CBZ, which can act as an agonist of the GABAA receptor in humans, can also induce alterations in the GABAergic system in fish. Overall, this study improves understanding of the neurotoxicity and behavioral toxicity of zebrafish exposed to CBZ and generates data to be used to understand mechanisms of action that may underlie antiepileptic drug exposures.


2013 ◽  
Vol 16 (1) ◽  
pp. 77-84 ◽  
Author(s):  
J. Małaczewska ◽  
A.K. Siwicki

Abstract The growing popularity of nanotechnology in the past decade has increased nanomaterial concentrations in the environment and the risk of their toxicity for aquatic organisms. Metal nanoparticles, which are easily absorbed and accumulated by fish, are probably able to interact directly with their immunocompetent cells. The objective of this study was to evaluate the in vitro effect of commercially available silver, gold and copper nanocolloids on the rainbow trout leukocyte and splenocyte activity. At high concentrations, all of the nanocolloids studied had adverse effects on the proliferative response of trout lymphocytes, and the most toxic of them, silver, decreased also the respiratory burst activity of splenocytes. Low concentrations of silver nanocolloid, however, had a stimulating effect on the lymhocyte proliferation.


Parasitology ◽  
1973 ◽  
Vol 67 (2) ◽  
pp. 219-228 ◽  
Author(s):  
E. S. Upatham ◽  
R. F. Sturrock

Groups of mice were exposed to Schistosoma mansoni cercariae in a large volume of water. A factorial design was used to investigate the effects of cercarial concentration and length of exposure on infection rates and worm burdens. Low exposure times and cercarial concentrations gave no infections, but prolonged exposure to high concentrations gave high infection rates and worm burdens. Prolonged exposure to low concentrations gave low worm burdens and moderate infection rates: short exposure to high concentrations gave moderate infection rates and worm burdens. Statistical analysis showed that both infection rates and mean worm burdens were significantly related to the two main factors, but the relationship was complicated in each case by curvilinear effects and by a significant interaction between the main factors. Field cercarial concentrations are generally low on St Lucia, a fact suggesting that brief human water contacts, such as fording and filling domestic water containers, play little part in transmission. Prolonged contact during swimming, bathing and washing clothes may produce significant infection rates accompanied by low worm burdens. However, on the rare occasions when high cercarial concentrations occur, even the briefest exposure may produce significant infection rates and moderate worm burdens.


1992 ◽  
Vol 68 (05) ◽  
pp. 570-576 ◽  
Author(s):  
Mary A Selak

SummaryWe have previously demonstrated that human neutrophil cathepsin G is a strong platelet agonist that binds to a specific receptor. This work describes the effect of neutrophil elastase on cathepsin G-induced platelet responses. While platelets were not activated by high concentrations of neutrophil elastase by itself, elastase enhanced aggregation, secretion and calcium mobilization induced by low concentrations of cathepsin G. Platelet aggregation and secretion were potentiated in a concentration-dependent manner by neutrophil elastase with maximal responses observable at 200 nM. Enhancement was observed when elastase was preincubated with platelets for time intervals of 10–60 s prior to addition of a low concentration of cathepsin G and required catalytically-active elastase since phenylmethanesulphonyl fluoride-inhibited enzyme failed to potentiate cell activation. Neutrophil elastase potentiation of platelet responses induced by low concentrations of cathepsin G was markedly inhibited by creatine phosphate/creatine phosphokinase and/or indomethacin, indicating that the synergism between elastase and cathepsin G required the participation of ADP and thromboxane A2. On the other hand, platelet responses were not attenuated by the PAF antagonist BN 52021, signifying that PAF-acether did not play a role in elastase potentiation. At higher concentrations porcine pancreatic elastase exhibits similar effects to neutrophil elastase, demonstrating that the effect of elastase was not unique to the neutrophil protease. While neutrophil elastase failed to alter the ability of cathepsin G to hydrolyze a synthetic chromogenic substrate, preincubation of platelets with elastase increased the apparent affinity of cathepsin G binding to platelets. In contrast to their effect on cathepsin G-induced platelet responses, neither neutrophil nor pancreatic elasatse potentiated aggregation or dense granule release initiated by ADP, PAF-acether, arachidonic acid or U46619, a thromboxane A2 mimetic. Moreover, unlike its effect on cathepsin G, neutrophil elastase inhibited thrombin-induced responses. The current observations demonstrate that elastase can potentiate platelet responses mediated by low concentrations of cathepsin G, suggesting that both enzymes may function synergistically to activate platelets under conditions where neutrophil degranulation occurs.


1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.


1970 ◽  
Vol 23 (03) ◽  
pp. 601-620 ◽  
Author(s):  
Th. B Tschopp

SummaryAggregation of cat platelets in the citrated plasma is examined by means of Born’s absorptiometer. A marked tendency of the platelets of this species to spontaneous aggregation necessitated first of all the development of an improved technique of blood collection.A hypothesis according to which 5-HT is released from the platelets, explains the absence of oscillations on the base line of the absorptiometer, the absence of platelet swelling, when ADP is added, and the effect of stirring on the aggregation curves in cat PRP. The average volume of cat platelets amounts to 10.46 μ3 when directly fixed in the blood, when fixed from PRP to 12.17 μ3, when fixed from stirred PRP to 13.51 μ3.In low concentrations (0.3-2 μM) ADP produce reversible aggregation; in narrowly restricted, individually dissimilar mean concentrations irreversible aggregation in two phases and in high concentrations, irreversible aggregation in one phase. Like ADP serotonin produces 2 phase irreversible aggregation in concentrations of 3-10 μM, but unlike ADP, the aggregation velocity decreases again with high 5-HT concentrations (>100 μM). Adrenaline does not produce aggregation and it is likely that adenosine and adenosine monophosphate inhibit the aggregation by serotonin but not by ADP. Species differences in the aggregation of human, rabbit and cat platelets are discussed.


1971 ◽  
Vol 26 (01) ◽  
pp. 145-166
Author(s):  
E Deutsch ◽  
K Lechner ◽  
K Moser ◽  
L Stockinger

Summary1. The aniline derivative AN 162, Donau Pharmazie, Linz, Austria, has a dual action on the blood coagulation: an anticoagulant and an coagulation enhancing effect.2. The anticoagulant action may only be demonstrated with high concentrations (over 1 X 10”3 M related to plasma) preferentially in PPP. It is partially caused by an inhibition of the endogenous way of generation of the prothrombin converting principle. In addition it is suggested that it interferes with the fibrinogen-fibrin reaction in a manner not yet understood.3. The coagulant action is caused by a greater availability of platelet constituents at low concentrations of AN 162 (over 1 × 10-4 M) and by the induction of a release reaction at higher concentrations. The platelet factors 3 and 4, serotonin, adenine, and acid phosphatase are released.4. AN 162 inhibits platelet aggregation. This inhibition can be demonstrated by the PAT of Breddin and in the stirred aggregation test of Born. It is more effective to inhibit the collagen-induced and the second phase of the adrenaline-induced aggregation than the ADP induced one. The platelet retention (test of Hellem) is also reduced.5. The action of AN 162 on the platelets is caused by a damage of the platelet membrane which becomes permeabel for both, soluble platelet constitutents and granula.6. AN 162 interferes with the energy metabolism of the platelets. It causes a loss of ATP, and inhibits the key-enzymes of glycolysis, citric acid cycle, fatty acid oxydation and glutathione reduction.7. AN 162 inhibits the growth of fibroblasts without influence on mitosis.


1986 ◽  
Vol 55 (01) ◽  
pp. 136-142 ◽  
Author(s):  
K J Kao ◽  
David M Shaut ◽  
Paul A Klein

SummaryThrombospondin (TSP) is a major platelet secretory glycoprotein. Earlier studies of various investigators demonstrated that TSP is the endogenous platelet lectin and is responsible for the hemagglutinating activity expressed on formaldehyde-fixed thrombin-treated platelets. The direct effect of highly purified TSP on thrombin-induced platelet aggregation was studied. It was observed that aggregation of gel-filtered platelets induced by low concentrations of thrombin (≤0.05 U/ml) was progressively inhibited by increasing concentrations of exogenous TSP (≥60 μg/ml). However, inhibition of platelet aggregation by TSP was not observed when higher than 0.1 U/ml thrombin was used to activate platelets. To exclude the possibility that TSP inhibits platelet aggregation by affecting thrombin activation of platelets, three different approaches were utilized. First, by using a chromogenic substrate assay it was shown that TSP does not inhibit the proteolytic activity of thrombin. Second, thromboxane B2 synthesis by thrombin-stimulated platelets was not affected by exogenous TSP. Finally, electron microscopy of thrombin-induced platelet aggregates showed that platelets were activated by thrombin regardless of the presence or absence of exogenous TSP. The results indicate that high concentrations of exogenous TSP (≥60 μg/ml) directly interfere with interplatelet recognition among thrombin-activated platelets. This inhibitory effect of TSP can be neutralized by anti-TSP Fab. In addition, anti-TSP Fab directly inhibits platelet aggregation induced by a low (0.02 U/ml) but not by a high (0.1 U/ml) concentration of thrombin. In conclusion, our findings demonstrate that TSP is functionally important for platelet aggregation induced by low (≤0.05 U/ml) but not high (≥0.1 U/ml) concentrations of thrombin. High concentrations of exogenous TSP may univalently saturate all its platelet binding sites consequently interfering with TSP-crosslinking of thrombin-activated platelets.


1992 ◽  
Vol 26 (3-4) ◽  
pp. 907-914 ◽  
Author(s):  
A. Attal ◽  
M. Brigodiot ◽  
P. Camacho ◽  
J. Manem

The purpose of this study is to gain a better understanding of the biological phenomena involved in the production of hydrogen sulfide in urban wastewater (UWW) systems. It is found that the UWW itself naturally possesses the biomass needed to consume the sulfates. These heterotrophic sulfate-reducing bacteria populations, though immediately active in strict anaerobic conditions, are present only in very low concentrations in the UWW. A concentration of them was studied within the pressure pipes, in the form of deposits, and this justifies the high concentrations of sulfides measured in certain wastewater networks. There are two reasons why the ferrous sulfate used as a treatment in any wastewater networks should not cause the production of additional sulfides. Firstly, the sulfate consumption kinetics are always too slow, relative to the residence time of the water in the pipe, for all of the sulfates to be consumed anyway. Secondly, the amount of assimilable carbon, soluble carbon, and carbon from suspended solid (SS) hydrolysis is insufficient.


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