scholarly journals Stress response and toxicity studies on zebrafish exposed to endosulfan and imidacloprid present in water

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.

2019 ◽  
Vol 24 (40) ◽  
pp. 4726-4741 ◽  
Author(s):  
Orathai Tangvarasittichai ◽  
Surapon Tangvarasittichai

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.


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.


Nanomaterials ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 2471
Author(s):  
Su-Chun Wang ◽  
Fei-Fei Liu ◽  
Tian-Yuan Huang ◽  
Jin-Lin Fan ◽  
Zhi-Yin Gao ◽  
...  

Recently, the effects of nanoplastics (NPs) on aquatic organisms have attracted much attention; however, research on the toxicity of NPs to microalgae has been insufficient. In the present study, the effects of polystyrene nanoplastics (nano-PS, 50 nm) on growth inhibition, chlorophyll content, oxidative stress, and algal toxin production of the marine toxigenic dinoflagellate Amphidinium carterae Hulburt were investigated. Chlorophyll synthesis was promoted by nano-PS on day 2 but was inhibited on day 4; high concentrations of nano-PS (≥50 mg/L) significantly inhibited the growth of A. carterae. Moreover, despite the combined effect of superoxide dismutase (SOD) and glutathione (GSH), high reactive oxygen species (ROS) level and malondialdehyde (MDA) content were still induced by nano-PS (≥50 mg/L), indicating severe lipid peroxidation. In addition, the contents of extracellular and intracellular hemolytic toxins in nano-PS groups were significantly higher than those in control groups on days 2 and 8, except that those of extracellular hemolytic toxins in the 100 mg/L nano-PS group decreased on day 8 because of severe adsorption of hemolytic toxins to the nano-PS. Hence, the effects of nano-PS on A. carterae are closely linked to nano-PS concentration and surface properties and exposure time. These findings provide a deep understanding of the complex effects of NPs on toxigenic microalgae and present valuable data for assessing their environmental risks.


2018 ◽  
Author(s):  
Robert PL Wisse ◽  
Jonas JW Kuiper ◽  
Timothy RDJ Radstake ◽  
Jasper CA Broen

AbstractPurposeThe pathogenesis of keratoconus (KC) is multifactorial and associated with oxidative stress and subsequent DNA damage. The aim of this study was to investigate differences in DNA damage and replicative stress in patients with KC, and in both healthy and diseased controls.MethodsSixty-four corneal buttons were obtained from 27 patients with KC after corneal transplant surgery, 21 patients with a decompensated graft (DG), and 16 healthy controls (HC). The amount of intact Alu elements per genome copy as measured by qPCR was used to quantify intact DNA. Telomere length was measured as a proxy for replicative stress. In addition, telomerase reverse transcriptase (hTERT) gene expression level was assessed.ResultsMean (±SD) DNA damage was similar between the KC (5.56 ±14.08), DG (3.16 ±8.22), and HC (3.51 ±6.66) groups (P=0.807). No associations were found between DNA damage and patient age (P=0.523), atopic constitution (P=0.240), or contact lens wear (P=0.393). Telomere length differed (P=0.034), most notably in the KC group, and hTERT was not detected in any corneal sample. Three cross-linked (CXL) KC corneas did not contain significant more DNA damage (2.6x, P = 0.750).ConclusionsBased on these findings, differences in actual corneal DNA damage in KC could not be identified, and the longer telomere length in KC did not support replicative stress as a major etiological factor in the pathogenesis of KC. Future longitudinal investigations on KC etiology should assess progressive early cases to better comprehend the cellular and molecular processes preceding the archetypical morphological changes.PrecisOxidative stress is allegedly linked with the development of keratoconus. Whether these stressors actually lead to persisting DNA damage and replicative stress is debated. DNA damage was comparable with control samples, and a shortened telomere length was not identified.


APOPTOSIS ◽  
2012 ◽  
Vol 17 (9) ◽  
pp. 964-974 ◽  
Author(s):  
Fulvia Zanichelli ◽  
Stefania Capasso ◽  
Giovanni Di Bernardo ◽  
Marilena Cipollaro ◽  
Eleonora Pagnotta ◽  
...  

2018 ◽  
Vol 69 (2) ◽  
pp. 154-168 ◽  
Author(s):  
Mirta Milić ◽  
Suzana Žunec ◽  
Vedran Micek ◽  
Vilena Kašuba ◽  
Anja Mikolić ◽  
...  

AbstractIn this 28 day-study, we evaluated the effects of herbicide glyphosate administered by gavage to Wistar rats at daily doses equivalent to 0.1 of the acceptable operator exposure level (AOEL), 0.5 of the consumer acceptable daily intake (ADI), 1.75 (corresponding to the chronic population-adjusted dose, cPAD), and 10 mg kg−1 body weight (bw) (corresponding to 100 times the AOEL). At the end of each treatment, the body and liver weights were measured and compared with their baseline values. DNA damage in leukocytes and liver tissue was estimated with the alkaline comet assay. Oxidative stress was evaluated using a battery of endpoints to establish lipid peroxidation via thiobarbituric reactive substances (TBARS) level, level of reactive oxygen species (ROS), glutathione (GSH) level, and the activity of glutathione peroxidase (GSH-Px). Total cholinesterase activity and the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) were also measured. The exposed animals gained less weight than control. Treatment resulted in significantly higher primary DNA damage in the liver cells and leukocytes. Glyphosate exposure significantly lowered TBARS in the liver of the AOEL, ADI, and cPAD groups, and in plasma in the AOEL and cPAD group. AChE was inhibited with all treatments, but the AOEL and ADI groups significantly differed from control. Total ChE and plasma/liver ROS/GSH levels did not significantly differ from control, except for the 35 % decrease in ChE in the AOEL and ADI groups and a significant drop in liver GSH in the cPAD and 100xAOEL groups. AOEL and ADI blood GSH-Px activity dropped significantly, but in the liver it significantly increased in the ADI, cPAD, and 100xAOEL groups vs. control. All these findings show that even exposure to low glyphosate levels can have serious adverse effects and points to a need to change the approach to risk assessment of low-level chronic/sub-chronic glyphosate exposure, where oxidative stress is not necessarily related to the genetic damage and AChE inhibition.


Molecules ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 368 ◽  
Author(s):  
Adriana Nowak ◽  
Małgorzata Zakłos-Szyda ◽  
Dorota Żyżelewicz ◽  
Agnieszka Koszucka ◽  
Ilona Motyl

Acrylamide (AA) toxicity remains an interesting subject in toxicological research. The aim of the research performed in this paper was to determine mechanisms of cyto- and genotoxic effects of AA on the human colon adenocarcinoma cell line Caco-2, to estimate the inhibitory concentration (IC)50 values in cell viability assays, to measure the basal and oxidative DNA damage as well as the oxidative stress leading to apoptosis, and to assess the morphological changes in cells using microscopic methods. It has been proven that AA induces cytotoxic and genotoxic effects on Caco-2 cells. Higher cytotoxic activity was gained in the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay compared with the PrestoBlue assay, with IC50 values of 5.9 and 8.9 mM after 24 h exposure, respectively. In the single-cell gel electrophoresis assay, the greatest DNA damage was caused by the highest concentration of acrylamide equal to 12.5 mM (89.1% ± 0.9%). AA also induced oxidative DNA damage and generated reactive oxygen species (ROS), which was concentration dependent and correlated with the depletion of mitochondrial membrane potential and apoptosis induction. In the microscopic staining of cells, AA in the dosage close to the IC50 induced morphological changes typical for apoptosis. Taken together, these results demonstrate that AA has a pro-oxidative effect on Caco-2 cells, leading to apoptotic cell death.


2018 ◽  
Vol 81 (1) ◽  
pp. 25-38
Author(s):  
O.B. Leonenko ◽  
N.S. Leonenko ◽  
V.А. Movchan ◽  
A.O. Lukianenko

The data of literature and own researches concerning features of toxic action of welding aerosols are generalized. Which have a different chemical composition and dimensions. Their damaging effect depends on many factors. Prolonged exposure may occur in low concentrations. Most of the negative effects are determined by oxidative stress and DNA damage. There are the most dangerous components of welding electrodes are chromium and nickel. Key words: welding aerosol, nanoparticles, cytotoxicity, damaging effect.


2014 ◽  
Vol 20 (1) ◽  
pp. 45-61 ◽  
Author(s):  
Teresa Korniłłowicz

In the present paper low concentrations (l -10 mcg/ml) of DNOC, in general, were not found to restrain germination of fungal spores. High concentrations (25-200 mcg/ml) were sporostatic and sporocidal Disturbances of fungal spore germination in the presence of DNOC were often accompanied by morphological changes of spores and germ tubes, <i>Mucor mucedo</i> under the influence of DNOC developed budding cels besides hyphae.


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