scholarly journals Toxicological Effects of Inorganic Nanoparticle Mixtures in Freshwater Mussels

Environments ◽  
2020 ◽  
Vol 7 (12) ◽  
pp. 109
Author(s):  
Joelle Auclair ◽  
Patrice Turcotte ◽  
Christian Gagnon ◽  
Caroline Peyrot ◽  
Kevin J. Wilkinson ◽  
...  

The toxicological effects of nanoparticles mixtures in aquatic organisms are poorly understood. The purpose of this study was to examine the tissue metal loadings and sublethal effects of silver (nAg), cerium oxide (nCeO), copper oxide (nCuO) and zinc oxide (nZnO) nanoparticles individually at 50 µg/L and in two mixtures to freshwater mussels Dreissena bugensis. The mixtures consisted of 12.5 µg/L of each nanoparticle (Mix50) and 50 µg/L of each nanoparticles (Mix200). After a 96-h exposure period, mussels were analyzed for morphological changes, air time survival, bioaccumulation, inflammation (cyclooxygenase or COX activity), lipid peroxidation (LPO), DNA strand breaks, labile Zn, acetylcholinesterase (AChE) and protein–ubiquitin levels. The data revealed that mussels accumulated the nanoparticles with nCeO and nAg were the least and most bioavailable, respectively. Increased tissue metal loadings were observed for nCeO and nCuO in mixtures, while no mixture effects were observed for nAg and nZnO. The weight loss during air emersion was lower in mussels exposed to nCuO alone but not by the mixture. On the one hand, labile Zn levels was increased with nZnO but returned to control values with the Mix50 and Mix200, suggesting antagonism. On the other hand, DNA strand breaks were reduced for both mixtures compared to controls or to the nanoparticles individually, suggesting potentiation of effects. The same was found for protein–ubiquitin levels, which were decreased by nCeO and nCuO alone but not when in mixtures, which increased their levels. In conclusion, the data revealed that the behavior and effects of nanoparticles were influenced by other nanoparticles where antagonist and potentiation interactions were identified.

1989 ◽  
Vol 92 (1) ◽  
pp. 37-49
Author(s):  
D.A. Jackson ◽  
C.K. Pearson ◽  
D.C. Fraser ◽  
K.M. Prise ◽  
S.Y. Wong

The survival of cells cultured in medium containing the chemotherapeutic drug methotrexate (MTX) is related directly to drug concentration. Changes in DNA resulting from a severe imbalance in the cells' nucleotide pools are thought to account for this cytotoxicity. We have attempted to clarify the gross biochemical changes that might lead to cell death. DNA strand breaks occur in cells treated with high concentrations of MTX but it is not clear that these are sufficient to account for cytotoxicity at lower doses. We observed dramatic changes in cytoskeletal morphology. Gross reorganization of the cytoskeleton is shown by immunolabelling but is high-lighted dramatically when cells are lysed to leave ‘nucleoids’. The nature of the changes seen in MTX-treated cells is characteristic of the cells’ general stress response, seen originally following heat shock. This study shows that other factors, such as changes in cytoskeletal function, must be considered together with any contribution from DNA damage, in order to account for the lethal effects of MTX.


2013 ◽  
Vol 61 (4) ◽  
pp. 215-222 ◽  
Author(s):  
Fabio Matsu Hasue ◽  
Maria José de Arruda Campos Rocha Passos ◽  
Thaís da Cruz Alves dos Santos ◽  
Arthur José da Silva Rocha ◽  
Caroline Patrício Vignardi ◽  
...  

In the environment, anthracene is characterized as being persistent, bioaccumulative and toxic to aquatic organisms. Biotransformation of xenobiotic substances, such as anthracene, produces reactive oxygen species that may induce DNA strand breaks. The aim of the present study was to evaluate the DNA damage in juvenile T. carolinus exposed to different concentrations (8, 16 and 32 µg.L-1) of anthracene for 24 h in the dark then subsequently allowed to depurate in clean water for different periods of time (48, 96 or 144 h) using the comet assay. Our results show that anthracene is genotoxic to T. carolinus and that DNA damage was dose- and depuration/time- dependent. Anthracenegenotoxicity was observed in all experimental concentrations. Depuration seemed to be more efficient in fish exposed to thelowest anthracene concentration and maintained in clean water for 96 h.


2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
J. Auclair ◽  
P. Turcotte ◽  
C. Gagnon ◽  
C. Peyrot ◽  
K. J. Wilkinson ◽  
...  

Nanomaterials could be modified with various coatings which could modulate their behavior in the environment, bioavailability and toxicity. The purpose of this study was to determine if the selected coatings of silver nanoparticles (nAg) could influence the fate, bioavailability, and toxicity toward suspension feeding freshwater mussels, Elliptio complanata. Mussels were exposed for 96 h to 50 μg/L of nAg with the following surface coatings: citrate, silicate (Si), polyvinylpyrrolidone (PVP), and branched polyethylenimine (bPEI). After the exposure period, mussels were analyzed for total Ag, resistance to air emersion, oxidative stress, genotoxicity, and autophagosome protein uptake (protein ubiquitinylation) in gills and digestive glands. The data revealed that citrate- and PVP-coated nAg were 2 times more abundant in the digestive gland compared to bPEI- and Si-coated nAg with estimated bioaccumulation factors between 5 and 10. The data revealed that tissue Ag levels were closely associated with air survival time, weight loss during air exposure, DNA strand breaks, LPO, and protein-ubiquitin levels in the digestive gland. The data supports the hypothesis that the coatings could influence bioavailability and toxicity in freshwater mussels.


1997 ◽  
Vol 45 (7) ◽  
pp. 923-934 ◽  
Author(s):  
Jae A. Collins ◽  
Cynthia A. Schandl ◽  
Kristy K. Young ◽  
Josef Vesely ◽  
Mark C. Willingham

Apoptosis, the terminal morphological and biochemical events of programmed cell death, is characterized by specific changes in cell surface and nuclear morphology. In addition, DNA fragmentation in an internucleosomal pattern is detectable in mass cultures of apoptotic cells. However, DNA fragmentation and nuclear morphological changes may not necessarily be associated events. In this study, we examined OVCAR-3 and KB human carcinoma cells using time-lapse video phase-contrast microscopy to characterize the surface and nuclear morphological features of apoptosis in response to treatment with either taxol or ricin. The surface morphological features of apoptosis were the same in both cell types and with both drugs. Using an in situ nick-translation histochemical assay, these single cells were also examined for DNA strand breaks during apoptosis. Surface morphological changes demonstrated discrete stages of cell rounding, surface blebbing, followed by cessation of movement and the extension of thin surface microspikes, followed much later by surface blistering and cell lysis. Nuclear features examined by DAPI cytochemistry demonstrated apoptotic nuclear condensation very early in this sequence, usually at the time of initial surface blebbing. The nick-translation assay, however, demonstrated DNA strand breaks at a much later time, only after the formation of separated apoptotic bodies or after final cell lysis. This study points out the differences between surface and nuclear morphological changes in apoptosis, and the large temporal separation between nuclear morphological changes and major DNA fragmentation detectable by this in situ technique. This result suggests caution in using in situ nick-translation as a direct correlate of internucleosomal DNA fragmentation in apoptosis.


2001 ◽  
Vol 21 (21) ◽  
pp. 7191-7198 ◽  
Author(s):  
John R. Vance ◽  
Thomas E. Wilson

ABSTRACT In Saccharomyces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathways for the removal of various 3′-terminal blocking lesions from DNA strand breaks and in the repair of abasic sites, which both result from oxidative DNA damage. Here we demonstrate that Tpp1, a homologue of the 3′ phosphatase domain of polynucleotide kinase, is a third member of this group of redundant 3′ processing enzymes. Unlike Apn1 and Apn2, Tpp1 is specific for the removal of 3′ phosphates at strand breaks and does not possess more general 3′ phosphodiesterase, exonuclease, or AP endonuclease activities. Deletion ofTPP1 in an apn1 apn2 mutant background dramatically increased the sensitivity of the double mutant to DNA damage caused by H2O2 and bleomycin but not to damage caused by methyl methanesulfonate. The triple mutant was also deficient in the repair of 3′ phosphate lesions left by Tdp1-mediated cleavage of camptothecin-stabilized Top1-DNA covalent complexes. Finally, the tpp1 apn1 apn2 triple mutation displayed synthetic lethality in combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3′-terminal lesions resulting from endogenous damage. Taken together, these results demonstrate a clear role for the lesion-specific enzyme, Tpp1, in the repair of a subset of DNA strand breaks.


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