Cadmium Protection Strategies—A Hidden Trade-Off?

Sandbichler, Adolf Michael; Höckner, Martina

doi:10.3390/ijms17010139

Cited by 85 publications

(40 citation statements)

References 193 publications

(190 reference statements)

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“…Its high expression also induced GSH accumulation (2.6-fold increase) and provided a sufficient amount of GSH under Cd exposure. Similar results were obtained in rat proximal tubule cells 51 . It was proposed that the increasing GSH contents provided a protective response to Cd toxicity.…”

Section: Resultssupporting

confidence: 88%

Cadmium effects on DNA and protein metabolism in oyster (Crassostrea gigas) revealed by proteomic analyses

Meng

Wang

et al. 2017

Sci Rep

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Marine molluscs, including oysters, can concentrate high levels of cadmium (Cd) in their soft tissues, but the molecular mechanisms of Cd toxicity remain speculative. In this study, Pacific oysters (Crassostrea gigas) were exposed to Cd for 9 days and their gills were subjected to proteomic analysis, which were further confirmed with transcriptomic analysis. A total of 4,964 proteins was quantified and 515 differentially expressed proteins were identified in response to Cd exposure. Gene Ontology enrichment analysis revealed that excess Cd affected the DNA and protein metabolism. Specifically, Cd toxicity resulted in the inhibition of DNA glycosylase and gap-filling and ligation enzymes expressions in base excision repair pathway, which may have decreased DNA repair capacity. At the protein level, Cd induced the heat shock protein response, initiation of protein refolding as well as degradation by ubiquitin proteasome pathway, among other effects. Excess Cd also induced antioxidant responses, particularly glutathione metabolism, which play important roles in Cd chelation and anti-oxidation. This study provided the first molecular mechanisms of Cd toxicity on DNA and protein metabolism at protein levels, and identified molecular biomarkers for Cd toxicity in oysters.

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Section: Resultssupporting

confidence: 88%

Cadmium effects on DNA and protein metabolism in oyster (Crassostrea gigas) revealed by proteomic analyses

Meng

Wang

et al. 2017

Sci Rep

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“…Cd treatment upregulates ROS and lipid peroxidation, reduces NO bioavailability, and induces peroxynitrite production and protein nitration One of the mechanisms of heavy metal cytotoxicity is partly related to the generation of oxidative stress, through a heterogeneous mechanism that includes both the reduction of anti-oxidative defense and the production of ROS by mitochondrial damage (Sandbichler and Höckner 2016). Numerous findings have shown that Cd exposure produces O 2 − and NO.…”

Section: Resultsmentioning

confidence: 99%

Recombinant heat shock protein 27 (HSP27/HSPB1) protects against cadmium-induced oxidative stress and toxicity in human cervical cancer cells

Alvarez-Olmedo

Biaggio

Koumbadinga

et al. 2017

Cell Stress and Chaperones

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Cadmium (Cd) is a carcinogen with several well-described toxicological effects in humans, but its molecular mechanisms are still not fully understood. Overexpression of heat shock protein 27 (HSP27/HSPB1)-a multifunctional protein chaperone-has been shown to protect cells from oxidative damage and apoptosis triggered by Cd exposure. The aims of this work were to investigate the potential use of extracellular recombinant HSP27 to prevent/counteract Cd-induced cellular toxicity and to evaluate if peroxynitrite was involved in the development of Cd-induced toxicity. Here, we report that the harmful effects of Cd correlated with changes in oxidative stress markers: upregulation of reactive oxygen species, reduction in nitric oxide (NO) bioavailability, increment in lipid peroxidation, peroxynitrite (PN), and protein nitration; intracellular HSP27 was reduced. Treatments with Cd (100 μM) for 24 h or with the peroxynitrite donor, SIN-1, decreased HSP27 levels (~50%), suggesting that PN formation is responsible for the reduction of HSP27. Pre-treatments of the cells either with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) (a pharmacological inhibitor of NO synthase) or with recombinant HSP27 (rHSP27) attenuated the disruption of the cellular metabolism induced by Cd, increasing in a 55 and 52%, respectively, the cell viability measured by CCK-8. Cd induced necrotic cell death pathways, although apoptosis was also activated; pre-treatment with L-NAME or rHSP27 mitigated cell death. Our findings show for the first time a direct relationship between Cd-induced toxicity and PN production and a role for rHSP27 as a potential therapeutic agent that may counteract Cd toxicity.

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“…On the other hand, in our study spinosad application caused a significant increase in HSP70 concentration in the body of the insects from the Cd-strain in comparison to the insects from the control strain. Enhanced synthesis of heat shock proteins is, in general, regarded as a protective mechanism against environmental stress (Multhoff et al 2015;Sandbichler and Höckner 2016). However, the reports can be found presenting examples of adapted ecotypes of invertebrates, that are insensitive to pollutants, including cadmium, and, at the same time, they have low HSP concentration (Haap and Köhler 2009;Haap et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Cross tolerance in beet armyworm: long-term selection by cadmium broadens tolerance to other stressors

et al. 2017

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Long lasting exposure of animals to stressing factor may lead to the selection of population able to cope with the stressor at lower cost than unexposed individuals. The aim of this study was to assess whether 130-generational selection of a beet armyworm to cadmium in food might have induced tolerance also to other stressors. The potential tolerance was assessed by means of unspecific stress markers: HSP70 concentration, DNA damage level, and energy budget indices in L5 larval instars of beet armyworm. The animals originated from Cd-exposed and control strains exposed additionally in a short-term experiment to high/low temperature or pesticide-spinosad. The application of the additional stressors caused, in general, an increase in the levels of studied parameters, in a straindependent manner. The most significant increase was found in HSP70 level in the individuals from the Cd-strain exposed to various spinosad concentration. Therefore, multigenerational contact with cadmium caused several changes that enable the insect to survive under a chronic stress, preparing the organism to the contact with an additional, new stressor. This relationship may be described as a sort of cross tolerance. This may, possibly, increase the probability of population survivorship and, at the same time, decrease the efficiency of pesticide-based plant protection efforts.

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Cadmium Protection Strategies—A Hidden Trade-Off?

Cited by 85 publications

References 193 publications

Cadmium effects on DNA and protein metabolism in oyster (Crassostrea gigas) revealed by proteomic analyses

Cadmium effects on DNA and protein metabolism in oyster (Crassostrea gigas) revealed by proteomic analyses

Recombinant heat shock protein 27 (HSP27/HSPB1) protects against cadmium-induced oxidative stress and toxicity in human cervical cancer cells

Cross tolerance in beet armyworm: long-term selection by cadmium broadens tolerance to other stressors

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