Lack of p53 induction in fish cells by model chemotherapeutics

Embry, Michelle R.; Billiard, Sonya M.; Giulio, Richard T. Di

doi:10.1038/sj.onc.1209238

Cited by 29 publications

(11 citation statements)

References 44 publications

(48 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this regard, Puisieux et al (1991) verified that AFB 1 -epoxide can bind to codon 249 and generate mutations in p53 gene in vitro. Although p53 has been found in bony fish genomes, further studies are needed to determine if mutations may occur at p53 sites in rainbow trout exposed to AFB 1 (Embry et al 2006). Recent studies reported that an overexpression of mdm2 (negative regulator of p53) occurred both in Xenopus and in zebrafish, leading to tumor formation in the former, and no tumor development in the latter, suggesting phylogenetic differences in p53 regulation in lower vertebrates (Thisse et al 2000;Embry et al 2006).…”

Section: Mutagenicitymentioning

confidence: 96%

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Santacroce

Conversano

Casalino

et al. 2007

Rev Fish Biol Fisheries

157

119

View full text Add to dashboard Cite

Among all known mycotoxins, aflatoxins represent the most investigated, widespread and worrisome source of contamination of foods and feed worldwide. In the early 1960s, soon after the finding of aflatoxin B 1 (AFB 1 ) in the feedstuffs of aquacultured rainbow trout that had died in an epizootic of hepatomas, great scientific discoveries were made in several areas by a number of researchers under the direction of scientists like J. Halver, R. 0. Sinnhuber, G. S. Bailey, J. D. Hendricks and colleagues. Since that time, several studies have focused on the identification of new isoenzymes involved in AFB 1 metabolism and on the discovery of new modulators in AFB 1 -induced cancer initiation and progression. However, metabolic and toxicological studies on aflatoxins in marine aquacultured species are fragmented and restricted to a limited number of fish species. Aflatoxins exert a substantial impact on the fish farming production, causing disease with high mortality and a gradual decline of reared fish stock quality, thus representing a significant problem in aquaculture systems. Based on these considerations, the goals of this review article are: (1) to gather the currently available scientific information, summarising existing data on aflatoxin contamination on feeds and fishmeals, and toxicological effects induced in reared aquatic species; (2) to make a comparative analysis of AFB 1 metabolism in the most representative species studied; (3) to gain new insights on the risk of DNA damage caused by aflatoxins on fish genomes and their role in cancer development.

show abstract

Section: Mutagenicitymentioning

confidence: 96%

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Santacroce

Conversano

Casalino

et al. 2007

Rev Fish Biol Fisheries

157

119

View full text Add to dashboard Cite

show abstract

“…This clearly supports the existence of a conserved DNA damage-induced apoptosis pathway in vertebrates with the transcriptional factor p53 playing a key role activating Puma, which, through activation of Bax, leads to MMP, release of cytochrome c and apoptosis. On the other hand, comparing to higher vertebrates, several differences in p53 expression and regulation have been reported in fish such as absence of tumorigenesis in zebrafish embryos injected with the p53-negative regulator Mdm2 [136] as well as lack of p53 induction in fish cells by model chemotherapeutics, albeit those same chemotherapeutics induced apoptosis [137]. Moreover, the low prevalence of p53 mutations found in wild fish [138,139] as well as in laboratory-exposed fish [129,130,140], compared to the high prevalence (>50%) of p53 mutations in human cancers, further suggest that p53 activation and function in fish species may differ from that of other vertebrates [137].…”

Section: Intrinsic Pathway In Fishmentioning

confidence: 99%

“…On the other hand, comparing to higher vertebrates, several differences in p53 expression and regulation have been reported in fish such as absence of tumorigenesis in zebrafish embryos injected with the p53-negative regulator Mdm2 [136] as well as lack of p53 induction in fish cells by model chemotherapeutics, albeit those same chemotherapeutics induced apoptosis [137]. Moreover, the low prevalence of p53 mutations found in wild fish [138,139] as well as in laboratory-exposed fish [129,130,140], compared to the high prevalence (>50%) of p53 mutations in human cancers, further suggest that p53 activation and function in fish species may differ from that of other vertebrates [137]. However, it should be further investigated whether the differences mentioned above may be due to the fact that the experiments have been performed in vitro, as well as whether the low prevalence of p53 mutations reported in fish are associated to the fact that the studied fish were not old enough or were not allowed to live long enough in captivity for mutations to occur.…”

Section: Intrinsic Pathway In Fishmentioning

confidence: 99%

Fish and Apoptosis: Molecules and Pathways

Santos¹,

Vale²,

Reis³

et al. 2008

CPD

View full text Add to dashboard Cite

Apoptosis is a genetically controlled and evolutionarily conserved form of active cell death, albeit with an increase in complexity with continuing development. A high conservation at the functional and molecular level has been described between the players of the apoptotic machinery in invertebrates (Caenorhabditis elegans and Drosophila) and mammals. However, fish represent an excellent and advantageous model for the study of vertebrate development and disease, bridging the gap between the C. elegans/Drosophila and mouse/human models. Moreover, contrary to C. elegans and Drosophila, fish can be used for studying the development and function of vertebrate-specific organs and have a fully developed immune system similar to that of mammals. Last but not less important, both the environment and human health will obviously gain by using the knowledge generated through the use of fish models, for developing better prophylactic and therapeutic measures with impact on the aquaculture industry. In the present article, structural and functional data on the most important apoptosis related molecules, namely death-receptor, Bcl-2 and caspase families, and mechanisms are reviewed. The data point to the existence in fish of apoptotic pathways equivalent to those of mammals, making fish useful animal models for studying apoptosis, which may have great applicability for the advance of the knowledge on the role of apoptotic cell death in human apoptosis-related disorders as well as in pharmaceutical design.

show abstract

“…In the present study, we therefore investigated the role of AVD and ion fluxes in cells from fish, trying to elucidate some of the principle mechanisms operative in lower vertebrate apoptosis. Previous examination of the molecular apoptotic machinery of fish has revealed both highly conserved features as well as potentially interesting dissimilarities compared to the molecular network established in mammals [12][13][14][15]. We thus aimed at elucidating how physiological aspects of apoptosis in fish cells compare to those described in mammals.…”

Section: Introductionmentioning

confidence: 95%

Staurosporine-induced cell death in salmonid cells: the role of apoptotic volume decrease, ion fluxes and MAP kinase signaling

et al. 2007

View full text Add to dashboard Cite

Apoptotic cell death in mammalian models is frequently associated with cell shrinkage. Inhibition of apoptotic volume decrease (AVD) is cytoprotective, suggesting that cell shrinkage is an important early event in apoptosis. In salmonid hepatoma and gill cells staurosporine induced apoptosis, as assessed by activation of effector caspases, nuclear condensation, and a decrease of mitochondrial membrane potential (MMP), and these changes were accompanied by cell shrinkage. The Cl- transport inhibitor DIDS and the K+ channel inhibitor quinidine prevented AVD, but only DIDS inhibited apoptosis. Other Cl- flux inhibitors, as well as a pan-caspase inhibitor, did not prevent cell shrinkage, but still prevented caspase activation. Furthermore, regulatory volume decrease (RVD) under hypotonic conditions was not facilitated, but diminished in apoptotic cells. Since all transport inhibitors used blocked RVD, but only DIDS and quinidine inhibited AVD, the ion transporters involved in both processes are apparently not identical. In addition, our data indicate that inhibition of Cl- fluxes rather than blocking cell shrinkage or K+ fluxes is important for preventing apoptosis. In line with this, inhibition of MAP kinases reduced RVD and not AVD, but still diminished caspase activation. Finally, we observed that MAP kinases were activated upon staurosporine treatment and that at least activation of ERK was prevented when AVD was inhibited.

show abstract

Lack of p53 induction in fish cells by model chemotherapeutics

Cited by 29 publications

References 44 publications

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Aflatoxins in aquatic species: metabolism, toxicity and perspectives

Fish and Apoptosis: Molecules and Pathways

Staurosporine-induced cell death in salmonid cells: the role of apoptotic volume decrease, ion fluxes and MAP kinase signaling

Contact Info

Product

Resources

About