Cytotoxic Response Profiles of Cultured Renal Epithelial and Mesenchymal Cells toSelected Aromatic Hydrocarbons

Parrish, Alan R.; Alejandro, Napoleon F.; Bowes, Russell C.; Ramos, Kenneth S.

doi:10.1016/s0887-2333(97)00118-5

Cited by 20 publications

(14 citation statements)

References 26 publications

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“…In the Krebs cycle, succinate can be converted into fumarate by succinate dehydrogenase (Lankadurai et al, 2013). The alteration of succinate and fumarate levels means a possible disruption in the conversion of succinate to fumarate induced by the released Ag + (Lankadurai et al, 2011;Parrish et al, 1998). Since succinate dehydrogenase is the only enzyme bound to the inner mitochondrial membrane in the Krebs cycle, Ag + released from AgNPs probably disrupts the functioning of succinate dehydrogenase by binding to the inner mitochondrial membrane and affecting its stabilization (Horton et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Peijnenburg

et al. 2014

Nanotoxicology

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To disentangle the contribution of ionic and nanoparticulate Ag to the overall toxicity to the earthworm Eisenia fetida, a semi-permeable membrane strategy was used to separate Ag + released from silver nanoparticles (AgNPs) in an aqueous exposure. Internal Ag fractionation, activities of antioxidant enzymes and metabolites in E. fetida were determined after 96 h of exposure to two sizes of polyvinylpyrrolidone-coated AgNPs. The response of the antioxidant system combined with the content of malondialdehyde indicated that the Ag + released from AgNPs induced significant oxidative stress to the earthworms. Ag accumulated from AgNPs was predominantly associated with the granules and cell membrane compartments, whereas dissolved Ag was localized in the cytosol-containing fraction. In both Ag + exposures, two intermediates in the Krebs cycle, succinate and fumarate, were significantly elevated and depleted, respectively. A similar alteration pattern was seen in groups exposed to both smaller AgNPs (S AgNP, 10 nm) and larger AgNP (L AgNP, 40 nm), indicating that these effects in E. fetida were induced by exposure to released Ag + . In addition, unique metabolic responses including decreased malate and glucose levels in S AgNP-exposed earthworms could be associated with exposure to nanoparticulate silver. Increased leucine and arginine and decreased ATP and inosine levels were observed in L AgNP exposures only, which clearly demonstrated a size-specific effect of AgNPs. Collectively, this study provided strong evidence that nanosilver acts by a different mechanism than ionic silver to cause acute toxicity to E. fetida, but further verification under different environmental conditions is needed.

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Section: Discussionmentioning

confidence: 99%

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Peijnenburg

et al. 2014

Nanotoxicology

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“…A transitory impairment of energy metabolism or mitochondrial function appears to be an action of BaP that had previously gone unnoticed, but the literature contains hints of a similar phenomenon. Parrish et al [35] found an increase in mitochondrial membrane fragility upon exposure of rat renal epithelial and mesenchymal cells to BaP, and this effect was greater after 4 hours as compared to 24 hours of exposure.…”

Section: Transitory Metabolic Disruptionmentioning

confidence: 98%

Transitory metabolic disruption and cytotoxicity elicited by benzo<[>a<]>pyrene in two cell lines from rainbow trout liver

Schirmer

Chan

Bols

2000

J. Biochem. Mol. Toxicol.

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Two cell lines, RTL‐W1 and R1, from rainbow trout liver were used to investigate the effects of benzo[A]pyrene (BaP). BaP induced a catalytic measure of CYP1A, 7‐ethoxyresorufin‐O‐deethylase (EROD) activity, in the rainbow trout liver cell line RTL‐W1 but not in R1. Geldanamycin inhibited EROD induction by BaP. Potential BaP metabolites, BaP‐7,8‐dihydrodiol (BDP) and 6,12‐BaP quinone (BQ) also induced EROD activity in RTL‐W1. Very low BaP concentrations slightly stimulated cell proliferation in both cell lines. Higher BaP concentrations caused cytotoxicity in RTL‐W1 but not in R1. Cytotoxicity was detected in a cell viability assay with 5‐carboxyfluorescein diacetate acetoxymethyl ester, and as a decline in cell number. In both cell lines, BaP exposure impaired the reduction of the redox dye, alamar Blue (AB). After BaP removal, AB reduction recovered. Similar results were observed with BQ. As AB monitors metabolic activity, this novel phenomenon was termed transitory metabolic disruption. This decline in AB readings that was caused by BaP was ameliorated in RTL‐W1 by α‐naphthoflavone and geldanamycin, which suggests a role for CYP1A, and in R1 by indomethacin, which suggests involvement of prostaglandin‐H‐synthase. The significance of the response to BaP that is detected with AB and whether other PAHs cause it will be interesting future questions. © 2000 John Wiley & Sons, Inc. J Biochem Toxicol 14:262–276, 2000

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“…Some PAHs are classified as human carcinogens, and also may exert their negative effects on the human organism by induction of the oxidative stress. Exposure to PAHs results in a variety of molecular responses in an organism such as enzyme activation, oxidation, and/or signal transduction (Kelley et al, 1997;Parrish et al, 1998;Kang et al, 2010). These responses are mainly mediated by the AHR/aryl hydrocarbon nuclear translocator (ARNT) signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…The toxicity of aromatic hydrocarbons often involves cellular alternations associated with oxidative stress (Parrish et al, 1998). Although many PAHs have been shown to interfere with immune responses, the mechanisms underlying immunotoxicity of these compounds are not fully understood (Hwang et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Docosahexaenoic acid regulates gene expression in HUVEC cells treated with polycyclic aromatic hydrocarbons

et al. 2015

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Cytotoxic Response Profiles of Cultured Renal Epithelial and Mesenchymal Cells toSelected Aromatic Hydrocarbons

Cited by 20 publications

References 26 publications

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Transitory metabolic disruption and cytotoxicity elicited by benzo<[>a<]>pyrene in two cell lines from rainbow trout liver

Docosahexaenoic acid regulates gene expression in HUVEC cells treated with polycyclic aromatic hydrocarbons

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Cytotoxic Response Profiles of Cultured Renal Epithelial and Mesenchymal Cells toSelected Aromatic Hydrocarbons

Cited by 20 publications

References 26 publications

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Both released silver ions and particulate Ag contribute to the toxicity of AgNPs to earthwormEisenia fetida

Transitory metabolic disruption and cytotoxicity elicited by benzo<&lsqb;>a<&rsqb;>pyrene in two cell lines from rainbow trout liver

Docosahexaenoic acid regulates gene expression in HUVEC cells treated with polycyclic aromatic hydrocarbons

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Transitory metabolic disruption and cytotoxicity elicited by benzo<[>a<]>pyrene in two cell lines from rainbow trout liver