Cytotoxicity and DNA-damage in human lung epithelial cells exposed to respirable α-quartz

Fanizza, Carla; Ursini, Cinzia Lucia; Paba, Emilia; Ciervo, Aureliano; Francesco, A. Di; Maiello, Raffaele; Simone, Paolo De; Cavallo, Delia

doi:10.1016/j.tiv.2006.12.002

Cited by 42 publications

(36 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In an our previous study (Fanizza et al, 2007), SEM analysis of cells (A549) exposed to quartz for 4 h revealed evident changes in the cellular surface after treatment in a concentration-dependent response. Cells exposed to 25 and 50 µg ml −1 (52.35 or 104.71 µg cm −2 ) of quartz showed small bleb development, while microvilli morphological changes were detected in cells treated with 100 µg ml −1 (104.71 µg cm −2 ) of quartz, in which they became shorter and embedded in the cell surface.…”

Section: Discussionmentioning

confidence: 75%

“…In general the reactivity of the particle surface is closely related to the ability of quartz to generate ROS (Fubini et al, 1990), and since ROS are implicated in both DNA damage and carcinogenesis (Marnett, 2000), it was postulated that the particle surface is involved in DNA damage induced by quartz. Cytotoxic and genotoxic eff ects of crystalline silica were evidenced in some in vitro studies (Elias et al, 2000;Lin et al, 2006;Wang et al, 2007;Fanizza et al, 2007). Moreover silicainduced cytokine release from human epithelial lung cell line (Hetland et al, 2001) and from human alveolar macrophages (Gosset et al, 1991) was found.…”

Section: Introductionmentioning

confidence: 95%

“…Studies conducted in diff erent urban areas of the USA (Davis et al, 1984) and in Italy (Puledda et al, 1999;De Berardis et al, 2007) (Rome) found crystalline silica levels in the PM10 range. In vitro (Balduzzi et al, 2004;Fanizza et al, 2007) and in vivo (Porter et al, 2002) studies demonstrated that aged fractured quartz also may exert adverse eff ects.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

Fanizza¹,

Fresegna

Maiello

et al. 2009

J of Applied Toxicology

Self Cite

View full text Add to dashboard Cite

A causal pathway between quartz, silicosis and lung cancer has been postulated. The aim of our study was to assess cytotoxic effects induced in a human lung epithelial cell line (A549) by exposure to alpha-quartz. Cells were exposed to respirable alpha-quartz (SRM1878a, NIST) at 25, 50 or 100 microg ml(-1 )for 24 h and at 50 or 100 microg ml(-1) for 48 h. Cytotoxic effects were analyzed by scanning electron microscopy (SEM), apoptotic morphology analysis with Hoechst staining and lactate dehydrogenase (LDH) release assay. In cells exposed to alpha-quartz for 24 h, a concentration-dependent bleb development and in particular the localization of blebs at the cell edge at higher concentrations were observed. The blebbing phenomenon was more evident after 48 h of exposure to 50 or to 100 microg ml(-1) of alpha-quartz and large blebs were localized at the cell edge. At the same concentrations surface smoothing was also observed. Moreover the presence of holes and tears was detected at the highest concentration both at 24 and 48 h. Results of morphological analysis with Hoechst stain evidenced an increase concentration-time dependent of apoptotic cell percentage that was more marked after 48 h exposure to 100 microg ml(-1) and a prevalence of late apoptosis stage with the increase of exposure time and concentration. Cells exposed to 50 or 100 microg ml(-1) of alpha-quartz for 24 and 48 h produced a significant increase in LDH release. The concentration-time-dependent bleb induction evidenced by SEM correlates with the increase of apoptotic cells and LDH activity release, demonstrating the onset of cytotoxic effects in human lung cells exposed to alpha-quartz.

show abstract

Section: Discussionmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

Fanizza¹,

Fresegna

Maiello

et al. 2009

J of Applied Toxicology

Self Cite

View full text Add to dashboard Cite

show abstract

“…A549 cells are considered as target cells for lung carcinogenesis induced by inhalable xenobiotics and have been already used in other studies on eff ects of Cr(VI) (Hodges et al, 2001;Hodges and Chipman, 2002;Liu et al, 2001). These cells have structural and biochemical characteristics of human type II cells and have been successfully applied to investigate the presence of DNA damage by several xenobiotics (Kim et al, 2001;Fanizza et al, 2007;Don Porto Carero et al, 2001;Hodges et al, 2001;Knaapen et al, 2002;Liu et al, 2001). Since cellular response to Cr(VI) may diff er in diff erent cell types, we also used BEAS-2B that derived from normal human bronchial epithelial cells and are potential targets of chromium lung toxicity (Samet et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Direct‐oxidative DNA damage and apoptosis induction in different human respiratory cells exposed to low concentrations of sodium chromate

Cavallo

Ursini

Fresegna

et al. 2009

J of Applied Toxicology

Self Cite

View full text Add to dashboard Cite

The mechanism of Cr(VI) genotoxicity has still not been elucidated. We used Fpg-modified comet assay to assess direct-oxidative DNA damage on human lung (A549) and bronchial (BEAS-2B) cells exposed to 0.1, 0.5, 1.0 and 10 microm sodium chromate for 0.5, 1 and 4 h. Moreover we evaluated apoptosis by morphological analysis and caspase-3 activity, also after 24 h. On A549 cells a time-dependent DNA damage, expressed as tail DNA%, beginning from 0.5 microm was found. For oxidative DNA damage an induction after 30 min to 0.5 microm decreasing with time, and a time-dependent increase at 10 microm was found, indicating for low Cr(VI) concentration the oxidative stress as the first event followed by direct DNA damage and for the highest concentration a time-dependent increase in oxidative DNA damage. On BEAS-2B cells DNA damage was induced within 1 h at 0.5-10 microm, without changes with time, showing that BEAS-2B cells are able to resist to Cr(VI) genotoxicity. Early oxidative DNA damage at 0.1 microm decreasing with time was also found. Significant apoptosis was observed by morphological analysis in A549 cells and to a lower extent in BEAS-2B at 10 microm. The exposure to 10 microm induced caspase-3 activity after 4 h in BEAS-2B and after 24 h in A549 cells. The findings show a higher responsiveness of A549 cells to genotoxic effect of Cr(VI) and early transient oxidative DNA damage in BEAS-2B. The results emphasize the suitability of this experimental model to evaluate the early genotoxic response of different cells to non-cytotoxic concentrations of Cr(VI) on target organ.

show abstract

“…Membrane damage was evaluated by measuring the LDH release in the culture medium (Fanizza et al, 2007). The HeLa cells were cultured in the absence of doxycycline for 3 days and treated with 500 nM 2-ME or the vehicle for 24 h, before the media was collected for the LDH release assay.…”

Section: Cytotoxicity Assaysmentioning

confidence: 99%

Targeting human 8-oxoguanine DNA glycosylase to mitochondria protects cells from 2-methoxyestradiol-induced-mitochondria-dependent apoptosis

et al. 2008

View full text Add to dashboard Cite

Cytotoxicity and DNA-damage in human lung epithelial cells exposed to respirable α-quartz

Cited by 42 publications

References 50 publications

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

Evaluation of cytotoxic concentration–time response in A549 cells exposed to respirable α‐quartz

Direct‐oxidative DNA damage and apoptosis induction in different human respiratory cells exposed to low concentrations of sodium chromate

Targeting human 8-oxoguanine DNA glycosylase to mitochondria protects cells from 2-methoxyestradiol-induced-mitochondria-dependent apoptosis

Contact Info

Product

Resources

About