Vanadium pentoxide induces pulmonary inflammation and tumor promotion in a strain-dependent manner

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Alison K. Bauer (Creator)
Elizabeth A. Rondini (Creator)
Dianne M. Walters (Creator)
East Carolina University (ECU )
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Abstract: Background: Elevated levels of air pollution are associated with increased risk of lung cancer. Particulate matter (PM) ontains transition metals that may potentiate neoplastic development through the induction of oxidative stress and nflammation a lung cancer risk factor. Vanadium pentoxide (V2O5) is a component of PM derived from fuel ombustion as well as a source of occupational exposure in humans. In the current investigation we examined the nfluence of genetic background on susceptibility to V2O5-induced inflammation and evaluated whether V2O5 unctions as a tumor promoter using a 2-stage (initiation-promotion) model of pulmonary neoplasia in mice. esults: A/J BALB/cJ (BALB) and C57BL/6J (B6) mice were treated either with the initiator 3-methylcholanthrene (MCA; 0 μg/g; i.p.) or corn oil followed by 5 weekly aspirations of V2O5 or PBS and pulmonary tumors were enumerated 20 eeks following MCA treatment. Susceptibility to V2O5-induced pulmonary inflammation was assessed in ronchoalveolar lavage fluid (BALF) and chemokines transcription factor activity and MAPK signaling were quantified n lung homogenates. We found that treatment of animals with MCA followed by V2O5 promoted lung tumors in both /J (10.3 ± 0.9 tumors/mouse) and BALB (2.2 ± 0.36) mice significantly above that observed with MCA/PBS or V2O5 lone (P < 0.05). No tumors were observed in the B6 mice in any of the experimental groups. Mice sensitive to tumor romotion by V2O5 were also found to be more susceptible to V2O5-induced pulmonary inflammation and yperpermeability (A/J>BALB>B6). Differential strain responses in inflammation were positively associated with levated levels of the chemokines KC and MCP-1 higher NFκB and c-Fos binding activity as well as sustained ERK1/2 ctivation in lung tissue. onclusions: In this study we demonstrate that V2O5 an occupational and environmentally relevant metal oxide unctions as an in vivo lung tumor promoter among different inbred strains of mice. Further we identified a positive elationship between tumor promotion and susceptibility to V2O5-induced pulmonary inflammation. These findings uggest that repeated exposures to V2O5 containing particles may augment lung carcinogenesis in susceptible ndividuals through oxidative stress mediated pathways. Originally published Particle and Fibre Toxicology Vol. 7 No. 9 Apr 2010

Additional Information

Particle and Fibre Toxicology. 7:9(April 2010) p. 1-13.
Language: English
Date: 2011
particulate matter, vanadium pentoxide, Lungs--Cancer

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