Inhalative exposure to vanadium pentoxide causes DNA damage in workers: results of a multiple end point study

Area of Science:

• Environmental Health
• Toxicology
• Genetics

Background:

• Inhalative exposure to vanadium pentoxide (V(2)O(5)) is a known cause of lung cancer in rodent models.
• Occupational exposure to V(2)O(5) necessitates an understanding of its genotoxic effects in humans.

Purpose of the Study:

• To investigate the impact of V(2)O(5) exposure on DNA stability in workers from a V(2)O(5) factory.
• To assess biomarkers of DNA damage and chromosomal instability in exposed individuals.

Main Methods:

• The alkaline comet assay was used to determine DNA strand breaks in leukocytes from 52 workers and controls.
• The cytokinesis-block micronucleus (MN) cytome method was employed to evaluate chromosomal instability in lymphocytes from 23 workers and 24 controls.
• Lesion-specific enzymes were used to identify oxidized purines and pyrimidines.

Main Results:

• Workers exhibited significantly higher plasma vanadium concentrations (7-fold increase).
• Increased DNA migration due to oxidized purines (7%) and pyrimidines (30%) was observed in workers.
• Workers showed a 2.5-fold higher MN frequency, with 7-fold and 3-fold increases in nucleoplasmic bridges (NPBs) and nuclear buds (Nbuds), respectively.
• Reduced repair of bleomycin-induced DNA lesions and higher rates of necrosis were noted in the exposed group.

Conclusions:

• Vanadium pentoxide exposure induces DNA base oxidation and affects DNA repair mechanisms in occupationally exposed individuals.
• The formation of micronuclei, NPBs, and Nbuds indicates significant chromosomal instability.
• These findings suggest that V(2)O(5)-exposed workers face an elevated risk of cancer and other diseases associated with DNA instability.