Lisa Tran

Mentor:

Dr. Xinxin Ding

Department: 

Pharmacology and Toxicology

Abstract: 

Chronic exposure to inorganic arsenic (iAs) is associated with increased incidence of lung diseases in humans, posing a significant health risk to populations residing near superfund sites. iAs exposure may occur via inhalation of dust particles and ingestion of contaminated water or food. iAs inhibits wound healing in vitro in human lung epithelial cells, but it is unclear whether iAs inhibits lung tissue repair in vivo. This study examines the effects of NaAsO₂ exposure via drinking water on lung tissue repair in an airway injury mice model induced by an intraperitoneal injection of naphthalene (NA, 200 mg/kg). Acute lung toxicity and subsequent tissue repair were monitored on day 1 (6 weeks after starting 25 ppm iAs exposure) and day 14 after NA exposure, respectively, by measuring the abundance of Club Cell Secretory Protein (CCSP)-positive cells in the airways. Percentage of CCSP-positive cells was significantly decreased in the distal airways of (NaAsO₂ + NA)-treated mice compared to (water + NA)-treated mice (by ~30%, p<0.05). The predominant As species in the serum and lungs of mice exposed to NaAsO₂ in drinking water for 1-28 days was found to be dimethylarsinic acid, not As(III) or As(V). These data indicate that iAs exposure via drinking water inhibits lung tissue repair and suggest the need to identify the As species responsible for the inhibition in vivo and assess whether inhalation exposure to iAs can cause greater inhibition.