Modulation of silica-induced lung injury by reducing lung non-protein sulfhydryls with buthionine sulfoximine

Abstract

A role for non-protein sulfhydryl moieties (NPSH) (e.g., glutathione) in silica (SI)-induced cellular inflammation and fibrosis was examined in C57B1/6 mice depleted of lung NPSH by buthionine sulfoximine (BSO). Lung NPSH levels in the BSO-treated groups were reduced to approx. 50% of the non-BSO-treated animals. In BSO-treated Si-injected (2 mg/mouse) animals, the number of pulmonary alveolar macrophages (PAM) lavaged from the lungs was significantly increased on day 1 and decreased on day 7. Moreover, BSO-treated Si-exposed mice evidenced significantly more lavage protein and albumin on days 1 and 3, respectively, than non-BSO-treated Si-exposed mice. Si-induced collagen deposition, however, was decreased by 18% in the BSO-treated animals. These data suggest that lung NPSH lessens the potential of silica to elicit acute lung injury.