Int. J. Environ. Res. Public Health 2012, 9 487 Figure 10. 2-D gel profile of tubulins, MAPs, and other cytoskeletal proteins in As3+-treated cells. Growth-arrested RFL6 cells were labeled with [35S]methionine (50 Ci/mL) in the absence (A) or presence (B) of 10 µM As3+ for 24 h. Cells treated without (C) or with (D) 5 µg/mL nocodazole, an MT depolymerization agent, at the last 3 h of the metabolic labeling, were used as a positive control. The MT protein-rich extracts with identical redioactivity from control and treated cells were processed for 2-D gel analysis (α, β and A indicate α tubulin, β tubulin and actin, respectively). For MAP nomenclature, e.g., MAP56/6.5, the numbers refer to their apparent molecular weight (MW in kDa) and isoelectric point (pI), respectively. Protein quantitation was measured by the 1 D Scan EX software. Arrowheads indicate altered MAPs. 4. Discussion Our previous studies have shown As3+ perturbation of the cytoskeletal organization and cellular glutathione homeostasis in Swiss 3T 3 cells [21]. The lung is a major target organ for arsenic. In this report, we further evaluated As3+ effects on the organization of MTs, a critical element of the cytoskeleton, in vitro, in cultured rat fetal lung fibroblasts and in lungs of the animal model. RFL6 cells were selected as an in vitro model in this study because they display a typical MT morphology sensitive to As3+ injury (Figure 1). Results indicated that As3+ disrupted MT assembly by targeting